Knowledge, attitudes, practices, and self-efficacy of the Chinese public regarding cardiopulmonary resuscitation: an online cross-sectional survey.

Objective: To evaluate the current status of Chinese public's knowledge, attitudes, practices (KAP) and self-efficacy regarding cardiopulmonary resuscitation (CPR), and to analyze the factors that influence KAP and self-efficacy. Methods: An online cross-sectional survey was conducted from February to June 2022 in Mainland China via a self-designed self-filled questionnaire. Potential participants were recruited through WeChat by convenience sampling and snowball sampling methods. Descriptive and quantitative analyses were used for statistical analysis. Results: The survey included 4,450 participants from 31 provinces, autonomous regions, or municipalities across Mainland China, aged 18 or above. The public's average understanding (clear and very clear) of the knowledge regarding CPR was 67.4% (3,000/4,450), with an average proportion of positive attitudes at 96.8% (4,308/4,450). In practice, the average proportion of good practices was 92.8% (4,130/4,450), while the percentage of good self-efficacy averaged at 58.9% (2,621/4,450), only 42.4% (1,885/4,450) of the participants had confidence in the correct use of automated external defibrillator (AED). Pearson correlation analysis showed a significantly positive correlation among knowledge, attitude, practice, and self-efficacy (p < 0.01). Multiple linear regression analysis revealed that several factors have a significant influence on the public's CPR KAP and self-efficacy, including ever having received CPR training (p < 0.001), hearing about AED (p < 0.001), performing CPR on others (p < 0.001), hearing about CPR (p < 0.001), occupation (p < 0.001), personal health status (p < 0.001), education level (p < 0.001), gender (p < 0.001), and encountering someone in need of CPR (p = 0.021). Conclusion: The Chinese public demonstrates good knowledge of CPR, positive attitude, and high willingness to perform CPR. However, there is still room for improvement in the mastery of some professional knowledge points related to CPR and AED. It should be noted that knowledge, attitude, practice, and self-efficacy are interrelated and influence each other. Factors such as prior CPR training, hearing about AED, having performed CPR before, hearing about CPR, occupation, personal health status, education level, gender, and having encountered someone in need of CPR have a significant impact on the public's KAP and self-efficacy.

[Protective effect of metformin on pulmonary fibrosis caused by paraquat through activating AMP-activated protein kinase pathway].

OBJECTIVE: To observe whether metformin (MET) inhibits transforming growth factor-ß1 (TGF-ß1)/Smad3 signaling pathway by activating adenosine activated protein kinase (AMPK), so as to alleviate the pulmonary fibrosis caused by paraquat (PQ) poisoning in mice. METHODS: Male C57BL/6J mice were randomly divided into the Control group, PQ poisoning model group (PQ group), MET intervention group (PQ+MET group), AMPK agonist group (PQ+AICAR group), and AMPK inhibitor group (PQ+MET+CC group), according to a random number table method. A mouse model of PQ poisoning was established by one-time peritoneal injection of 1 mL PQ solution (20 mg/kg). The Control group was injected with the same volume of normal saline. After 2 hours of modeling, the PQ+MET group was given 2 mL of 200 mg/kg MET solution by gavage, the PQ+AICAR group was given 2 mL of 200 mg/kg AICAR solution by intraperitoneal injection, the PQ+MET+CC group was given 2 mL of 200 mg/kg MET solution by gavage and then 1 mL complex C (CC) solution (20 mg/kg) was intraperitoneally injected, the Control group and PQ group were given 2 mL of normal saline by gavage. The intervention was given once a day for 21 consecutive days. The 21-day survival rate of ten mice in each group was calculated, and the lung tissues of remaining mice were collected at 21 days after modeling. The pathological changes of lung tissues were observed under light microscope after hematoxylin-eosin (HE) staining and Masson staining, and the degree of pulmonary fibrosis was evaluated by Ashcroft score. The content of hydroxyproline in lung tissue and oxidative stress indicators such as malondialdehyde (MDA) and superoxide dismutase (SOD) were detected. The protein expressions of E-cadherin, α-smooth muscle actin (α-SMA), phosphorylated AMPK (p-AMPK), TGF-ß1 and phosphorylated Smad3 (p-Smad3) in lung tissue were detected by Western blotting. RESULTS: Compared with the Control group, the 21 days survival rate was significantly reduced, lung fibrosis and Ashcroft score were significantly increased in PQ group. In addition, the content of hydroxyproline, MDA and the protein expressions of α-SMA, TGF-ß1 and p-Smad3 in lung tissue were significantly increased, while the activity of SOD and the protein expressions of E-cadherin and p-AMPK were significantly decreased in PQ group. Compared with the PQ group, the 21 days survival rates of mice were significantly improved in the PQ+MET group and PQ+AICAR group (70%, 60% vs. 20%, both P < 0.05). The degree of pulmonary fibrosis and the Ashcroft score were significantly reduced (1.50±0.55, 2.00±0.63 vs. 6.67±0.52, both P < 0.05). The content of hydroxyproline and MDA in lung tissue, as well as α-SMA, TGF-ß1 and p-Smad3 protein expressions were significantly reduced [hydroxyproline (mg/L): 2.03±0.11, 3.00±0.85 vs. 4.92±0.65, MDA (kU/g): 2.06±1.48, 2.10±1.80 vs. 4.06±1.33, α-SMA/GAPDH: 0.23±0.06, 0.16±0.06 vs. 1.00±0.09, TGF-ß1/GAPDH: 0.28±0.03, 0.53±0.05 vs. 0.92±0.06 p-Smad3/GAPDH: 0.52±0.04, 0.69±0.06 vs. 1.11±0.10, all P < 0.05], SOD activity and the protein expressions of E-cadherin and p-AMPK were significantly increased [SOD (µmol/g): 39.76±1.35, 33.03±1.28 vs. 20.08±1.79, E-cadherin/GAPDH: 0.91±0.08, 0.72±0.08 vs. 0.26±0.04, p-AMPK/GAPDH: 0.62±0.04, 0.60±0.01 vs. 0.20±0.04, all P < 0.05]. However, these protective effects of MET were inhibited by the addition of AMPK inhibitor CC solution. CONCLUSIONS: MET can effectively alleviate the degree of pulmonary fibrosis in mice poisoned with PQ, and its mechanism may be related to the activation of AMPK and inhibition of TGF-ß1/Smad3 signaling pathway, which can be inhibited by AMPK inhibitor CC.

A typically progressive dissection of the internal carotid artery with recurrent hiccups: A case report with continuous 2-year data recording.

Patients with internal carotid artery dissection (ICAD) usually report headache, neck pain, Horner's syndrome, and ischemic stroke. Because the posterior cranial nerve is involved, some patients may show different forms of posterior cranial nerve paralysis. There have been no reports of patients with ICAD showing repeated hiccups. Here, to help clinicians identify ICAD early and gain a better understanding of the atypical manifestations of the disease, we report an atypical case of recurrent hiccup symptoms caused by ICAD.

Therapeutic and adverse effects of adrenaline on patients who suffer out-of-hospital cardiac arrest: a systematic review and meta-analysis.

OBJECTIVE: The efficacy and safety of epinephrine in patients with out-of-hospital cardiac arrest (OHCA) remains controversial. The meta-analysis was used to comprehensively appraise the influence of epinephrine in OHCA patients. METHODS: We searched all randomized controlled and cohort studies published by PubMed, EMBASE, and Cochrane Library from the inception to August 2022 on the prognostic impact of epinephrine on patients with OHCA. Survival to discharge was the primary outcome, while the return of spontaneous circulation (ROSC) and favorable neurological outcome were secondary outcomes. RESULTS: The meta-analysis included 18 studies involving 863,952 patients. OHCA patients with adrenaline had an observably improved chance of ROSC (RR 2.81; 95% CI 2.21-3.57; P = 0.001) in randomized controlled studies, but the difference in survival to discharge (RR 1.27; 95% CI 0.58-2.78; P = 0.55) and favorable neurological outcomes (RR 1.21; 95% CI 0.90-1.62; P = 0.21) between the two groups was not statistically significant. In cohort studies, the rate of ROSC (RR 1.62; 95% CI 1.14-2.30; P = 0.007) increased significantly with the adrenaline group, while survival to discharge (RR 0.73; 95% CI 0.55-0.98; P = 0.03) and favorable cerebral function (RR 0.42; 95% CI 0.30-0.58; P = 0.001) were lower than the non-adrenaline group. CONCLUSION: We found that both the randomized controlled trials (RCTs) and cohort studies showed that adrenaline increased ROSC in OHCA patients. However, they were unable to agree on a long-term prognosis. The cohort studies showed that adrenaline had an adverse effect on the long-term prognosis of OHCA patients (discharge survival rate and good neurological prognosis), but adrenaline had no adverse effect in the RCTs. In addition to the differences in research methods, there are also some potential confounding factors in the included studies. Therefore, more high-quality studies are needed to fully confirm the effect of adrenaline on the long-term results of OHCA.

[Research progress of S-nitrosoglutathione reductase inhibitors in the regulation of cerebral injury after cardiac arrest-cardiopulmonary resuscitation].

The cerebral ischemia-reperfusion injury (CIRI) after the cardiac arrest (CA)-cardiopulmonary resuscitation (CPR) was a complex pathophysiology process. Nitric oxide (NO) is a small molecule that mediates cell signal transduction in vivo and plays an important role in the regulation of brain function during ischemia/reperfusion (I/R). S-nitrosoglutathione reductase (GSNOR) inhibitor can regulate the synthesis and release of NO in vivo and has a protective effect on CIRI. Therefore, early administration of GSNOR to CA-CPR patients could be the main treatment method to improve the prognosis of those patients. A large number of studies have been done to improve the prognosis of CA-CPR in recent years. In order to provide reference for further research on the treatment and brain protection of CIRI after CA-CPR, the article reviewed the main mechanisms of brain injury after CA-CPR, the protective effect and mechanism of NO on cerebral I/R injury, the production and regulation of NO, in vivo, and the protective effect of GSNOR inhibitors on CIRI, especially the research progress of GSNOR inhibitors.

[Advances in the study of optimum chest compression point for adult cardiopulmonary resuscitation].

Chest compressions are a key component of cardiopulmonary resuscitation (CPR). The determination of the optimal compression point (OCP) in adult CPR is an indispensable critical factor for high quality chest compressions (CCs). At present, the OCP for adult CPR is still controversial, which still needs further research and discussion. To provide theoretical reference for determining the OCP, this paper reviews the research progress of the OCP of adult CPR from the development process of compression point and hemodynamic mechanism, so as to improve the quality of CCs and the outcome of cardiac arrest (CA) patients.

[Research progress on the relationship between diquat poisoning and nuclear factor E2-related factor 2 signaling pathway].

Since the production and use of paraquat was banned in China in 2016, the use of diquat (DQ) has been increasing and the clinical cases of DQ poisoning have also shown an increasing trend every year. The treatment of DQ poisoning is a worldwide medical problem, and there is no specific antidote. Studies have found that oxidative stress, lipid peroxidation, neurotoxicity, reproductive and developmental toxicity play an important role in DQ poisoning. Nuclear factor E2-related factor 2 (Nrf2) can inhibit oxidative stress, lipid peroxidation and inflammation by regulating the protein expression of upstream and downstream signaling molecules. Therefore, the role of Nrf2 signaling pathway in the poisoning and treatment of DQ has become a hot spot of attention for emergency critical care researchers in recent years. This paper reviews the relationship between Nrf2 signal pathway and DQ poisoning, in order to provide a theoretical basis for improving the treatment strategy for DQ poisoning.

Effects of Different Hypothermia on the Results of Cardiopulmonary Resuscitation in a Cardiac Arrest Rat Model.

Objective: To investigate the optimal temperature of hypothermia treatment in rats with cardiac arrest caused by ventricular fibrillation (VF) after the return of spontaneous circulation (ROSC). Methods: A total of forty-eight male Sprague-Dawley rats were induced by VF through the guidewire with a maximum of 5 mA current and untreated for 8 min. Cardiopulmonary resuscitation (CPR) was performed for 8 min followed by defibrillation (DF). Resuscitated rats were then randomized into the normothermia (37°C) group, milder (35°C) group, mild (33°C) group, or moderate (28°C) group. Hypothermia was immediately induced with surface cooling. The target temperature was maintained for 4 h before rewarming to 37 ± 0.5°C. Moreover, at the end of the 4 h, a rat in each group was randomly selected to be sacrificed for the cerebral cortex electron microscopy observation (n = 1). The other resuscitated animals were observed for up to 72 h after ROSC (n = 7). Left ventricular ejection fraction (LVEF) and left ventricular end diastolic volume (LVEDV) were measured. Survival time, survival rate, and neurological deficit score (NDS) were recorded for 72 h. Results: During hypothermia, higher LVEF was observed in the hypothermia groups when compared with normothermia group (35°C vs. 37°C, p < 0.05, 33°C and 28°C vs. 37°C, p < 0.01). Among the hypothermia groups, LVEF was higher in the 28°C group than that of 35°C (p < 0.05). However, both the heart rate (HR) (p < 0.01) and LVEDV (28°C vs. 35°C, p < 0.01, 28°C vs. 37°C and 33°C, p < 0.05) were lowest in the 28°C group when compared with the other groups. There were no significant differences of LVEF and LVEDV between the group 35°C and 33°C (p > 0.05). After rewarming, the LVEF of 35°C group was higher than that of group 37°C, 33°C, and 28°C (35°C vs. 37°C and 28°C, p < 0.01, 35°C vs. 33°C, p < 0.05). Group 35°C and 33°C resulted in longer survival (p < 0.01), higher survival rate (p < 0.01), and lower NDS (35°C vs. 37°C and 28°C, p < 0.01, 33°C vs. 37°C and 28°C, p < 0.05) compared with the group 37°C and 28°C. The extent of damage to cerebral cortex cells in group of 35°C and 33°C was lighter than that in group of 37°C and 28°C. The 35°C group spent less time in the process of cooling and rewarming than the group 33°C and 28°C (p < 0.01). Conclusions: An almost equal protective effect of milder hypothermia (35°C) and mild hypothermia (33°C) in cardiac arrest (CA) rats was achieved with more predominant effect than moderate hypothermia (28°C) and normothermia (37°C). More importantly, shorter time spent in cooling and rewarming was required in the 35°C group, indicating its potential clinical application. These findings support the possible use of milder hypothermia (35°C) as a therapeutic agent for postresuscitation.

Human Amnion-Derived MSCs Alleviate Acute Lung Injury and Hinder Pulmonary Fibrosis Caused by Paraquat in Rats.

Methods: First, the purity of hAD-MSCs was determined by morphological observation and FCM, and the effects on the survival of paraquat-poisoned Sprague-Dawley rats were observed. All rats were randomly divided into three groups, defined as the sham control group (n = 8), model group (n = 15), and hAD-MSC-transplanted group (n = 17). Pneumonocyte damage and inflammatory cell infiltration were investigated in the three groups of rats, untreated control, paraquat only, and paraquat+hAD-MSC transplanted, using H&E staining. Fibrosis was investigated in three groups of rats using Masson's trichrome staining and Sirius red staining. The profibrotic factor TGF-ß1, the composition of fibrotic collagen HYP, and the hAD-MSC-secreted immunosuppressive factor HLA-G5 in serum were investigated in the three groups of rats using ELISA. Furthermore, the distribution of hAD-MSCs was investigated in the three groups of rats using immunohistochemistry and hematoxylin staining. Results: The hAD-MSCs exhibited typical hallmarks of MSCs, improved the state of being and survival of paraquat-poisoned rats, reduced both lung injury and inflammation, and inhibited the progression of pulmonary fibrosis by decreasing the deposition of collagen and the secretion of both TGF-ß1 and HYP. The hAD-MSCs could survive in damaged lungs and secreted appropriate amounts of HLA-G5 into the serum. Conclusion: The obtained results indicate that hAD-MSCs used to treat paraquat-induced lung injury may work through anti-inflammatory and immunosuppressive pathways and the downregulation of profibrotic elements. This study suggests that the transplantation of hAD-MSCs is a promising therapeutic approach for the treatment of paraquat-intoxicated patients.

An interpretable machine learning model based on a quick pre-screening system enables accurate deterioration risk prediction for COVID-19.

A high-performing interpretable model is proposed to predict the risk of deterioration in coronavirus disease 2019 (COVID-19) patients. The model was developed using a cohort of 3028 patients diagnosed with COVID-19 and exhibiting common clinical symptoms that were internally verified (AUC 0.8517, 95% CI 0.8433, 0.8601). A total of 15 high risk factors for deterioration and their approximate warning ranges were identified. This included prothrombin time (PT), prothrombin activity, lactate dehydrogenase, international normalized ratio, heart rate, body-mass index (BMI), D-dimer, creatine kinase, hematocrit, urine specific gravity, magnesium, globulin, activated partial thromboplastin time, lymphocyte count (L%), and platelet count. Four of these indicators (PT, heart rate, BMI, HCT) and comorbidities were selected for a streamlined combination of indicators to produce faster results. The resulting model showed good predictive performance (AUC 0.7941 95% CI 0.7926, 0.8151). A website for quick pre-screening online was also developed as part of the study.

[Progress in the study of pulmonary fibrosis signaling pathways caused by paraquat poisoning].

Paraquat is a quaternary ammonium herbicide, which can be distributed in lung, liver, kidney, heart, brain and other organs through blood circulation, leading to multiple organ failure, especially lung injury. Due to the lack of effective treatment methods and specific antidotes, the prognosis of most patients with paraquat poisoning is very poor. The treatment of paraquat poisoning was a big problem for emergency doctors. Previous studies have found that pulmonary fibrosis caused by paraquat poisoning is closely related to a variety of pathological processes, such as oxidative stress, inflammatory reaction, mitochondrial damage, imbalance of extracellular matrixproduction (ECM) and degradation, which involve the activation or inhibition of various signaling pathways. In recent years, many researchers focused on clarifying the mechanism of paraquat induced pulmonary fibrosis, and some signaling pathways related to paraquat poisoning leading to pulmonary fibrosis have been found. A large number of studies have found that adenosine monophosphate activated protein kinase (AMPK) related signaling pathway, transforming growth factor-ß/Smad (TGF-ß/Smad) signaling pathway, mitogen-activated protein kinase (MAPK) related signaling pathway, Ras homolog gene/Rho associated kinases (Ras/ROCK) and Wnt/ß-catenin signal pathways are closely related to paraquat induced pulmonary fibrosis. In this paper, we reviewed signaling pathways related to paraquat induced pulmonary fibrosis, in order to provide more ideas for the clinical treatment of paraquat induced pulmonary fibrosis.

Effects of endovascular and surface cooling on resuscitation in patients with cardiac arrest and a comparison of effectiveness, stability, and safety: a systematic review and meta-analysis.

OBJECTIVES: This study conducted a meta-analysis to assess the effectiveness, stability, and safety of mild therapeutic hypothermia (TH) induced by endovascular cooling (EC) and surface cooling (SC) and its effect on ICU, survival rate, and neurological function integrity in adult CA patients. METHODS: We developed inclusion criteria, intervention protocols, results, and data collection. The results included outcomes during target temperature management as well as ICU stay, survival rate, and neurological functional integrity. The characteristics of the included population and each study were analyzed. RESULTS: Four thousand nine hundred thirteen participants met the inclusion criteria. Those receiving EC had a better cooling efficiency (cooling rates MD = 0.31[0.13, 0.50], p < 0.01; induced cooling times MD = - 90.45[- 167.57, - 13.33], p = 0.02; patients achieving the target temperature RR = 1.60[1.19, 2.15], p < 0.01) and thermal stability during the maintenance phase (maintenance time MD = 2.35[1.22, 3.48], p < 0.01; temperature fluctuation MD = - 0.68[- 1.03, - 0.33], p < 0.01; overcooling RR = 0.33[0.23, 0.49], p < 0.01). There were no differences in ICU survival rate (RR = 1.22[0.98, 1.52], p = 0.07, I2 = 0%) and hospital survival rate (RR = 1.02 [0.96, 1.09], p = 0.46, I2 = 0%), but EC reduced the length of stay in ICU (MD = - 1.83[- 3.45, - 0.21], p = 0.03, I2 = 49%) and improved outcome of favorable neurological function at discharge (RR = 1.15[1.04, 1.28], p < 0.01, I2 = 0%). EC may delay the hypothermia initiation time, and there was no significant difference between the two cooling methods in the time from the start of patients' cardiac arrest to achieve the target temperature (MD = - 46.64[- 175.86, 82.58]). EC was superior to non-ArcticSun in terms of cooling efficiency. Although there was no statistical difference in ICU survival rate, ICU length of stay, and hospitalization survival rate, in comparison to non-ArcticSun, EC improved rates of neurologically intact survival (RR = 1.16 [1.01, 1.35], p = 0.04, I2 = 0%). CONCLUSIONS: Among adult patients receiving cardiopulmonary resuscitation, although there is no significant difference between the two cooling methods in the time from the start of cardiac arrest to achieve the target temperature, the faster cooling rate and more stable cooling process in EC shorten patients' ICU hospitalization time and help more patients obtain good neurological prognosis compared with patients receiving SC. Meanwhile, although EC has no significant difference in patient outcomes compared with ArcticSun, EC has improved rates of neurologically intact survival.

Metformin Activates the Protective Effects of the AMPK Pathway in Acute Lung Injury Caused by Paraquat Poisoning.

OBJECTIVE: To observe whether metformin (MET) plays a protective role in acute lung injury (ALI) induced by paraquat (PQ) poisoning in rats by activating the AMPK/NF-κB signaling pathway. METHODS: PQ exposure was used to construct a rat model of ALI and a model of acute type II alveolar epithelial cell (RLE-6TN) injury, and MET intervention was performed. Rat lung tissue samples were collected to evaluate pathological changes in rat lung tissue, the oxidation index, and inflammatory factors; cell viability was detected by CCK-8 assays, and the protein expression levels of phospho-AMPK and phospho-NF-κBp65 in rat lung tissue and RLE-6TN cells were observed by Western blotting. RESULTS: Compared with the PQ group, the MET treatment group showed significantly (1) reduced lung wet/dry ratio (W/D: 4.67 ± 0.31 vs. 5.45 ± 0.40, P < 0.001), (2) reduced pathological changes in lung tissue, (3) decreased MDA levels (nmol/mg prot: 2.70 ± 0.19 vs. 3.08 ± 0.15, P < 0.001) and increased SOD and GSH-Px activities (U/mg prot: 76.17 ± 5.22 vs. 45.23 ± 6.58, 30.40 ± 2.84 vs. 21.00 ± 3.20; all P < 0.001) in lung tissue homogenate, (4) reduced levels of IL-1ß, IL-6, and TNF-α in lung tissue homogenates (pg/mL: 47.87 ± 5.06 vs. 66.77 ± 6.55; 93.03 ± 7.41 vs. 107.39 ± 9.81; 75.73 ± 6.08 vs. 89.12 ± 8.94; all P < 0.001), (5) increased activity of RLE-6TN cells (%: 0.69 ± 0.09, 0.76 ± 0.06, and 0.58 ± 0.03 vs. 0.50 ± 0.05; all P < 0.05), (6) decreased protein levels of phospho-NF-κBp65 in lung homogenates and RLE-6TN cells (p-NF-κB/NF-κB: 0.47 ± 0.09 vs. 0.81 ± 0.13; 0.26 ± 0.07 vs. 0.79 ± 0.13; all P < 0.01), and (7) upregulated protein expression of phospho-AMPK in lung homogenates and RLE-6TN cells (p-AMPK/AMPK: 0.88 ± 0.05 vs. 0.36 ± 0.12; 0.93 ± 0.03 vs. 0.56 ± 0.15; all P < 0.01). After the addition of the AMPK inhibitor Compound C (Com C), the protein expression levels of phospho-AMPK and phospho-NF-κBp65 returned to baseline. CONCLUSION: MET can effectively alleviate ALI induced by paraquat poisoning and increase the viability of cells exposed to paraquat. The mechanism may be related to the activation of the AMPK/NF-κB pathway, downregulation of inflammatory mediators such as IL-6 and TNF-α, and upregulation of the SOD and GSH-Px oxidation index, and these effects can be inhibited by the AMPK inhibitor Com C.

A meta-analysis of the resuscitative effects of mechanical and manual chest compression in out-of-hospital cardiac arrest patients.

OBJECTIVES: To evaluate the resuscitative effects of mechanical and manual chest compression in patients with out-of-hospital cardiac arrest (OHCA). METHODS: All randomized controlled and cohort studies comparing the effects of mechanical compression and manual compression on cardiopulmonary resuscitation in OHCA patients were retrieved from the Cochrane Library, PubMed, EMBASE, and Ovid databases from the date of their establishment to January 14, 2019. The included outcomes were as follows: the return of spontaneous circulation (ROSC) rate, the rate of survival to hospital admission, the rate of survival to hospital discharge, and neurological function. After evaluating the quality of the studies and summarizing the results, RevMan5.3 software was used for the meta-analysis. RESULTS: In total, 15 studies (9 randomized controlled trials and 6 cohort studies) were included. The results of the meta-analysis showed that there were no significant differences in the resuscitative effects of mechanical and manual chest compression in terms of the ROSC rate, the rate of survival to hospital admission and survival to hospital discharge, and neurological function in OHCA patients (ROSC: RCT: OR = 1.12, 95% CI (0.90, 1.39), P = 0.31; cohort study: OR = 1.08, 95% CI (0.85, 1.36), P = 0.54; survival to hospital admission: RCT: OR = 0.95, 95% CI (0.75, 1.20), P = 0.64; cohort study: OR = 0.98 95% CI (0.79, 1.20), P = 0.82; survival to hospital discharge: RCT: OR = 0.87, 95% CI (0.68, 1.10), P = 0.24; cohort study: OR = 0.78, 95% CI (0.53, 1.16), P = 0.22; Cerebral Performance Category (CPC) score: RCT: OR = 0.88, 95% CI (0.64, 1.20), P = 0.41; cohort study: OR = 0.68, 95% CI (0.34, 1.37), P = 0.28). When the mechanical compression group was divided into Lucas and Autopulse subgroups, the Lucas subgroup showed no difference from the manual compression group in ROSC, survival to admission, survival to discharge, and CPC scores; the Autopulse subgroup showed no difference from the manual compression subgroup in ROSC, survival to discharge, and CPC scores. CONCLUSION: There were no significant differences in resuscitative effects between mechanical and manual chest compression in OHCA patients. To ensure the quality of CPR, we suggest that manual chest compression be applied in the early stage of CPR for OHCA patients, while mechanical compression can be used as part of advanced life support in the late stage.

[Effects between chest-compression-only cardiopulmonary resuscitation and standard cardiopulmonary resuscitation for patients with out-of-hospital cardiac arrest: a Meta-analysis].

OBJECTIVE: To comprehensively evaluate and compare the resuscitation efficacy of chest-compression-only cardiopulmonary resuscitation (CCPR) and standard cardiopulmonary resuscitation (SCPR) for patients with out-of-hospital cardiac arrest (OHCA). METHODS: Databases such as PubMed, Embase, Ovid, Cochrane Library, Wanfang, CNKI, VIP, CBM were searched from the date of their foundation to March 2nd 2018, and the studies on the difference of effects between CCPR and SCPR for patients with OHCA were retrieved. The outcomes included the return of spontaneous circulation (ROSC) rate, survival to hospital discharge, neurological function completion rate. Two reviewers independently screened the literature meeting the inclusion criteria, independently collected information and evaluated the literature quality. Meta-analysis was conducted using RevMan 5.3 software, and sensitivity analysis was conducted by selecting model analysis method and removing single research method. Funnel plot was used to evaluate publication bias. RESULTS: A total of 10 cohort studies were included, including 174 163 patients with OHCA, of which 95 157 undergone CCPR and 79 006 undergone SCPR. The scores of the Newcastle-Ottawa scale (NOS) were 8-9, indicating that the quality of the literatures included was high. It was shown by the Meta-analysis that CCPR had the higher rate of survival to hospital discharge [relative risk (RR) = 1.04, 95% confidence interval (95%CI) = 1.00-1.08, P = 0.04] and neurological function completion (RR = 1.11, 95%CI = 1.06-1.17, P < 0.000 1) than SCPR, but there was no significant difference in ROSC rate between the two groups (RR = 1.01, 95%CI = 0.98-1.04, P = 0.52). In the subgroup, there was no statistical significance between CCPR and SCPR in the rate of survival to hospital discharge in cardiac OHCA patients (RR = 1.13, 95%CI = 0.82-1.57, P = 0.45). However, in non-cardiac OHCA group, SCPR showed more benefits than CCPR in improving the rate of survival to hospital discharge (RR = 0.88, 95%CI = 0.80-0.96, P = 0.004). The above analysis results were consistent in the fixed effect model and random effect model, indicating that the results were reliable and stable. It was shown by the funnel plot that most of the studies were left-right inverted funnel type, indicating a low publication bias. However, the bias could not be completely excluded due to the small number of included literatures. CONCLUSIONS: For patients without OHCA etiological classification, CCPR was not less than SCPR in improving ROSC rate, discharge survival rate and good neurological function, and CCPR was more advantageous in learning and the willingness of bystanders to implement. However, when non-cardiogenic OHCA could be identified, SCPR should be recommended when conditions permit.

[Protective effect of 5-aminosalicylic acid on the kidney of paraquat poisoning rats by Nrf2-ARE signal pathway].

OBJECTIVE: To investigate the protective effect of 5-aminosalicylic acid (5-ASA) on renal injury poisoned by paraquat (PQ) in rats and its mechanism. METHODS: Twenty-four healthy clean male Sprague-Dawley (SD) rats were randomly divided into four groups: normal saline (NS) control group, 5-ASA control group, PQ model group and 5-ASA treatment group, with 6 rats in each group. The rat model of PQ poisoning was reproduced by intraperitoneal injection of 2% PQ solution 20 mg/kg, and the same volume of NS was given in NS control group and 5-ASA control group. Two hours later, the rats in 5-ASA control group and 5-ASA treatment group were intragastrically administered with 1 mL 5-ASA (75 mg/kg) for one time after NS or PQ administration, and those in NS control group and PQ model group were administered with 1 mL double distilled water. Behavioral changes were observed in rats. Then the rats were sacrificed at 24 hours after starting of the experiment for cardiac blood harvest which could be used to detect the biomarkers of renal injury and oxidative stress parameters. The kidney tissue was collected, and the hematein-eosin (HE) staining was conducted for observation of pathological changes in renal tissue, and protein expressions of Nrf2 and heme oxygenase-1 (HO-1) were determined by Western Blot. RESULTS: At 30 minutes after PQ poisoning, rats appeared obvious poisoning symptoms and signs. Twenty-four hours after PQ poisoned, hemocoel of glomerular capillary, swelling of renal tubular epithelial cell and serious micronecrosis appeared under the light microscope. Compared with NS control group, blood urea nitrogen (BUN), serum creatinine (SCr), superoxide dismutase (SOD), malondialdehyde (MDA), catalase (CAT) and glutathione (GSH) levels were significantly abnormal in PQ model group, and Nrf2 and HO-1 protein expressions in renal tissue were increased. After administration of 5-ASA, the morphological changes and pathological damage were mitigated as compared with those of PQ model group, the levels of BUN, SCr and MDA were decreased significantly [BUN (mmol/L): 11.98±1.81 vs. 18.56±2.32, SCr (µmol/L): 30.67±2.31 vs. 43.67±9.02, MDA (µmol/L): 5.28±0.43 vs. 6.81±1.00], and the SOD activity, CAT and GSH contents were significantly increased [SOD (kU/L): 125.49±7.63 vs. 106.76±7.94, CAT (ng/L): 30.68±3.51 vs. 23.05±1.55, GSH (µmol/L): 3.81±0.44 vs. 3.14±0.17], while the protein expressions of Nrf2 and HO-1 were further increased [Nrf2 protein (gray value): 0.76±0.04 vs. 0.52±0.03, HO-1 protein (gray value): 0.56±0.02 vs. 0.31±0.02, all P < 0.05]. Only 5-ASA intervention had no significant effect on behavior, pathology, renal injury markers and oxidative stress parameters, but it could induce the expressions of Nrf2 and HO-1 protein in renal tissue, which were significantly higher than those of NS control group [Nrf2 protein (gray value): 0.78±0.02 vs. 0.41±0.04, HO-1 protein (gray value): 0.51±0.03 vs. 0.23±0.01, both P < 0.01]. CONCLUSIONS: 5-ASA attenuates the damage of acute renal injury (AKI) caused by PQ, which mechanism may be related with the activation of Nrf2-antioxidant response element (ARE) signaling pathway.

[Therapeutic effects of gastric lavage with fuller earth combined with QingyiII catharsis in treatment of oral paraquat poisoning in rabbits].

OBJECTIVE: To observe the therapeutic effects of gastric lavage with fuller earth combined with Qingyi II catharsis in treatment of oral paraquat poisoning in rabbits. METHODS: Thirty healthy adult Japanese white rabbits were randomly divided into five groups: namely control group, model group, gastric lavage group (lavage of 10% fuller earth suspension), catharsis group (Qingyi II catharsis), and combination group (10 minutes after gastric lavage of fuller earth suspension liquid, giving Qingyi II for catharsis), with 6 rabbits in each group. All groups were challenged with paraquat (100 mg/kg) diluted to 5 mL with normal saline by lavage to reproduce the model of acute poisoning, while the control group was given 5 mL of normal saline instead. Each treatment group was treated accordingly at 1 hour after gavages of paraquat, and treatment continued for 3 days. The animal survival rate was observed. Venous blood samples were collected from ear marginal vein to determine the plasma concentration of paraquat by ultraviolet spectrophotometer at 1, 2, 4, 8 and 24 hours after the poisoning. The animals were sacrificed by intravenous air injection on the 8th day after the poisoning, and the right lower lobe of lung was harvested to observe the lung tissue pathological changes with hematoxylin-eosin (HE) staining. RESULTS: (1) Survival rate: the surviving rate of the combination group (6 rabbits) was higher than that of gastric lavage group (5 rabbits), catharsis group (2 rabbits) and model group (0 rabbit) on the 2nd day with statistically significant difference (P < 0.001). The survival rate on the 7th day in combination group (5 rabbits) was higher than that of gastric lavage group (3 rabbits), and catharsis group (0 rabbit ) with statistically significant difference (P = 0.003). (2) Plasma concentrations of paraquat: plasma paraquat concentration in all groups peaked at 2 hours after intoxication, and its levels in the gastric lavage, catharsis and combination groups were significantly lower than that of the model group ( mg/L: 1.830 ± 0.068, 1.890 ± 0.048, 1.800 ± 0.052 vs. 1.960 ± 0.063, all P < 0.01). As the time prolonged, the plasma concentration of paraquat was lowest in combination group than that of gastric lavage group and catharsis group (all P < 0.01). Gastric lavage and catharsis had interaction at 4 hours in combination group [F = 5.194, P = 0.034; the concentrations of paraquat (mg/L) was 0.670 ± 0.057 vs. 1.010 ± 0.018, 1.210 ± 0.052]. (3) Lung histopathology: obvious expansion and hyperemia of the alveolar capillary, widened alveolar septum, a large number of inflammatory cell infiltrations were observed in model group and catharsis group. Lung histopathology was more improved in combination group and gastric lavage group, and it was improved more obviously in combination group than that in gastric lavage group. CONCLUSIONS: Early start of gastric lavage with fuller earth combined with Qingyi II catharsis, can reduce the animal plasma concentrations of paraquat in oral paraquat poisoning rabbits. At the same time, it can alleviate the degree of lung injury and significantly improve survival rates compared with the single gastric lavage or catharsis alone. Gastric lavage with fuller earth combined with Qingyi II catharsis can improve the prognosis of animal synergistically.

[Protection of anisodamine on the mitochondrial injury induced by oxidative stress in swine with cardiac arrest].

OBJECTIVE: To investigate the protection of anisodamine on cardiac ischemia/reperfusion (I/R) injury by oxidative stress by observing the changes in oxidation and antioxidant markers in plasma and myocardium, and the damage of cardiac mitochondria structure in pigs with cardiac arrest (CA). METHODS: Twenty-three healthy male swine were divided into three groups using random digits table: sham group (n=5), epinephrine group (n=9), and anisodamine group (n=9). The CA model was reproduced by alternating current. Blood samples were collected before CA, 8 minutes after CA, and 0 minute, 30 minutes, 24 hours after recovery of spontaneous circulation (ROSC), and hearts were harvested at 24 hours after ROSC. The content of malondialdehyde (MDA) and the enzyme activity of superoxide dismutase (SOD) were analyzed by spectrophotography, the cardiac ATP content was assayed by high performance liquid chromatography, the generation of reactive oxygen species (ROS) was detected by laser confocal microscope, and the myocardial ultrastructures were observed with transmission electron microscope to assess mitochondrial damage score. RESULTS: At 30 minutes and 24 hours after ROSC, plasma MDA level of anisodamine group was lower than that of epinephrine group (30 minutes: 43.38±8.12 µmol/L vs. 55.47±10.97 µmol/L, 24 hours: 29.96±6.04 µmol/L vs. 37.87±7.85 µmol/L, both P<0.05). Compared with epinephrine group, the cardiac SOD activity and ATP content of anisodamine group were elevated (SOD: 1.35±0.50 U/mg vs. 0.54±0.19 U/mg, ATP: 4.17±1.06 µmol/g vs. 2.95±0.94 µmol/g, P<0.01 and P<0.05), and the mitochondrial ROS level (RFU) was lowered (88.00±17.67 vs. 107.00±21.35, P<0.05). Although the cardiac MDA content was also reduced, but the difference between two resuscitation groups showed no statistical significance (16.66±2.89 µmol/mg vs. 19.28±3.90 µmol/mg, P>0.05). Using electron microscope, in epinephrine group disordered arrangement of cardiac myocyte arrangement was observed, and the mitochondrial alignment and morphology were significantly different from the sham group (mitochondrial damage score: 0.41±0.08 vs. 0.12±0.01, P<0.01). The level of mitochondrial injury in anisodamine group was milder than that of epinephrine group (mitochondrial damage score: 0.21±0.05 vs. 0.41±0.08, P<0.05). CONCLUSION: Through regulating oxygen radical metabolism, anisodamine alleviates the injury to myocardial mitochondria structure and function injury as induced by oxidative stress.

[Protective effect of anisodamine against myocardial cell apoptosis through mitochondria impairment in cardiac arrest in pigs].

OBJECTIVE: To investigate the protective effect of anisodamine on myocardial mitochondrial damage in cardiac arrest (CA) in pigs. METHODS: Twenty-three male pigs were randomly divided into three groups, epinephrine group (n=9), anisodamine group (n=9) and control group (n=5). CA following ventricular fibrillation (VF) was induced by alternating current. The blood samples were collected before CA, 8 minutes after CA and instantly after recovery of spontaneous circulation (ROSC), and 30 minutes and 24 hours later. Hearts were obtained at 24 hours after ROSC. The changes in Cytochrome C (Cyt C) and caspase-3 in plasma and myocardium were analyzed by enzyme-linked immunosorbent assay (ELISA). The myocardial specimens were observed by transmission electron microscopy for ultrastructural changes, and apoptosis was assessed with Hoechst 33258 staining. RESULTS: The ROSC rate of the anisodamine group was elevated by 22.22% compared with the epinephrine group (77.78% vs. 55.56%, P>0.05). All animals with resumption of ROSC survived up to 24 hours. The plasma contents of Cyt C and caspase-3 in the epinephrine group and the anisodamine group gradually increased after ROSC, and were significantly higher than those in the control group. But the plasma Cyt C level in the anisodamine group was lower than that in the epinephrine group at 30 minutes and 24 hours after ROSC (48.68±19.50 nmol/L vs. 77.51±29.87 nmol/L, 48.98±20.26 nmol/L vs. 82.11±25.09 nmol/L, both P<0.05). There was no significant difference in protein contents of both Cyt C and caspase-3 in plasma and myocardium between two resuscitate groups. Both epinephrine and anisodamine could mitigate cardiac mitochondrial damage after CA, but the anisodamine showed better effect. The myocardium apoptosis ratio in the anisodamine group was lower than that of the epinephrine group [(0.15±0.04)% vs. (0.37±0.04)%, P<0.01]. CONCLUSION: By decreasing the protein content of Cyt C, and reducing the extent of damage to myocardial mitochondria, anisodamine can protect the myocardial ultrastructure, and restrain the mitochondria-induced cell apoptosis after resuscitation.