Efficacy of non-pharmacological interventions in pain relief and opioid consumption after cardiac surgery: A systematic review and Bayesian network meta-analysis.

OBJECTIVE: To investigate and rank the evidence for the efficacy of non-pharmacological interventions in relieving pain after cardiac surgery using comprehensive comparisons. BACKGROUND: Although several previous systematic reviews and meta-analyses showed that non-pharmacological interventions effectively control and reduce pain after cardiac surgery, none quantitatively compared the effect of these different types of interventions. DESIGN: Systematic review and Bayesian network meta-analysis based on the Preferred Reporting Items for Systematic Reviews and Meta-Analyses for Network Meta-Analysis guidelines. METHODS: Six databases were searched from inception to April 2021 to collect all published evidence from randomised clinical trials. One author extracted the relevant information from the eligible trials; a second author independently reviewed the data. Before analysing the extracted data, two investigators independently assessed the quality of the included studies. Conventional meta-analysis was conducted using either fixed- or random-effects models according to statistical heterogeneity. The Bayesian network meta-analysis was conducted using the consistency model. RESULTS: We identified 42 randomised clinical trials comparing 14 groups with 4253 patients. Transcutaneous electrical nerve stimulation, acupressure, music and massage were effective for pain relief, with transcutaneous electrical nerve stimulation being associated with the best probability of successful pain relief after cardiac surgery (cumulative ranking curve surface, 0.97; probability, 77.03%). Acupressure (cumulative ranking curve surface, 0.79; probability, 30.69%) was the second-best option. However, there was no evidence that any pair-up intervention significantly reduced opioid use or anxiety. CONCLUSIONS: These findings suggest that transcutaneous electrical nerve stimulation, acupressure, music and massage may effectively alleviate postoperative cardiac pain, with transcutaneous electrical nerve stimulation representing the best choice for pain relief. RELEVANCE TO CLINICAL PRACTICE: The results of this network meta-analysis can guide patients after cardiac surgery and healthcare providers to make optimal decisions in managing postoperative cardiac pain. TRIAL REGISTRATION: PROSPERO CRD42021246183.

Broadband dielectric spectroscopic detection of volatile organic compounds with ZnO nanorod gas sensors.

Metal-oxide (MO) semiconductor gas sensors based on chemical resistivity necessarily involve making electrical contacts to the sensing materials. These contacts are imperfect and introduce errors into the measurements. In this paper, we demonstrate the feasibility of using contactless broadband dielectric spectroscopy (BDS)-based metrology in gas monitoring that avoids distortions in the reported resistivity values due to probe use, and parasitic errors (i.e. tool-measurand interactions). Specifically, we show how radio frequency propagation characteristics can be applied to study discrete processes on MO sensing material, such as zinc oxide (i.e. ZnO) surfaces, when exposed to a redox-active gas. Specifically, we have used BDS to investigate the initial oxidization of ZnO gas sensing material in air at temperatures below 200 °C, and to show that the technique affords new mechanistic insights that are inaccessible with the traditional resistance-based measurements.

MicroRNA-574-5p promotes cell growth of vascular smooth muscle cells in the progression of coronary artery disease.

Coronary artery disease (CAD) is caused by atherosclerotic plaque development in the walls of coronary arteries. Aberrant proliferation of vascular smooth muscle cells (VSMCs) promotes atherosclerotic plaque formation, whereas VSMC apoptosis may promote CAD-related inflammation. microRNAs are potential diagnostic biomarkers in cardiovascular disease, especially CAD. Previous reports found that, among patients with CAD, microRNA-574-5p (miR-574-5p) expression was significantly increased and associated with disease severity. However, the specific mechanism by which miR-574-5p affects CAD is unknown. We used quantitative real-time PCR to detect the mRNA expression levels of miR-574-5p in the sera and VSMCs of patients with CAD. We also detected cell proliferation by MTT assay and apoptosis by the Cell Death Detection ELISA-Plus apoptosis assay. We found that miR-574-5p expression was elevated in the sera and VSMCs of patients with CAD. Additionally, miR-574-5p overexpression promoted cell proliferation and inhibited apoptosis in VSMCs. A dual-luciferase reporter assay showed that miR-574-5p directly targets ZDHHC14. In conclusion, our findings indicate that miR-574-5p promotes cell proliferation and inhibits apoptosis by inhibiting ZDHHC14 gene expression, suggesting that miR-574-5p is a CAD-related factor that may serve as a potential molecular target for CAD treatment.

Monitoring the end-tidal concentration of sevoflurane for preventing awareness during anesthesia (MEETS-PANDA): A prospective clinical trial.

OBJECTIVE: It was hypothesized that monitoring end-tidal sevoflurane (ETS) during endoscopic surgery could reduce the incidence of intraoperative awareness in patients undergoing general anesthesia. Herein, the incidence of intraoperative awareness and other correlative factors was recorded and compared. METHODS: Two thousand five hundred ASA I-III patients aged 18-80 years who underwent general anesthesia were randomly divided into 2 groups (n = 1250): routine care group (R) and ETS concentration group (E). ETS concentration was monitored in group E and maintained at a sevoflurane minimum alveolar concentration (MAC) of 0.7-1.3; group R was monitored using routine care, and the sevoflurane was maintained. Patients were assessed for intraoperative awareness with a questionnaire on their explicit memory 24-48 h after surgery. RESULTS: A total of 2532 patients were selected, and 86 patients were excluded. As for the groups, 1219 patients were assigned to group E, and 1227 patients were assigned to group R. As for intraoperative awareness, group E had 2 patients, and group R had 14. Compared with group R, the incidence of intraoperative awareness in group E was significantly lower (p = 0.003); the time-averaged ETS concentration and sevoflurane dosage were lower in group E (p < 0.05); and no significant changes were found in tracheal extubation time, intravenous general anesthetic dosage, or postoperative complication incidence in either group (p > 0.05). The incidence of intraoperative awareness was higher in women than men in group R (p < 0.05). CONCLUSION: Using ETS-guided anesthesia and maintaining the sevoflurane concentration (0.7-1.3 MAC) can decrease the incidence of patient awareness during endoscopic surgery.

Involvement of AQP 1 in the cardio-protective effect of remifentanil post-conditioning in ischemia/reperfusion rats.

BACKGROUND: our research aim to study the role of AQP1 in the cardioprotective effect of remifentanil post-conditioning for myocardial ischemia/reperfusion injury. METHODS: Ninety Sprague-Dawley (SD) rats were divided into 6 groups: sham operation group (Sham group), myocardial ischemia and reperfusion group (I/R group), postconditioning of remifentanil group (R-post), postconditioning of remifentanil plus AQP1 inhibitor acetazolamide group (R-post +Ace), postconditioning of remifentanil plus opioid-receptor antagonist compounds (R-post +AC), postconditioning of remifentanil plus AQP1 enhancer arginine vasopressin (R-post +AV). All groups except the sham operation group were given 30 min ischemia in left anterior descending (LAD) coronary arteries. All groups were then given 120 min reperfusion to the LAD. Before reperfusion, the R-post, R-post +Ace, R-post +AC, R-post +AV groups were given 10 min remifentanil post-conditioning. Hemodynamic data were measured every 30 min after initiation of ischemia. The rats' hearts were exercised for detecting infarct size and water content in the left ventricle, and AQP1 expression were also detected. RESULTS: The R-post group showed a significant reduction of the infarct size compared to the I/R group. The effect of R-post for reducing infarct size was slightly enhanced by adding acetazolamide to R-post, so significant differences could still be found when compared R-post+Ace group to the I/R group. The effect of infarct size reduction brought by R-post was blocked by the opioid-receptor antagonist compounds. This effect was also blocked by the AQP1 enhancer. Similar outcomes were found considering the water content of the left ventricle and the AQP1 expression. CONCLUSION: Cardioprotective effect of remifentanil post-conditioning may initiate through inhibiting the function of AQP1.

[Effects of sevoflurane preconditioning on cardiomyocyte apoptosis and myocardial inflammation in rats with sepsis].

OBJECTIVE: To observe the effects of preconditioning with different concentrations of sevoflurane on cariomyocyte apoptosis and myocardial inflammation in rats with sepsis and explore the possible mechanism of sevoflurane for myocardial protection. METHODS: Forty adult male Sprague-Dawley rats were randomly divided into 4 groups (n=10), namely the control group, LPS group, low-concentration sevoflurane group and high-concentration sevoflurane group. Following sevoflurane pretreatment for 30 min and a washout period for 10 min, all the rats received intraperitoneal injection of LPS or normal saline (NS) and were sacrificed 12 h later to observe the myocardial histopathology. Apoptosis of the ardiomyocytes was detected with TUNEL assay, and enzyme-linked immunosorbent assay was used to detect serum cTnI level and myocardial TNF-α level. RESULTS: Compared with the control group, the rats in the other 3 groups showed significantly increased serum cTnI level, myocardial TNF-α content, and apoptotic index of the cardiomyocytes (P<0.05). Compared with those in LPS group, serum cTnI level, myocardial TNF-α content, and apoptotic index of the cardiomyocytes were significantly decreased in the two sevoflurane preconditioning groups (P<0.05), and the effect was more obvious with a high dose of sevoflurane (P<0.05 CONCLUSION: Sevoflurane preconditioning can concentration-dependently reduce LPS-induced myocardial injury in rats possibly by decreasing cardiomyocyte apoptosis and alleviating myocardial inflammations.

Remifentanil induces L-type Ca2+ channel inhibition in human mesenteric arterial smooth muscle cells.

PURPOSE: Remifentanil is known to cause vasodilation at standard anesthetic concentrations. The intracellular mechanisms underlying its vasodilator action may involve the activation of ion channels. The purpose of this study was to examine whether remifentanil inhibits L-type calcium channels (Ca.(L)) and provides dose-dependent effects on L-type calcium channel Ba(2+) currents (I(Ba.L)) in human mesenteric arterial smooth muscle cells. METHODS: Using the whole-cell patch-clamp method, an in depth analysis of the mechanism of the I(Ba.L) induced by remifentanil was performed in cells which were enzymatically isolated from human mesenteric arterial smooth muscle. Ten millimolars Ba(2+) was used to replace 1.5 mM Ca(2+) to increase the amplitude of the inward current through Ca(2+)channels. L-type calcium channel Ba(2+) was elicited during 50 msec depolarizing test pulses (150 msec duration) to +80 mV (10 mV increments) from a holding potential of -60 mV. The effects of remifentanil on Ca.(L) were observed at the following concentrations: 1.21, 4.84, and 19.4 nmol.L(-1) and were compared with control. RESULTS: Remifentanil produced a concentration-dependent block of I(Ba,L) with IC(50) values of 38.90 +/- 3.96 x 10(-3) micromol.L(-1). The L-type calcium channel blocker, nifedipine, antagonized these remifentanil-induced currents. Remifentanil, at all concentrations, shifted the maximum of the current-voltage relationship in the hyperpolarizing direction of I(Ba.L). CONCLUSION: Remifentanil significantly inhibits Ca.(L) channels in a concentration-dependent manner in human mesenteric arteriolar smooth muscle cells.