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Objective:To establish the rat cardiac arrest model in high-altitude hypobaric hypoxia environment, and to explore the effect of the treatment time in the hypobaric oxygen chamber on the reproduction of high-altitude rat cardiac arrest model.Methods:SPF grade healthy male Sprague-Dawley (SD) rats were used as observation subjects. The experiment was conducted in two different altitude areas. The rats from the Plateau Branch of Institute of Cardiopulmonary and Cerebral Resuscitation of Sun Yat-sen University (Xining, Qinghai) were weighed and numbered, and they were placed in a hypobaric oxygen chamber (simulated altitude of 3 000 meters, speed of ascent and descent of 15 m/min, temperature of 20 ℃, cabin pressure of 69.5 kPa, cabin oxygen pressure of 14.5 kPa). After 30 days of feeding, the rats were obtained according to random number table method, and the cardiac arrest model was established by asphyxia method as the 30-day hypobaric hypoxia group. After 60 days of feeding, rats were randomly selected again, and the cardiac arrest model was established as the 60-day hypobaric hypoxia group. Thirty rats were randomly selected from the Institute of Cardiopulmonary Cerebral Resuscitation at Sun Yat-sen University (Guangzhou, Guangdong) by the same method, and the cardiac arrest model was established as the plain control group. The differences in the body weight of rat modeling precursors and the induction time of asphyxia during the modeling process among different groups were compared.Results:Finally, cardiac arrest model was established in 16 rats in the 30-day hypobaric hypoxia group and in 22 rats in the 60-day hypobaric hypoxia group. There was no significant difference in the body weight of rats before modeling among the plain control group, 30-day hypobaric hypoxia group and 60-day hypobaric hypoxia group [g: 429.00 (389.25, 440.75), 440.00 (415.50, 486.25), 440.00 (400.00, 452.50), all P > 0.05]. The asphyxia induction time of rats in the 60-day hypobaric hypoxia group was significantly longer than that in the 30-day hypobaric hypoxia group (s: 294.59±75.39 vs. 234.31±93.86, P < 0.01), even about 1.4 times of the plain control group (s: 294.59±75.39 vs. 208.73±30.88, P < 0.01). There was no significant difference in the asphyxia induction time between the 30-day hypobaric hypoxia group and the plain control group ( P > 0.05). Conclusion:Rats treated in a hypobaric oxygen chamber for 60 days are more suitable for the preparation of high-altitude cardiac arrest model, and are also consistent with the oxygen reserve and hypoxia tolerance of high-altitude rats.
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Objective:To investigate the effect of venous blood carbon dioxide binding capacity (CO 2-CP) on the short-term prognosis of patients with acute ischemic stroke (AIS) after thrombolytic therapy. Methods:A total of 86 AIS inpatients who received thrombolytic therapy in the emergency department of Sun Yat-Sen Memorial Hospital of Sun Yat-Sen University from April 2019 to May 2021 were analyzed retrospectively. According to the venous blood CO 2-CP levels at admission, the patients were divided into two groups: low CO 2-CP group (CO 2-CP < 23 mmol/L, n = 52) and high CO 2-CP group (CO 2-CP ≥ 23 mmol/L, n = 34). The CO 2-CP levels and changes between the two groups before and after thrombolytic therapy were compared. The National Institutes of Health Stroke scale (NIHSS) score was used to evaluate the improvement rate of patients after thrombolytic therapy [NIHSS score at admission-NIHSS score at discharge)/NIHSS score at admission ×100%] and in-hospital death was also recorded. The correlation between CO 2-CP levels and prognosis of patients with AIS during emergency visit was analyzed, the receiver operator characteristic curve (ROC curve) was drawn and the area under the ROC curve (AUC) was calculated to evaluate the predictive value of CO 2-CP in the prognosis of AIS patients. Results:The CO 2-CP levels of low CO 2-CP group and high CO 2-CP group after thrombolytic therapy were significantly higher than those before treatment (mmol/L: 23.08±2.34 vs. 20.46±1.51, 25.24±2.16 vs. 23.94±1.07, both P < 0.05). The differences of CO 2-CP before and after treatment in low CO 2-CP group were significantly higher than those in high CO 2-CP group (mmol/L: 2.62±0.83 vs. 1.30±1.09, P < 0.05). The improvement rate of CO 2-CP levels in the high CO 2-CP group (NIHSS improvement rate > 45%) was significantly higher than that in the low CO 2-CP group [85.29% (29/34) vs. 23.08% (12/52)], while the mortality in the low CO 2-CP group was significantly higher than that in the high CO 2-CP group [11.54% (6/52) vs. 0% (0/34), P < 0.05]. The AUC of CO 2-CP for the prognosis of patients with AIS thrombolysis was 0.820, the 95% confidence interval (95% CI) was 0.727-0.924, P = 0.000 1. Conclusion:AIS patients with CO 2-CP levels less than 23 mmol/L have a poor short-term prognosis, which has certain predictive and clinical reference value for choosing thrombolytic time in emergency stroke patients.
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Objective To investigate the effect of mild hypothermia on the myocardial and microcirculation dysfunction induced by epinephrine during early post-resuscitation in a rat model of cardiac arrest and cardiopulmonary resuscitation (CPR).Methods Transesophageal cardiac pacing was performed in order to elicit cardiac arrest for 5 min in SD male rats.Totally 40 rats were randomly (random number) divided into 4 groups (n=10):normothermic control group (N),normothermic epinephrine group (N+E),hypothermic control group (H),and hypothermic epinephrine group (H+E).Chest compression was then initiated.Epinephrine (0.02 mg/kg) or saline was administrated at 1 min during CPR.Restoration of spontaneous circulation (ROSC) was recorded,and the rates of ROSC were observed.Myocardial and microcirculatory function were observed at 1,2,3,and 4 h during early post-resuscitation.Serum lactate level was assessed at baseline and ROSC 4 h.Results The ROSC rates were 10/10 in the H+E group,9/10 in the N+E group,4/10 in the H group,and 1/10 in the N group,respectively.Ejection fraction (EF)and cardiac output (CO) in the H+E group were significantly higher than that of other groups (P<0.05).Total vessel density,perfused vessel density,proportion of perfused vessels,and microvascular flow index in the H+E group were also significantly higher than those of other groups during early post-resuscitation.The serum lactate level in the H+E group was significantly lower than that in the N+E and H groups..Conclusions Both epinephrine and mild hypothermia can improve the success rate of resuscitation.However,mild hypothermia can improve the epinephrine induced myocardial and microcirculatory dysfunction during postresuscitation in the rat cardiac arrest.
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Objective To investigate the pharmacological hypothermic effect of WIN55, 212-2 on neuronal apoptosis after cardiopulmonary resuscitation. Methods Cardiac Arrest ( CA ) was induced in Sprague-Dawley rats.Five minutes after onset of CA, cardiopulmonary resuscitation ( CPR) was carried out.At 30 minutes post-resuscitation, the animals were randomized into three groups (n=10 in each group): (1) WIN55, 212-2 hypothermia group [W group, WIN55, 212-2, 1 mg/(kg· h)].(2) Normothermia group (NT group, 5%DMSO);(3) WIN55, 212-2 with normothermia group (W+NT group, WIN55, 212-2, 1 mg/(kg· h).Animals in WIN55, 212-2 hypothermia group and WIN55, 212-2 with normothermia group were dealt with continuous intravenous infusion of WIN55, 212-2 [1 mg/(kg· h)] for 4 h, while rats in NT group were infused with equal volume of 5% DMSO instead.The survival time and neurological deficit score ( NDS) were observed.The CA models were established in three groups.After rats were sacrificed, the brains were harvested for detecting histopathological changes and apoptosis of neural cell at 24 h, 48 h and 72 h after ROSC respectively.Five animals of each group were chosen randomly ( random number ) .Results Body temperatures of rats in W group decreased from 37°C to 34°C in 4 hours.Accumulated survival rate in W group was higher than that in the other two groups ( P=0.02) .NDS was significantly improved in W group than that in the other two groups ( P<0.05) .Morphological change in W group was less serious than that in the other two groups.The number of neuron apoptosis in W group was smaller than that in the other two groups.Conclusions WIN55, 212-2 inducing pharmacologically hypothermia during post-resuscitation prolonged survival and improved cerebral function in rat cardiac arrest models.The beneficial effects of WIN55, 212-2 were associated with ameliorating the histopathological damage in brain and alleviating the neuron apoptosis.
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Objective To compare the impact of intra-arterial versus intravenous administration of epinephr-ine on the efficacy CPR in mice. Methods Transoesophageal cardiac pacing was performed to induce cardiac arrest for 4 minitues in 20 Kunming male mice. The mice were then randomized to two groups (n = 10 in each group), and received epinephrine of 0.02 mg/kg via either carotid artery (IA-gro) or jugular vein (IV-gro) injection. Chest compression and ventilation were performed; and the rate of restoration of spontaneous circulation (ROSC) and survival time were recorded. CPR was stopped if spontaneous circulation was not restored within 10 minutes. Results There was no significant difference in the rates of ROSC between IA-gro and IV-gro (10/10 vs. 8/10, P>0.05), nor in the time of ROSC or survival time [51 ± 13 s vs. 62 ± 24 s; 8.5 (6.0, 17.0) h vs. 6.5 (2.8, 21.3) h, P > 0.05]. Conclusions Neither intra-arterial nor intravenous administration of epinephrine has no obvious impact on the efficacy of CPR in mice.
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Objective Objectives To investigate the gender difference affecting the efficacy of cardiopulmonary resuscitation (CPR) in the mouse cardiac arrest (CA) model.Methods CA was induced in 30 Kunming mice (15 male and 15 female) by trans-oesophageal cardiac pacing for 4 minutes.Epinephrine was then administrated intra-artery,and CPR was performed.The time required for restoration of spontaneous circulation (ROSC) was observed,but if ROSC failed to appear at 10 minutes after CPR,resuscitation was discontinued.Blood pressure and electrocardiograms of resuscitated animals were invasively monitored for an additional 60 minutes.Blood pressure,heart rate,the restoration of spontaneous respiration (ROSR) and survival time were observed and recorded.Results All 15 female mice and 14 of 15 male mice had ROSC.There were no significant differences in the time required for ROSC,ROSR,and survival between the two groups [(50±17)svs.(46±12)s; (2.4±1)minvs.(2.5±1)min; 28 (1,72)h vs.16 (3,72)h,P > 0.05)].Moreover,neither blood pressure nor heart rate showed significant differences one hour after ROSC between the two groups.Conclusions Sex differences did not affect the efficacy of CPR,but the precise mechanism is still unclear,and further investigations are required.
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Objective To compare the effects between vasopressin and epinephrine during cardiopulmonary resuscitation(CPR)in a mouse model of cardiac arrest(CA).Method Transoesophageal cardiac pacing was performed so as to elicit cardiac arrest in 30 Kunming male mice.Four minutes after the initiation of cardiac pacing,the animals were prospectively randomized into three groups in equal number(n=10/group),namely,control group(saline 0.2 mL intra-arterial),vasopressin group(vasopressin 0.4U/kg intra-arterial)and epinephrine group(epinephrine 0.04 mg/kg intra-arterial),then CPR was initiated.Restoration of spontaneous circulation (ROSC)was observed.If ROSC failed to appear at 10 minutes after CPR,resuscitation was discontinued.Electrocardiogram and blood pressure of resuscitated animals were invasively monitored for an additional 60 minutes.Electrocardiogram and blood pressure.and the restoration of spontaneous respiration and survival time were observed and recorded.Results Rates of ROSC in vasopressin group and epinephrine group were significantly higher than those in saline group(9/10,10/10 vs.3/10,P<0.05,P<0.01 respectively),and there was signilieant difference between vasopressin and epinephrine group.All resuscitated mice treated with epinephrine restored sponlaneous respiration after ROSC,while only 4 of 9 animals trealed with vasopressin did(P<0.05).Survival time of anireals in epinephrine group was longer than that in vasopressin group or in saline group(P<0.05,P<0.05,respectively).Conclusions Both vasopressin and epinephrine increase the rates of ROSC.Epinephrine 0.04 mg/kg improved respiratory function and results in a longer survival time compared with vasopressin 0.4 U/kg in this mouse model.and the precise mechanism is not clear and further investigation is required.