To compare the early effects of hypertonic and isotonic saline resuscitation on heme oxygenase-1 （HO-1） expression in organs of rats with hemorrhagic shock. Rats were randomly divided into hypertonic saline resuscit...To compare the early effects of hypertonic and isotonic saline resuscitation on heme oxygenase-1 （HO-1） expression in organs of rats with hemorrhagic shock. Rats were randomly divided into hypertonic saline resuscitation （HTS）, normal saline resuscitation （NS） and sham groups. HO-1 mRNA, protein expression and apoptosis were evaluated in organs. In the HTS group, significant difference was noted in HO-1 protein in small intestinal mucosa and liver compared with the NS and sham groups, and in HO-1 mRNA in liver and kidney compared with the sham group. The apoptosis of small intestinal mucosa, liver, heart, and lung was significantly lower in the HTS group than that in the NS group. In this study, small volume resuscitation with HTS can efficiently up-regulate the expression level of HO-1 in small intestinal mucosa and liver, which may be one of the mechanisms alleviating organ damage.展开更多
BACKGROUND： Despite a large amount of resuscitation research, the survival rate after cardiac arrest remains low, and brain injury is the key issue. Neuroglobin （NGB） is an oxygen-binding heme protein found in the...BACKGROUND： Despite a large amount of resuscitation research, the survival rate after cardiac arrest remains low, and brain injury is the key issue. Neuroglobin （NGB） is an oxygen-binding heme protein found in the brain with a protection role against ischemic-hypoxic brain injury. Hemin is an effective activator of neuroglobin. This study was undertaken to assess the effect of hemin on expression of neuroglobin （NGB） in the cerebral cortex, neuro-defi cit score （NDS） and pathological changes after cardiopulmonary resuscitation （CPR） in rats.METHODS： A total of 120 male Sprague-Dawley （SD） rats were randomly divided into a control group （A）, a CPR group （B） and a Hemin group （C）. The animal model of cardiac arrest （CA） induced by asphyxia and CPR was established. NGB expression in the cerebral cortex with immunohistochemistry, NDS and pathological changes in the cerebral cortex were examined at 3, 6, 12, 24 hours after recovery of spontaneous circulation （ROSC） in each group. Experimental data were treated as one-factor analysis of variance and the Tukey test.RESULTS： In comparison with group A, NGB expression was increased signifi cantly at 12 and 24 hours after ROSC （P〈0.05 or P〈0.01）, NDS was decreased signifi cantly at each time point after ROSC （P〈0.01）, and pathological changes were severe at each time point after ROSC in group B. In comparison with group A, NGB expression was increased signifi cantly at 6, 12, 24 hours after ROSC （P〈0.05 or P〈0.01）, NDS was decreased signifi cantly at 3, 6, 12 hours after ROSC （P〈0.01） in group C. In comparison with group B, NGB expression was increased signifi cantly at 12 and 24 hours after ROSC, NDS was increased signifi cantly at 12 and 24 hours after ROSC, and pathological changes were milder in group C.CONCLUSION： There were increased NGB expression in the cerebral cortex, decreased NDS, and severe pathological changes after CPR in rats. Hemin treatment up-regulated expression of NGB, improved NDS, mitigated pathological changes, and alleviated cerebral injury after CPR.展开更多
BACKGROUND: Partial pressure of end-tidal carbon dioxide(PETCO2) has been used to monitor the effectiveness of precordial compression(PC) and regarded as a prognostic value of outcomes in cardiopulmonary resuscitation...BACKGROUND: Partial pressure of end-tidal carbon dioxide(PETCO2) has been used to monitor the effectiveness of precordial compression(PC) and regarded as a prognostic value of outcomes in cardiopulmonary resuscitation(CPR). This study was to investigate changes of PETCO2 during CPR in rats with ventricular fi brillation(VF) versus asphyxial cardiac arrest.METHODS: Sixty-two male Sprague-Dawley(SD) rats were randomly divided into an asphyxial group(n=32) and a VF group(n=30). PETCO2 was measured during CPR from a 6-minute period of VF or asphyxial cardiac arrest.RESULTS: The initial values of PETCO2 immediately after PC in the VF group were signifi cantly lower than those in the asphyxial group(12.8±4.87 mmHg vs. 49.2±8.13 mmHg, P=0.000). In the VF group, the values of PETCO2 after 6 minutes of PC were significantly higher in rats with return of spontaneous circulation(ROSC), compared with those in rats without ROSC(16.5±3.07 mmHg vs. 13.2±2.62 mmHg, P=0.004). In the asphyxial group, the values of PETCO2 after 2 minutes of PC in rats with ROSC were signifi cantly higher than those in rats without ROSC(20.8±3.24 mmHg vs. 13.9±1.50 mmHg, P=0.000). Receiver operator characteristic(ROC) curves of PETCO2 showed signifi cant sensitivity and specifi city for predicting ROSC in VF versus asphyxial cardiac arrest.CONCLUSIONS: The initial values of PETCO2 immediately after CPR may be helpful in differentiating the causes of cardiac arrest. Changes of PETCO2 during CPR can predict outcomes of CPR.展开更多
Background： Hemorrhagic shock （HS） results in myocardial contractile dysfunction. Studies showed that 17β-estradiol protects the myocardium against contractile dysfunction. The study investigated the cardioprotect...Background： Hemorrhagic shock （HS） results in myocardial contractile dysfunction. Studies showed that 17β-estradiol protects the myocardium against contractile dysfunction. The study investigated the cardioprotective effects of treatment with 17β-estradiol before resuscitation following 1 h of HS and resuscitation. Methods： Male Sprague-Dawley rats were assigned to 2 sets of experimental protocols： Ex vivo and in vivo treatment and resuscitation. Each set had three experimental groups （n = 6 per group）： Normotensive （N）, HS and resuscitation （HS-R） and HS rats treated with 17β-estradiol （E） and resuscitated （HS-E-R）. Rats were hemorrhaged over 60-rain to reach a mean arterial blood pressure of 40 mmHg. In the ex vivo group, hearts were resuscitated by perfusion in the Langendorff system. In the 17β-estradiol treated group, 17β-estradiol 280 μg/kg was added for the first 5 min. Cardiac function was measured. Left ventricular generated pressure （LVGP） and ＋dP/dt were calculated. In the in vivo group, rats were treated with 17β-estradiol 280 ±g/kg s.c. after 60-rain HS. Resuscitation was performed in vivo by the reinfusion of the shed blood for 30-min to restore normotension. Results： Treatment with 17β-estradiol before resuscitation in ex vivo treated and resuscitated isolated hearts and in the in vivo treated and resuscitated rats following HS improved myocardial contractile function. In the in vivo treated group, LVGP and ＋dP/dt max were significantly higher in 17β-estradiol treated rats compared to the untreated group （LVGP 136.40 ± 6.61 compared to 47.58 ± 17.55, and ＋dP/dt 661.85 ± 49.88 compared to 88.18 ± 0.85）. Treatment with 17β-estradiol improved LVGP following HS. Conclusions： The results indicate that treatment with 17β-estradiol before resuscitation following HS protects the myocardium against dysfunction.展开更多
基金supported by the Zhejiang Provincial Natural Science Foundation of China (No.Y2100430)the Zhejiang Provincial Education and Research Foundation of China (No. Y201019154)
文摘To compare the early effects of hypertonic and isotonic saline resuscitation on heme oxygenase-1 （HO-1） expression in organs of rats with hemorrhagic shock. Rats were randomly divided into hypertonic saline resuscitation （HTS）, normal saline resuscitation （NS） and sham groups. HO-1 mRNA, protein expression and apoptosis were evaluated in organs. In the HTS group, significant difference was noted in HO-1 protein in small intestinal mucosa and liver compared with the NS and sham groups, and in HO-1 mRNA in liver and kidney compared with the sham group. The apoptosis of small intestinal mucosa, liver, heart, and lung was significantly lower in the HTS group than that in the NS group. In this study, small volume resuscitation with HTS can efficiently up-regulate the expression level of HO-1 in small intestinal mucosa and liver, which may be one of the mechanisms alleviating organ damage.
文摘BACKGROUND： Despite a large amount of resuscitation research, the survival rate after cardiac arrest remains low, and brain injury is the key issue. Neuroglobin （NGB） is an oxygen-binding heme protein found in the brain with a protection role against ischemic-hypoxic brain injury. Hemin is an effective activator of neuroglobin. This study was undertaken to assess the effect of hemin on expression of neuroglobin （NGB） in the cerebral cortex, neuro-defi cit score （NDS） and pathological changes after cardiopulmonary resuscitation （CPR） in rats.METHODS： A total of 120 male Sprague-Dawley （SD） rats were randomly divided into a control group （A）, a CPR group （B） and a Hemin group （C）. The animal model of cardiac arrest （CA） induced by asphyxia and CPR was established. NGB expression in the cerebral cortex with immunohistochemistry, NDS and pathological changes in the cerebral cortex were examined at 3, 6, 12, 24 hours after recovery of spontaneous circulation （ROSC） in each group. Experimental data were treated as one-factor analysis of variance and the Tukey test.RESULTS： In comparison with group A, NGB expression was increased signifi cantly at 12 and 24 hours after ROSC （P〈0.05 or P〈0.01）, NDS was decreased signifi cantly at each time point after ROSC （P〈0.01）, and pathological changes were severe at each time point after ROSC in group B. In comparison with group A, NGB expression was increased signifi cantly at 6, 12, 24 hours after ROSC （P〈0.05 or P〈0.01）, NDS was decreased signifi cantly at 3, 6, 12 hours after ROSC （P〈0.01） in group C. In comparison with group B, NGB expression was increased signifi cantly at 12 and 24 hours after ROSC, NDS was increased signifi cantly at 12 and 24 hours after ROSC, and pathological changes were milder in group C.CONCLUSION： There were increased NGB expression in the cerebral cortex, decreased NDS, and severe pathological changes after CPR in rats. Hemin treatment up-regulated expression of NGB, improved NDS, mitigated pathological changes, and alleviated cerebral injury after CPR.
基金supported in part by grants from the National Natural Science Foundation of China(30700303)the National Clinical Key Subject Construction Project
文摘BACKGROUND: Partial pressure of end-tidal carbon dioxide(PETCO2) has been used to monitor the effectiveness of precordial compression(PC) and regarded as a prognostic value of outcomes in cardiopulmonary resuscitation(CPR). This study was to investigate changes of PETCO2 during CPR in rats with ventricular fi brillation(VF) versus asphyxial cardiac arrest.METHODS: Sixty-two male Sprague-Dawley(SD) rats were randomly divided into an asphyxial group(n=32) and a VF group(n=30). PETCO2 was measured during CPR from a 6-minute period of VF or asphyxial cardiac arrest.RESULTS: The initial values of PETCO2 immediately after PC in the VF group were signifi cantly lower than those in the asphyxial group(12.8±4.87 mmHg vs. 49.2±8.13 mmHg, P=0.000). In the VF group, the values of PETCO2 after 6 minutes of PC were significantly higher in rats with return of spontaneous circulation(ROSC), compared with those in rats without ROSC(16.5±3.07 mmHg vs. 13.2±2.62 mmHg, P=0.004). In the asphyxial group, the values of PETCO2 after 2 minutes of PC in rats with ROSC were signifi cantly higher than those in rats without ROSC(20.8±3.24 mmHg vs. 13.9±1.50 mmHg, P=0.000). Receiver operator characteristic(ROC) curves of PETCO2 showed signifi cant sensitivity and specifi city for predicting ROSC in VF versus asphyxial cardiac arrest.CONCLUSIONS: The initial values of PETCO2 immediately after CPR may be helpful in differentiating the causes of cardiac arrest. Changes of PETCO2 during CPR can predict outcomes of CPR.
文摘Background： Hemorrhagic shock （HS） results in myocardial contractile dysfunction. Studies showed that 17β-estradiol protects the myocardium against contractile dysfunction. The study investigated the cardioprotective effects of treatment with 17β-estradiol before resuscitation following 1 h of HS and resuscitation. Methods： Male Sprague-Dawley rats were assigned to 2 sets of experimental protocols： Ex vivo and in vivo treatment and resuscitation. Each set had three experimental groups （n = 6 per group）： Normotensive （N）, HS and resuscitation （HS-R） and HS rats treated with 17β-estradiol （E） and resuscitated （HS-E-R）. Rats were hemorrhaged over 60-rain to reach a mean arterial blood pressure of 40 mmHg. In the ex vivo group, hearts were resuscitated by perfusion in the Langendorff system. In the 17β-estradiol treated group, 17β-estradiol 280 μg/kg was added for the first 5 min. Cardiac function was measured. Left ventricular generated pressure （LVGP） and ＋dP/dt were calculated. In the in vivo group, rats were treated with 17β-estradiol 280 ±g/kg s.c. after 60-rain HS. Resuscitation was performed in vivo by the reinfusion of the shed blood for 30-min to restore normotension. Results： Treatment with 17β-estradiol before resuscitation in ex vivo treated and resuscitated isolated hearts and in the in vivo treated and resuscitated rats following HS improved myocardial contractile function. In the in vivo treated group, LVGP and ＋dP/dt max were significantly higher in 17β-estradiol treated rats compared to the untreated group （LVGP 136.40 ± 6.61 compared to 47.58 ± 17.55, and ＋dP/dt 661.85 ± 49.88 compared to 88.18 ± 0.85）. Treatment with 17β-estradiol improved LVGP following HS. Conclusions： The results indicate that treatment with 17β-estradiol before resuscitation following HS protects the myocardium against dysfunction.
