Esmaili Dehaj Mansour, Baharvand Babak, Rasoulian Bahram, Foadaddini Mohsen, Asgari Alireza, Noroozzadeh Ali, Poorkhalili Khalil, Wahhab Aghai Hannaneh, Khoshbaten Ali
Research Center for Trauma, Baqiyatallah University of Medical Sciences, Teheran, Iran.
J Surg Res. 2009 Jan;151(1):55-61. doi: 10.1016/j.jss.2007.12.802. Epub 2008 Feb 1.
Previous studies have shown that pretreatment with normobaric hyperoxia has cardioprotective effect in isolated rat heart. The present study was designed to test the hypothesis that pretreatment normobaric hyperoxia could induce delayed cardioprotection effect in an in vivo regional heart ischemia.
Experiment 1: Rats were exposed to normobaric normoxia or to normobaric hyperoxia (O(2) > 95%) for 15, 30, 60, 120, and 180 min (H15, H30, H60, H120, and H180 groups, respectively). After 24 h, they were subjected to 30 min regional ischemia and 90 min reperfusion. Then, the hearts were harvested for measurement of infarct size. Lead II of electrocardiogram was continuously recorded for analysis of ischemic arrhythmias. Experiment 2: Different oxygen concentrations were tested in the same model of heart ischemia.
Compared with normoxia group, infarct size significantly reduced in H120 and H180 groups (from 48.1 +/- 4 to 31.4 +/- 3.3 and 30 +/- 2.4, respectively); 120 and 180 min of >95% hyperoxia significantly reduced the number of ventricular beats (from 314 +/- 34.9 to 173 +/- 20.3 and 178 +/- 15.7, respectively) and incidence of ventricular fibrillation (from 66.8% to 30% and 22.2%, respectively). When the oxygen concentration decreased to 80%, its effect on infarct size was abolished; however, its antiarrhythmic effect persisted. Further reduction of oxygen concentration eliminated both the effects.
These results show that hyperoxia pretreatment may induce delayed anti-infarct and antiarrhythmic effects in anesthetized rats. These effects are dependent on the exposure time and oxygen concentration.
先前的研究表明，常压高氧预处理对离体大鼠心脏具有心脏保护作用。本研究旨在验证常压高氧预处理可在体内局部心脏缺血中诱导延迟性心脏保护作用这一假说。
实验1：将大鼠暴露于常压常氧或常压高氧（氧气浓度>95%）环境中15、30、60、120和180分钟（分别为H15、H30、H60、H120和H180组）。24小时后，对其进行30分钟局部缺血和90分钟再灌注。然后，取出心脏测量梗死面积。连续记录心电图II导联以分析缺血性心律失常。实验2：在相同的心脏缺血模型中测试不同的氧浓度。
与常氧组相比，H120和H180组的梗死面积显著减小（分别从48.1±4减小至31.4±3.3和30±2.4）；120和180分钟的>95%高氧显著减少室性早搏数量（分别从314±34.9减少至173±20.3和178±15.7）以及室颤发生率（分别从66.8%降至30%和22.2%）。当氧浓度降至80%时，其对梗死面积的影响消失；然而，其抗心律失常作用仍然存在。进一步降低氧浓度则两种作用均消失。
这些结果表明，高氧预处理可能在麻醉大鼠中诱导延迟性抗梗死和抗心律失常作用。这些作用取决于暴露时间和氧浓度。
