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首页> 外文期刊>Shock: Molecular, cellular, and systemic pathobiological aspects and therapeutic approaches = The official journal of the Shock Society, the European Shock Society, the Brazilian Shock Society, the International Federation of Shock Societies >Effects of positive end-expiratory pressure in an experimental model of acute myocardial infarct in wistar rats.
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Effects of positive end-expiratory pressure in an experimental model of acute myocardial infarct in wistar rats.

机译：呼气末正压通气的影响急性心肌梗死的实验模型wistar鼠。

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ABSTRACT: Our purpose in this study was to access the pulmonary effects of mechanical ventilation with positive end-expiratory pressure (PEEP; 10 cmH2O) or without PEEP (zero PEEP-ZEEP) in a rat model of acute myocardial infarction that resulted in hypotension but not in pulmonary congestion. METHODS: Wistar rats were anesthetized (1.5% isoflurane) and myocardial infarct was induced by ligature of the anterior interventricular coronary artery. Rats with myocardial infarct were compared with sham-operated (Sham) and closed thorax groups. RESULTS AND CONCLUSION: There was a significant decrease in MAP in the acute myocardial infarct group (92.5 +/- 4.2 mmHg) when compared with closed chest group (113.0 +/- 4.4 mmHg). There was no significant difference between acute myocardial infarct and Sham groups in PEEP or ZEEP. Mechanical ventilation for 120 min resulted in a significant increase in respiratory system elastance in the groups ventilated with ZEEP (2.59 +/- 0.17 and 2.32 +/- 0.17 cmH2O.mL, Sham and acute myocardial infarct groups, respectively). This effect of mechanical ventilation was not observed in the presence of PEEP in both groups. There was no significant increase in the amount of perivascular pulmonary edema measured in all groups studied. Mean airspace linear intercept and lung tissue distortion index also did not show statistically significant difference between Sham and acute myocardial infarct groups. We conclude that in this experimental model of acute myocardial infarct (12.4 +/- 4.1% area of necrotic tissue and 26.4 +/- 4.0% area of ischemic tissue), there was a protective pulmonary effect of PEEP.
机译：文摘:本研究的目的是访问机械通气肺的影响呼气末正压通气(偷看;cmH2O)或没有偷看(零PEEP-ZEEP)在一只老鼠急性心肌梗死模型导致低血压而不是肺交通堵塞。异氟烷麻醉(1.5%)和心肌梗塞被结扎诱导前室间冠状动脉。心肌梗死比较sham-operated(假的)和关闭胸腔组。结果与结论:有显著降低急性心肌梗塞的地图组(92.5 + / - 4.2毫米汞柱)相比闭胸组(113.0 + / - 4.4毫米汞柱)。急性之间没有显著差异心肌梗死和窥视或虚假的团体ZEEP。在呼吸系统的显著增加倒电容与ZEEP组通风(2.59 + / - 0.17和2.32 + / - 0.17 cmH2O。和急性心肌梗死组,分别)。通风的存在没有被观察到在两组偷看。增加血管周的肺水肿以所有组的研究。空域线性拦截和肺组织畸变指数统计上也没有显示虚假和急性显著区别心肌梗死组。这个实验模型的急性心肌梗塞(12.4 + / - 4.1%的坏死组织和26.4 + / - 4.0%的缺血性组织)是一种保护性肺偷看的效果。

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