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在56只麻醉开胸兔心脏上,观察了局部心肌缺氧、高血钾和乳酸性酸中毒对心肌电活动的影响。主要结果如下:(1)局部缺氧5分时MAPD_(50)和FRP分别缩短30±4.9%和10±1.5%(P<0.01),MAPA徊BEG未发生明显变化。(2)局部高钾(12~15mEq/l)时MAPA和BEGA分别降低26±3.2%和67±6.3%(P<0.01),BEGD延长79±23.5%(P<0.01),但MAPD_(50)与FRP仅轻度缩短(P>0.05)。(3)局部心肌乳酸性酸中毒对心肌电活动无明显影响。(4)用缺氧和高钾血浆灌流左室支时,MAP的变化与缺血时相似,表现为MAPA降低和MAPD_(50)缩短。根据以上结果,可认为,缺氧和高血钾是导致缺血心肌电生理学变化的重要因素,前者主要引起心肌不应期缩短,后者主要引起局部心肌传导减慢,二者均可促进折返性心律失常的发生。
The effects of local myocardial hypoxia, hyperkalemia and lactic acidosis on cardiac electrical activity were observed in 56 anesthetized open heart rabbits. The main results are as follows: (1) MAPD_ (50) and FRP decreased by 30 ± 4.9% and 10 ± 1.5% respectively at 5 min of hypoxia (P <0.01). (2) MAPA and BEGA decreased by 26 ± 3.2% and 67 ± 6.3% (P <0.01) and BEGD by 79 ± 23.5% (P <0.01) at local high potassium (12-15 mEq / ) And FRP only slightly shortened (P> 0.05). (3) Local myocardial lactic acidosis had no significant effect on myocardial electrical activity. (4) When the left ventricular branches were perfused with hypoxic and hyperkalemic plasma, the change of MAP was similar to that of ischemia, which showed the decrease of MAPA and the shortening of MAPD_ (50). Based on the above results, it can be considered that hypoxia and hyperkalemia are the important factors leading to electrophysiological changes in ischemic myocardium. The former mainly causes shortening of myocardial refractory period, and the latter mainly causes slowing of local myocardial conduction, both of which can promote reentry The occurrence of arrhythmia.