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在兔在体心脏上对比观察了阻断冠脉血流(心肌缺血)和阻断冠脉血流后用缺氧液体灌流(心肌缺氧)时心肌电活动与超微结构的变化。结果如下:(1)心肌缺血时引起 MAP 振幅(MAPA)与双极心外膜下电图振幅(BEGA)的降低(P<0.01)以及 MAP 复极达50%的时程(MAPD_(50))与功能不应期(FRP)的缩短(P<0.01);(2)心肌缺氧时只引起 MAPD_(50)和 FRP的缩短(P值分别小于0.01和0.05),而未引起 MAPA 和 BEGA 的明显变化;(3)超微结构的观察表明,心肌缺血10分钟时,多数线粒体内出现不定形的致密小体,核染色质明显周边化,而心肌缺氧10分钟时,仅在少数线粒体内出现致密体,核染色质分散,有的呈现早期周边化。上述结果提示,在心肌缺血早期,缺氧是造成不应期缩短的主要原因,而代谢产物和 K~+的蓄积则可能是引起传导阻抑的重要因素,并有加强缺氧所致心肌损伤的作用。
The changes of myocardial electrical activity and ultrastructure in rabbits were observed on the body of the heart in order to block the coronary flow (myocardial ischemia) and to block the perfusion of coronary artery with hypoxic fluid (myocardial hypoxia). The results were as follows: (1) The decrease of MAP amplitude and BEGA (P <0.01) and MAPD 50 (50% ) And shortening of FRP (P <0.01). (2) Myocardial hypoxia caused only MAPD 50 and FRP shortening (P values less than 0.01 and 0.05, respectively), but not MAPA and BEGA obvious changes; (3) ultrastructure of the observation showed that myocardial ischemia at 10 minutes, the majority of mitochondria appear amorphous dense bodies, nuclear chromatin significantly peripheral, and myocardial hypoxia 10 minutes, only in the A small number of mitochondria appear dense, nuclear chromatin scattered, and some showed early peripheral. The above results suggest that in the early stage of myocardial ischemia, hypoxia is the main reason for the shortening of refractory period, while the accumulation of metabolites and K ~ + may be an important factor that leads to conduction inhibition, as well as to strengthen myocardial oxygen caused by hypoxia Damage effect.