Engedal H, Skagseth E, Saetersdal T S, Myklebust R
J Thorac Cardiovasc Surg. 1978 Apr;75(4):548-54.
Transmural left ventricular biopsies from 13 patients undergoing cardiopulmonary bypass were studied. The hypertrophic myocardium was protected by deep hypothermia (15 degrees C.) during ischemic arrest for a maximal period of 96 minutes. Biopsies were taken at the start of bypass, at the end of aortic cross-clamping, and after 20 minutes of reperfusion. The structure of the mitochondria remained normal, whereas cellular alterations in the form of widened intercalated discs, interstitial and intracellular edema, myelin figures, and slight myofibrillar lysis were observed in all stages. As no clear correlation between these structural injuries and aortic cross-clamping time was seen, they are a result of cardiac hypertrophy rather than intraoperative ischemia.
对13例接受体外循环的患者进行了经壁左心室活检。在缺血性停搏期间,肥厚心肌通过深度低温(15摄氏度)进行保护,最长时间为96分钟。在体外循环开始时、主动脉阻断结束时以及再灌注20分钟后进行活检。线粒体结构保持正常,而在所有阶段均观察到以闰盘增宽、间质和细胞内水肿、髓鞘样结构以及轻微肌原纤维溶解形式出现的细胞改变。由于未发现这些结构损伤与主动脉阻断时间之间存在明确相关性,因此它们是心脏肥大的结果,而非术中缺血所致。