Smith H J, Kent K M, Epstein S E
J Thorac Cardiovasc Surg. 1978 Mar;75(3):452-57.
The patterns of regional contractile function were examined with ultrasonic crystals in "open-chest" anesthetized dogs. In normal myocardium, the base-line end-diastolic segment length (EDL) was 1.63 +/- 0.12 cm. and the mean systolic length (MSL) was 1.47 +/- 0.17 cm. Mean velocity of shortening over the first one third of systole (V1/3) was 15.9 +/- 2.3 mm. per second. Coronary occlusion induced regional ischemia with segmental dyskinesia (MSL = 1.84 +/- 0.12 cm). Reperfusion after 5 or 10 minutes of occlusion induced rapid recovery of contractile function that was independent of catecholamine release, as demonstrated in animals pretreated with 6-OH dopamine. After initial recovery, however, contractile function deteriorated. There were an increase in EDL (from 1.73 +/- 0.11 to 1.78 +/- 0.11; p less than 0.001) and the appearance of early systolic dyskinesia. V1/3 diminished from 5.6 +/- 4.6 to -6.6 +/- 2.5 mm. per second (p less than 0.005). Thus reperfusion damage, defined as late deterioration after recovery from brief periods of ischemia, may be partly distinct from ischemic damage per se. It is possible that the deterioration of myocardial function which accompanies reperfusion of previously ischemic myocardium may be a contributing factor in the transient myocardial dysfunction that is occasionally seen following cardiopulmonary bypass.
在“开胸”麻醉犬身上,用超声晶体检查区域收缩功能模式。在正常心肌中,基线舒张末期节段长度(EDL)为1.63±0.12厘米,平均收缩期长度(MSL)为1.47±0.17厘米。收缩期前三分之一的平均缩短速度(V1/3)为每秒15.9±2.3毫米。冠状动脉闭塞导致局部缺血并伴有节段性运动障碍(MSL = 1.84±0.12厘米)。闭塞5或10分钟后再灌注,可使收缩功能迅速恢复,且与儿茶酚胺释放无关,这在预先用6-羟基多巴胺处理的动物中得到了证实。然而,在最初恢复后,收缩功能恶化。EDL增加(从1.73±0.11增加到1.78±0.11;p<0.001),并出现早期收缩期运动障碍。V1/3从每秒5.6±4.6毫米降至-6.6±2.5毫米(p<0.005)。因此,再灌注损伤定义为短暂缺血恢复后的晚期恶化,可能部分有别于缺血损伤本身。先前缺血心肌再灌注时伴随的心肌功能恶化,可能是体外循环后偶尔出现的短暂心肌功能障碍的一个促成因素。