Jorge P A, Curti H V, Metze K
Faculdade de Ciéncias Médicas, Unicamp, SP.
Arq Bras Cardiol. 1991 Jun;56(6):471-6.
The study of the ultrastructural features of the coronary microvessels in postischemic reperfusion.
Five mongrel dogs of either sex, weighing 2 to 17 kg were studied Each dog was anesthetized with 30 mg. of pentobarbital and ventilated with room air. A thoracotomy was done and the left descendent coronary artery was isolated. Aorta and right atria pressures, electrocardiogram and coronary blood flow was measured. After 90 minutes of coronary occlusion and 20 minutes of reperfusion carbon black was injected into the anterior descending coronary artery to identify the area of impaired perfusion. The heart was excised and placed in a ice-cold saline. The left ventricle was cut transversely in six slices of 1 cm thickness parallel to the atrioventricular sulcus. Tissue specimens were taken from the subendocardial, mid-myocardial (in the non reperfused area) subepicardial and control layers for electron microscopic examination. Each slice was then incubated in a 1% solution of triphenyltetrazolium chloride (TTC) at 37 degrees C for 10 minutes.
The infarcted areas showed widespread tissue damage with relaxed myofibrils cellular edema, swollen mitochondria with fractured cristae and nuclear changes. The vascular endothelium demonstrated severe injury with edema, cytoplasmic clearing, loss of pinocytotic vesicles, nuclear changes, formation of blebs into the vascular lumen and intravascular neutrophil. In the mid-myocardial layer, near the non reperfused vessels, a striking contrast was observed between the vessel and myocardium cells patterns. The usual picture was a severe vascular damage without myocyte injury.
This study showed that prominent capillary damage with coagulation necrosis was the morphologic pattern observed in areas of myocardial infarction. In the mid-myocardium, near the non reperfused vessel, severe capillary damage was found in areas of preserved myocytes. Obstruction of flow at the capillary level, correlates well with the decrease of the coronary flow reserve observed during the post-ischemic reperfusion.
研究缺血后再灌注时冠状动脉微血管的超微结构特征。
对5只体重2至17千克的杂种犬进行研究，雌雄不限。每只犬用30毫克戊巴比妥麻醉，并用室内空气通气。进行开胸手术，分离左冠状动脉降支。测量主动脉和右心房压力、心电图和冠状动脉血流量。在冠状动脉闭塞90分钟和再灌注20分钟后，将炭黑注入冠状动脉前降支以确定灌注受损区域。取出心脏并置于冰冷盐水中。将左心室平行于房室沟切成6片1厘米厚的切片。从心内膜下、心肌中层（在未再灌注区域）、心外膜下和对照层取组织标本进行电子显微镜检查。然后将每片切片在37℃的1%氯化三苯基四氮唑（TTC）溶液中孵育10分钟。
梗死区域显示广泛的组织损伤，包括肌原纤维松弛、细胞水肿、线粒体肿胀伴嵴断裂以及细胞核改变。血管内皮显示严重损伤，表现为水肿、细胞质清亮、吞饮小泡丢失、细胞核改变、向血管腔内形成泡状突起以及血管内中性粒细胞。在心肌中层，靠近未再灌注血管处，观察到血管和心肌细胞模式之间形成鲜明对比。常见情况是严重的血管损伤而无心肌细胞损伤。
本研究表明，在心肌梗死区域观察到的形态学模式是显著的毛细血管损伤伴凝固性坏死。在心肌中层，靠近未再灌注血管处，在保存的心肌细胞区域发现严重的毛细血管损伤。毛细血管水平的血流阻塞与缺血后再灌注期间观察到的冠状动脉血流储备减少密切相关。
