[Coronary microcirculation in myocardial reperfusion. The phenomenon of no-reperfusion]

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.