Blood Supply of the Myocardium after Temporary Coronary Occlusion

Abstract

A coronary artery and the accompanying vein were ligated temporarily for 30, 60 and 120 minutes in 39 cats. By labelling the blood with the fluorescent dye acridine orange, the intravital blood supply of the myocardium was investigated 5 minutes to 6 hours after release of the ligature. The region supplied by the temporarily ligated coronary artery (RSCA) was demonstrated by postmortal perfusion of this vessel using the dye light green. Resumption of circulation in the deeper layers of the RSCA was delayed after a prior coronary occlusion, even occasionally after occlusions lasting only 30 minutes. After a coronary ligation of 60 to 120 minutes the inner layers of the RSCA became the sites of prolonged disturbance of blood supply. The circulatory abnormality observed immediately following release of the ligature did not result from intraluminal vascular obstruction. Even after a temporary ischemia lasting 120 minutes it was still possible, immediately after removal of the liga-ture, to perfuse an intravitally ischemic portion of the RSCA. The significance of these results for the determination of the so-called "revival-time" of the cardiac muscle is pointed out. ADDITIONAL KEY WORDS temporary cardiac ischemia intravital staining acridine orange coronary perfusion intracellular and interstitial edema revival-time of cardiac muscle anesthetized cats • After temporary interruption of the coronary circulation, survival of the myocardium depends primarily on whether a sufficient blood supply is established before irreversible injury has occurred. Detailed studies of the resumption of circulation in the myocardium after temporary occlusion of coronary vessels have not been done, so far as we know. Therefore, we examined the circulation in involved myocardium after a coronary artery had been occluded temporarily for 30, 60 or 120 minutes. Moreover, we wished to determine whether it might be possible to perfuse the myocardial vessels artificially in a region of prior ischemia. Methods Thirty-nine cats weighing 1.5 to 2.5 kg and unselected, were anesthetized with sodium pento-barbital (25 mg/kg). Respiration was maintained through an endotracheal tube attached to a respirator pump. Arterial pressures were monitored continuously by a Statham strain gauge attached to a catheter in the femoral artery. Left thoracot-omy and pericardotomy incisions remained un-closed throughout the experiment. The anterior descending branch of the left main coronary artery (together with the accompanying vein) was ligated temporarily 2 to 3 mm distal to its origin. The duration of coronary ligation was 30, 60 or 120 minutes after which the ligature was removed , allowing resumption of coronary flow for periods of five minutes to six hours before the beating heart was excised for study. Table 1 lists the experiments done and the number of animals in each category.

Complications of Coronary Intervention

“…This phenomenon was initially described by Krug et al 16 during induced myocardial infarction in the canine model in 1966 and again by Kloner et al 15 in 1974 in which it occurred for 90 min after temporary epicardial coronary artery occlusion followed by reperfusion. Electron microscopic examination showed severe myocardial capillary damage with loss of pinocytonic vesicles in the endothelial cells, endothelial blisters or blebs and endothelial gaps with neutrophil infiltration.…”

“…15 The underlying cause of no-reflow is microvascular obstruction, which may be produced by various mechanisms. The concept of no-reflow was first described in experimental models in 1966 16 and then in the clinical setting of reperfusion after myocardial infarction in 1985. 17 No-reflow has been documented in ≥30% of patients after thrombolysis 18 or mechanical intervention for acute myocardial infarction.…”

Original Research: Porcine model for observing changes due to ischemia/reperfusion injury secondary to intra-abdominal endovascular balloon occlusion

“…16 Postischemia/reperfusion data were compared with the baseline data. During the observational period, all pigs were resuscitated with normal saline solution if the mean arterial pressure (MAP) was less than 65 mmHg as an MAP of at least 65 mmHg is essential to maintain normal organ circulation.…”

Looking Beyond Reperfusion

“…In the 1960s, well before the first human reperfusion studies were carried out, Jennings RB et al [28] and Krug et al [29] demonstrated impaired reperfusion after release of a temporary coronary occlusion. Kloner RA et al [30] reported that reperfusion caused microvascular damage with swelling of capillary endothelial cells and of myocytes, leading to what was termed the 'no reflow phenomenon.…”