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The effect of collateral circulation on regional myocardial flow and wall motion of left ventricle was studied on 5 anesthetized dogs with a surgically implanted constrictor on the left circumflex coronary artery (LC). The grade of LC stenosis and wall motion of left ventricle (LV) were determined by cineangiography of the coronary artery and LV at the period of acute and chronic occlusion. Regional myocardial flow was determined by tracer microspheres (TM), labeled with four different isotopes, Sr85, Cr51, Sc46, Ce141. The first TM1 was infused after LC stenosis, TM2 during a temporary complete LC occlusion at the period of acute occlusion; TM3 and TM4 in a similar way 3 to 4 weeks after the acute LC stenosis. Three to four weeks after LC stenosis, i.e. chronic period of occlusion, the degree of LC stenosis progressed from 70--80% to 100% occlusion, but collateral flow and collateral vessels to the ischemic LC area were increased together with an improvement of wall motion of the ischemic LC area. The results may support the idea that collaterals may be an effective compensatory mechanism for ischemia. In contrast to an increase of collateral flow to the ischemic LV free wall in all five dogs, an increase to the posterior papillary muscle was found only in two out of five dogs.

For the experimental studies on chronic coronary stenosis, an ameroid constrictor was modified to facilitate serial cineangiographic evaluation of the degree of arterial narrowing. A radiolucent plastic ring instead of a stainless frame was used to prevent outward swelling of the ameroid material. Coronary cineangiography was performed 10, 20 and 30 days after the implantation of the modified ameroid constrictor on the left circumflex coronary artery (LCX), which could prove the progressive coronary stenosis of 57, 78 and 88% on the respective days. Collateral channels from the anterior descending branch of the left coronary artery to the LCX were demonstrated angiographically in 5 out of the 6 dogs on the 30th day.

The effects of intravenous administration of nitroglycerin or dipyridamole on distribution of myocardial blood flow in the heart after coronary underperfusion were investigated. In 18 open chest, anesthetized dogs, flow of the tubing supplying the left circumflex coronary artery (LCA) was reduced and kept constant, and then the drug was given intravenously. Before and after an administration of saline, nitroglycerin (0.04 mg/kg) and dipyridamole (0.2 mg/kg), myocardial blood flow was measured by tracer microspheres (TM). The first and second carbonized 15 mu spheres (TM1 and TM2) were injected into the left atrium and the cannulated LCA perfusion system respectively before medication. Similarly, the third and fourth spheres were given after drug. Thus, by using four different TMs (141Ce, 51Cr, 85Sr, 46Sc) regional myocardial blood flow from the LCA perfusion route (TM2 and TM4) was measured separately from that of the other normally perfused coronary route (TM1 and TM3). The effect of drugs on flow distribution of these two independent routes was measured. The LCA underperfusion produced a significant diminution of regional flow and its end/epi ratio in the LCA territory. Nitroglycerin increased end/epi ratio in the ischemic myocardium in the LCA perfusion route, but dipyridamole increased the normally perfused coronary flow but caused a shift of flow from the ischemic left ventricle to the atria and right ventricle within the LCA territory.

The effect of graded coronary stenosis on resting regional myocardial flow and left ventricular (LV) wall motion was studied in 18 anesthetized dogs. The left circumflex coronaary artery (LC) was constricted. The degree of LC stenosis and the changes in LV wall motion were determined by cineangiography of the coronary artery and LV. Regional myocardial flow was determined by tracer microspheres (TM), labeled with two different isotopes, Sr85, Sc46 or Ce141. The first TM1 and the second TM2 were infused after LC stenosis, and during a temporary complete LC occlusion respectively. Resting flow in areas with 70% stenosis was reduced, with a greater reduction of subendocardium and posterior papillary muscle, but minimum impairment of LV wall motion. No ST elevation was found. Animals with 80--90% stenosis showed a marked reduction of flow and wall motion, a significant ST-elevation and a delayed antegrade run-off in coronary arteriography.

The purpose of this study was to develop a technique measuring the perfusion area of the coronary artery preocclusively and to study the relationship between the perfusion area and infarct size. 125I tracer microspheres were selectively injected into the left circumflex coronary artery (LCX) preocclusively, and then the LCX was ligated. 48 hours later the heart was removed, rapidly frozen, and 50-mu transverse sections were obtained from base, middle and apex of the canine left ventricle, and used for autoradiography to measure perfusion area and for tetrazolium staining to measure infarct size. Dogs were divided into 2 groups: group 1 in which the main trunk of the LCX was occluded to produce large infarct (n = 10) and group 2 in which the distal branch of the LCX was occluded to produce small infarct (n = 10). There was a linear correlation between the perfused and infarcted area regardless of a size or location of the perfusion area involved. These results indicate that the extent of infarction is directly proportional to the perfusion area and is not altered by the location in the ventricle.

Effects of alpha adrenergic stimulation on diameter change of the epicardial coronary artery were studied in in-situ canine heart. The diameter of the left circumflex coronary artery (LCX) was continuously measured by 10 MHz PZT crystals applied to the external wall of the LCX. Aortic pressure was measured using high fidelity catheter-tip manometer. Enhanced activity of alpha adrenergic receptor by humoral and/or somatic nerve stimulations caused a reduction of the LCX diameter despite of the systemic pressure rise.