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In 10 conscious dogs, a model was developed for studying regional contractile responses in a coronary collateral-dependent bed. Regional myocardial function was compared after terminating a maximum paced rate of 240 beats/min maintained for 3 minutes (postpacing period) with that during telemetry-monitored exercise at comparable heart rates (average 252 +/- 34 beats/min, duration 2.4 minutes) at different times during collateral development. Ultrasonic dimension gauges were used to measure control and ischemic segment (CS and IS) lengths and ischemic zone regional wall thickness (IW). An ameroid constrictor and a Doppler flow probe were placed around the left circumflex coronary artery, and pacing electrodes were sutured to the right ventricle. An average of 23 days postoperatively, coronary obstruction was complete. Studies at that time showed that percent shortening (% delta L) of IS and percent wall thickening (% delta W) of IW decreased after pacing to 57% and 35% of control, respectively, and during exercise to 37% of control. One week later (average 30 days postoperatively), significant depression of regional function no longer occurred postpacing. However, exercise at a comparable heart rate still provoked regional dysfunction in the collateral-dependent zone: Both IS% delta L and IW% delta W decreased to 51% of control. Regional function at rest did not differ during these studies. Thus, the effectiveness of the postpacing response for detecting limited collateral reserve was eliminated by further collateral development, but regional myocardial dysfunction during exercise stress served to detect ischemia despite increased collateral circulation.

The form of the ocular pulse in anesthetized dogs resembled an arterial pressure tracing. Obstructing the carotid artery reduced the amplitude of the pulse in the ipsilateral eye, but if collateral circulation through the basilar artery remained intact, the pulse soon returned to normal. Division of the basilar artery by itself temporarily increased the pulse amplitude in both eyes, probably reflecting increased collateral circulation through the carotid arteries. A 14% reduction in carotid blood flow or a 4% reduction in carotid blood pressure reduced the amplitude of the ocular pulse by 10% in dogs.

The increased exercise capacity after physical training in patients with coronary artery disease has been attributed to improved oxygen supply to the myocardium by way of increased collateral circulation or reduction of myocardial oxygen consumption by extracardiac factors, or both. Fourteen patients aged 43 to 61 years (mean 51 years) with 50 percent or greater obstruction in one, two or three vessels (three, six and five patients, respectively) underwent 13 months of physical training. Clinical status was either stable or improved with training. Treadmill exercise capacity, as measured by oxygen consumption, increased 25 percent from 21.9 ± 4.8 (standard deviation) to 27.4 ± 4.1 ml/kg-min at heart rates of 154 ± 17 and 156 ± 12 beats/min, respectively. After training, new collateral vessels, apparently secondary to progression of the disease, were observed in 2 of 21 arteries significantly but not completely obstructed before training. These data are in contrast to those reported for trained dogs with incomplete obstruction. Coronary arterial lesions progressed in only 4 of 14 patients. Coronary arteriographic data from this laboratory do not support the hypothesis that the increased exercise capacity after training in patients with coronary disease can be attributed to the development of collateral circulation. It is possible that physical training may retard the progression of coronary artery disease.

To evaluate the effect of coronary collateral development on ventricular fibrillation threshold (VFT), we determined VFT and the anastomotic index (AI) of coronary collateral development in 26 anesthetized, open-chest dogs before and 15 minutes after coronary artery occlusion. The current required to induce VFT was measured by passing constant current pulses through non-ischemic left ventricular myocardium during the vulnerable period of the cardiac cycle. Fifteen minutes after coronary occlusion VFT was significantly (P

Summary Six Macaca mulatta monkeys (4 males and 2 females) were given a diet free of choline, low in protein (5%) and rich in cholesterol (2%) for a period of 16 months. All six animals developed abnormal liver function and marked nutritional lipidic infiltration. Three male monkeys had well developed Laennec's cirrhosis. Two of these cirrhotic monkeys had slightly elevated splenic pulp pressure and portal vein pressure and showed evidence of increased collateral circulation on splenoportogram. One cirrhotic monkey died after 15 ½ months on the diet with no cause other than cirrhosis. The technique of esophagoscopy, barium swallow, percutaneous splenoportography and splenic pulp manometry in the monkey are described.