Quantitative study of intramyocardial compression in the fibrillating heart.

Extravascular compression inhibits coronary blood flow in fibrillating hearts. Pressure-flow curves from spontaneously fibrillating hearts whose coronary arteries were maximally dilated were examined to see whether this inhibition involves a vascular waterfall mechanism as has been found in the beating heart. Waterfall behavior is indicated when pressure-flow curves are linear and experience a zero-flow intercept at pressures greater than venous pressure. Regional pressure-flow curves revealed a zero flow intercept of 28.4 mmHg for the inner quarter of the left ventricle, indicating that compression is quite high in that region. A zero-pressure intercept of only 15.1 was found at the outer quarter, which was not significantly different from venous pressure. We conclude that the spontaneously fibrillating heart experiences a gradient of compression falling from 28 mmHg at the subendocardium to near zero at the subepicardium.

Effects of sodium nitroprusside on function of regional ischemic myocardium.

In the presence of regional myocardial ischemia, a 20% decrease in systemic arterial pressure following nitroprusside caused a 25% decrease in coronary perfusion pressure in animals with normal left ventricular end-diastolic pressures. This pressure decrement resulted in a significant decrease in the shortening of the regionally ischemic segment during the ejection phase of systole. A comparable arterial pressure drop of 21% with nitroprusside infusion during ischemia in the animals with elevated diastolic pressures caused a similar 28% decrease in coronary perfusion pressure, but resulted in a simultaneous increase in regional shortening. For the entire group there was no significant change in stroke volume. Even in the 11 animals where stroke volume increased, systolic regional shortening increased in only 4. An increase in stroke volume cannot be used to infer a parallel increase in the performance of a regionally ischemic segment. Nitroprusside appears to improve regional performance only in the presence of severe failure.

Accumulation of technetium-99m stannous pyrophosphate in contused myocardium.

The uptake of technetium-99m stannous pyrophosphate in contused myocardium was measured as a function of time from the insult. The free wall of the dog's left ventricle was surgically exposed and struck with a spring-loaded paddle. Pyrophosphate was injected intravenously from 1 1/2 to 47 1/2 hr after the injury. After 1/2 hr of incubation the hearts were removed and the Tc-99m content of contused and noncontused myocardium was measured. Pyrophosphate was concentrated in contused myocardium at all of the time periods tested. Contused-to-normal ratios for pyrophosphate uptake ranged from 8.1 (8 hr) to 41.9 (48 hr).

Inhibitory effect of cardiac contraction on coronary collateral blood flow.

The present study was undertaken to determine the effect of contraction on overall flow in an area supplied by collateral vessels. Changes in the distribution of blood flow across the wall of ischemic and normally perfused regions of the left ventricle were observed during normal beating and during vagal arrest. The main left coronary artery was cannulated and perfused at constant pressure (125 mmHg) using a servo pump apparatus. An ischemic area supplied by collaterals was created by ligating the left anterior descending artery. Radiomicrospheres (15 micrometer) were injected into the perfusion apparatus during beating. Then spheres with a different label were administered to the same heart during arrest. The results revealed that beating caused a gradient of blood flow inhibition from near zero at the epicardium to about 50% at the endocardium in both zones. Inhibition to flow at the mid wall of the ischemic zone, 71%, was significantly greater than that seen at the corresponding depth in the normally perfused region, 33%. These results indicate that contraction not only inhibits collateral blood flow to an ischemic region, but also that the inhibition is actually magnified at the mid wall.

Selective coronary embolization in closed-chest dogs.

A method is described for occluding a branch of the canine left coronary arterial system, without the use of X-ray equipment or the need for a surgical thoracotomy. For the creation of experimental myocardial infarction, either a solid embolus or a diffusible medium is introduced into the coronary vessels via a rigid cannula which is inserted through a carotid artery. This technique produces infarcts of reproducible size with a minimum of equipment and surgical complication.

The effect of cardiac contraction on collateral resistance in the canine heart.

We determined whether the coronary collateral vessels develop an increased resistance to blood flow during systole as does the cognate vascular bed. Collateral resistance was estimated by measuring retrograde flow rate from a distal branch of the left anterior descending coronary artery while the main left coronary artery was perfused at a constant pressure. Retrograde flow rate was measured before and during vagal arrest. We found that in 10 dogs the prolonged diastole experienced when the heart was stopped caused no significant change in the retrograde flow rate, which indicated that systole has little effect on the collateral resistance. However, when left ventricular end-diastolic pressure was altered by changing afterload or contractility, a direct relationship between end-diastolic pressure and collateral resistance was noted.

Functional abnormalities in nonoccluded regions of myocardium after experimental coronary occlusion.

The performance characteristics of both ischemic and "adjacent" and "remote" nonischemic myocardium were studied in open chest dogs by three mercury-in-Silastic length gauges sutured to the anterior surface of the left ventricle before and after occlusion of the distal left anterior descending coronary artery. The adjacent gauge was separated from the ischemic segment by one large nonoccluded diagonal branch of the left anterior descending artery. Remote myocardium was separated from the ischemic area by two such branches. At the time of occlusion epicardial S-T segment elevation appeared in the ischemic region but not in the adjacent or remote regions. Immediately after occlusion, typical changes of ischemic dysfunction appeared. Late systolic lengthening, depression of systolic shortening and increased diastolic compliance occurred consistently and simultaneously in ischemic and adjacent regions and inconsistently in the remote region. Five minutes after occlusion, fiber shortening was depressed to 21, 58 and 67 percent of control values in ischemic, adjacent and remote regions, respectively. Heart rate did not change, and mean arterial pressure decreased slightly. These changes persisted over time. In 11 of these dogs, end-diastolic pressure was maintained constant 20 minutes after occlusion. Systolic shortening was depressed to 40 and 74 percent of control values in the ischemic and adjacent regions, respectively. In six dogs, end-diastolic pressure was varied form 5 to 20 mm Hg by rapid volume loading during the control state and 30 minutes after occlusion. Systolic shortening in ischemic, adjacent and remote regions was depressed to 20, 40 and 65 percent of control values, respectively. The severity of all functional alterations after coronary occlusion was directly related to proximity to the ischemic region. These results indicate that depression of left ventricular function after coronary occlusion may be partially related to previously unrecognized depression of function in apparently "nonischemic" myocardium.

Hemodynamic and metabolic effects of sodium nitroprusside on the performance and metabolism of regional ischemic myocardium;.

To assess the effects of sodium nitroprusside (5-10 mug/min) on total and regional cardiac performance, energetics, and lactate metabolism during acute ischemia, studies were performed in 21 open-chest dogs. For studies of regional function and metabolism, length gauges were sutured to the epicardial surface and an epicardial vein adjacent to the artery to be occluded was cannulated. Following occlusion of the left anterior descending coronary artery, cardiac output, mean arterial pressure, epicardial vein blood flow, and systolic shortening of the ischemic segment decreased significantly, In the blood samples from the ischemic zone, but not in those from the coronary sinus, lactate extraction shifted to production. In seven control dogs these alterations persisted throughout the experiment. In 14 animals treated with nitroprusside, cardiac output increased while peripheral resistance and mean arterial pressure decreased. Systolic shortening in the ischemic segment increased from 1.10 +/- 0.24 (SEM) to 1.77 +/- 0.30 mm (P less than 0.005). In eight dogs, regional venous outflow increased from 1.9 +/- 0.1 to 3.0 +/- 0.4 ml/min despite a slight reduction in mean arterial pressure. Concomitantly, regional negative lactate balance was reduced from -61.0 +/- 20.0 to -23.2 +/- 5.7% (P less than 0.05). These results indicate that nitroprusside significantly improves both total cardiac performance and the mechanical performance of regional ischemic myocardium. Moreover, this improvement in mechanical function occurred concomitantly with apparent increase in regional perfusion and reduction in lactate production, suggesting that nitroprusside simultaneously alleviates ischemia.