Ejection- and isovolumic contraction-phase wall thickening in nonischemic myocardium during coronary occlusion

Abstract

During acute regional ischemia in open-chest anesthetized dogs, contraction is augmented in nonischemic myocardium. The effectiveness of enhanced contraction, however, has been questioned based on recent studies (using midwall segment length measurements) that reported that most of the increase occurred only during the isovolumic contraction phase (ICP) and not the ejection phase (EP) of systole. We evaluated this issue retrospectively using a different means of measuring regional myocardial function, systolic wall thickening (measured with sonomicrometers). In open-chest anesthetized dogs we observed a significant increase in both ICP and EP wall thickening. With circumflex occlusion, ICP and EP thickening each contributed an average of 50% to the augmentation in total thickening. With left anterior descending occlusion, ICP thickening contributed a significantly greater proportion (71%) to the total increase, but the change in EP thickening was also significant (29%). Therefore, in open-chest dogs we observed evidence of intraventricular unloading (in that ICP thickening increased), but we also observed an increase in effective (EP) thickening. In a series of conscious dogs, however, we observed no significant change in total nonischemic thickening after circumflex coronary occlusion. There was a statistically significant increase in the ICP component acutely after coronary occlusion, but its contribution to total wall thickening was small. In a group of dogs studied at intervals for 2 wk after circumflex occlusion, there was no evidence of intraventricular unloading beyond 3-5 days postocclusion. Therefore, we conclude that significant intraventricular unloading is restricted to the acute phases of myocardial infarction, and we suggest that its functional importance is smaller in conscious closed-chest chest dogs than in open-chest dogs.

Contribution of asynchrony and nonuniformity to mechanical interaction in normal and stunned myocardium

“…It has been postulated that, during regional ischemia, either a difference in contractility (''weak and strong muscles in series'') or a difference in timing (''asynchrony'') between ischemic and nonischemic regions is responsible for the mechanical interaction (2,16,17,20,23,28). In the present study, we confirmed a role for both mechanisms in regionally stunned myocardium.…”

“…During ischemia, three independent factors have been identified to contribute to mechanical interaction: 1) changes in sympathetic tone, 2) the Frank-Starling mechanism, and 3) direct myocardial unloading (2,7,8,10,12,16,17,20,23,28,30). The proposed mechanism to explain mechanical interaction during ischemia is discussed for the present experimental conditions.…”

Inducible Nitric Oxide Synthase Expression and Cardiomyocyte Dysfunction During Sustained Moderate Ischemia in Pigs

“…37 Apart from NOS-derived NO, we have recently demonstrated NOS-independent NO accumulation within the myocardial interstitium during myocardial ischemia in vivo. 38 Although NOS-independent NO production may thus have contributed to nitrite formation during ischemia, cellular contractile dysfunction triggered by L-arginine in ISCH was reversible by iNOS inhibition, suggesting that iNOSdependent NO formation confined to the cardiomyocyte was most important for the measured functional alterations.…”

Effects of gradual coronary artery occlusion and exercise training on gene expression in swine heart

“…physiologic vs. pathologic) and magnitude of the resultant cardiac hypertrophy have not been reported. Abrupt occlusion of a coronary artery in mammals leads to myocardial infarction and hypertrophy of the remaining viable tissue that is phenotypically pathological (13)(14)(15). It is not clear, however, whether gradual LCX occlusion stimulates changes in gene expression that are associated with the physiological or pathological phenotype.…”