SUMMARY The contractile state of the noninfarcted myocardium was examined in adult cats after myocardial infarction produced by ligation of several branches of the left coronary artery. At 2 days, 7 days, and 6 weeks after infarction, and after determination of intracardiac pressures, papillary muscles were excised from the noninfarcted segment of the right ventricle and attached to a myograph for analysis of contractile function. One week after infarction there was a decline in actively developed force at L msx , caused by a decrease in the rate of force development. In addition, the response to procedures that augment myocardial contractility, such as paired stimulation and increasing the frequency of electrical stimulation, was significantly depressed. Two days after infarction, changes were less significant, although similar in direction. Six weeks after infarction, developed force at L max had returned to normal values. The response to procedures augmenting contractility also had returned to normal. There appears to be a distinct, reversible loss of contractility in the remaining viable myocardium in the early phase after experimental infarction.AFTER MYOCARDIAL infarction, the uninvolved portion of the heart generally is thought to maintain function and metabolism, unless coexisting stenosis of additional vessels causes ischemia of the noninfarcted segments. However, after experimental myocardial infarction, the clearly nonischemic portion of the heart muscle shows changes in its energy metabolism as well as a reversible decline in norepinephrine content.1 * 3 The functional significance of these changes, however, remains largely unknown because determinations of ventricular function after infarction fail to differentiate the infarcted and the surviving areas. Theroux et al. 4 demonstrated an increased extent of shortening of noninfarcted areas early after infarction which was caused by regional operation of the Frank-Starling mechanism; an alternate explanation could be that unloading of the ischemic segment permits increased active shortening as well. In the present study we analyzed myocardial function after isolation of the surviving heart muscle, to exclude any effect of the infarct itself. To avoid the ill-defined changes which occur in the zone which borders the infarct, we studied right ventricular papillary muscles after left ventricular infarction. We thus attempted to determine the effect of an acute myocardial infarction on the contractile properties of surviving, noninfarcted heart muscle. MethodsMyocardial infarction was produced in adult cats by ligation of several branches of the left coronary artery. Under general anesthesia (halothane, N 2 O, and O 2 ), the cats were intubated, and a thoractomy was performed through the 5th left intercostal space. After opening the pericardial sac, we ligated between three and five branches of the left coronary artery which lead to the free wall of the left ventricle. Infarctions produced in this way were comparable in extent and location in different cat...
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.