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Published on: July 27, 2015
Stress damage to nonischemic divisions of the heart in experimental infarction and its prevention
Insights
Emotional-painful stress, not just ischemia, impairs nonischemic heart function after myocardial infarction. Propranolol and membrane stabilizers can prevent these stress-induced contractile deficits in heart muscle.
Area of Science:
- Cardiology
- Cardiovascular Physiology
- Stress Physiology
Background:
- Myocardial infarction (MI) creates ischemic zones, but nonischemic areas also show functional deficits.
- These deficits in nonischemic regions are hypothesized to stem from infarction-associated emotional-painful stress.
Purpose of the Study:
- To investigate the role of emotional-painful stress in the contractile dysfunction of nonischemic heart regions following myocardial infarction.
- To assess the effects of stress and potential therapeutic interventions on myocardial contractility.
Main Methods:
- Studied contractile function of the isolated right auricle (a nonischemic cardiac region) in rats post-left ventricle myocardial infarction.
- Induced stress in control rats to replicate infarction-induced stress effects.
- Administered propranolol, antioxidant ionol, nicotinamide, and chloroquine to evaluate their preventative effects.
Main Results:
- Myocardial infarction led to reduced atrial extensibility, depressed Starling curve, decreased maximal systolic tension, and lower resistance to hypoxia and calcium excess.
- These contractile disturbances were fully replicated by emotional-painful stress alone and largely prevented by propranolol.
- Membrane-stabilizing agents (ionol, nicotinamide, chloroquine) mitigated stress-induced contractile dysfunction in the context of infarction.
Conclusions:
- Emotional-painful stress significantly contributes to the contractile dysfunction observed in nonischemic heart regions after myocardial infarction.
- Propranolol and agents stabilizing cardiomyocyte membranes show potential for preventing or limiting these stress-mediated cardiac deficits.
- Further research is warranted to explore therapeutic applications of these findings in ischemic heart disease.
Abstract:
Recently, it has been shown that nonischemic parts of the heart in myocardial infarction were separated from ischemic damaged ones by a sharp border zone. In this connection, the disturbance of contractile function of the myocardium of nonischemic parts is suggested to result from the infarction-concomitant emotional-painful stress. In order to test this assumption, the contractile function of the right auricle, which is an a priori nonischemic heart division, was studied in rats subjected to myocardial infarction of the left ventricle. In the study of the isolated auricle the following facts were established: 1 day after the induced infarction the atrial myocardium shows reduced extensibility, depression of the Starling curve, a concomitant approximately twofold decrease of the maximal systolic tension, and a reduced myocardial resistance to hypoxia and calcium excess. This complex of shifts, first, is completely reproduced without myocardial infarction by emotional-painful stress and, second, can be prevented to a considerable extent by propranolol indicating that it is essentially stress induced. In infarction, these above said stress-induced disturbances of the contractile function of nonischemic divisions of the heart were found to be prevented or limited by factors stabilizing the membranous lipid bilayer of cardiomyocytes, i.e., by antioxidant ionol, by nicotinamide, a lipase inhibitor, and by chloroquine, a phospholipase inhibitor. The aspects of application of these factors for the therapy of ischemic heart disease requires further studies.
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