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Taylor AL, Murphree S, Buja LM, et al. Segmental systolic responses to brief ischemia and reperfusion in the hypertrophied canine left ventricle. J Am Coll Cardiol. 1992;20(4):994-1002doi: 10.1016/0735-1097(92)90203-y.
Taylor, A. L., Murphree, S., Buja, L. M., Villarreal, M. C., Pastor, P., & Eckels, R. (1992). Segmental systolic responses to brief ischemia and reperfusion in the hypertrophied canine left ventricle. Journal of the American College of Cardiology, 20(4), 994-1002. https://doi.org/10.1016/0735-1097(92)90203-y
Taylor, A L, et al. "Segmental systolic responses to brief ischemia and reperfusion in the hypertrophied canine left ventricle." Journal of the American College of Cardiology vol. 20,4 (1992): 994-1002. doi: https://doi.org/10.1016/0735-1097(92)90203-y
Taylor AL, Murphree S, Buja LM, Villarreal MC, Pastor P, Eckels R. Segmental systolic responses to brief ischemia and reperfusion in the hypertrophied canine left ventricle. J Am Coll Cardiol. 1992 Oct;20(4):994-1002. doi: 10.1016/0735-1097(92)90203-y. PMID: 1388184.
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Elsevier Science

J Am Coll Cardiol. 1992 Oct;20(4):994-1002. doi: 10.1016/0735-1097(92)90203-y.

Segmental systolic responses to brief ischemia and reperfusion in the hypertrophied canine left ventricle.

Journal of the American College of Cardiology

A L Taylor, S Murphree, L M Buja, M C Villarreal, P Pastor, R Eckels

Affiliations

  1. Pauline and Adolph Weinberger Laboratory for Cardiopulmonary Research, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas.

PMID: 1388184 DOI: 10.1016/0735-1097(92)90203-y
Free Article

Abstract

OBJECTIVES AND BACKGROUND: Left ventricular hypertrophy is associated with increased mortality, increased myocardial infarct size and an increased incidence of sudden death. Although reperfusion after ischemia has been shown to result in decreased infarct size and recovery of systolic thickening, it is unknown how left ventricular hypertrophy might influence recovery of regional systolic thickening after ischemia and reperfusion. We hypothesized that left ventricular hypertrophy might attenuate or abolish the functional response to reperfusion.

METHODS: Three groups of chronically instrumented, conscious dogs (dogs with left ventricular hypertrophy and hypertension; dogs with left ventricular hypertrophy and reduced blood pressure and a control group without hypertrophy and with normal blood pressure) underwent 15 min of ischemia and 24 h of reperfusion. Segmental systolic thickening was measured by sonomicrometers and myocardial segments were grouped by percent of control segmental systolic thickening retained at 15 min of ischemia (class 1 greater than or equal to 67%, class 2 from 0% to 66%, class 3 less than 0% control systolic thickening). The recovery of each class of segment was measured serially during reperfusion. Hemodynamic variables and regional myocardial blood flow were also measured.

RESULTS: There were no differences among groups in recovery of segmental systolic thickening for class 1 segments. Systolic thickening in class 2 (hypokinetic) segments was significantly depressed (p less than 0.05 compared with control value) in the group with left ventricular hypertrophy and reduced blood pressure (but not in the group with hypertrophy and hypertension) during early reperfusion; systolic thickening in class 3 (dyskinetic) segments showed a similar trend in the group with hypertrophy and reduced pressure.

CONCLUSIONS: Although left ventricular hypertrophy with hypertension did not attenuate the contractile response to reperfusion, hypertrophy with reduced blood pressure was associated with significantly greater depression of segmental systolic thickening early during reperfusion.

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