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Leukocytes and Ischemia-Induced Myocardial Injury

Leukocytes and Ischemia-Induced Myocardial Injury Benedict R. Lucchesi Department of Pharmacology. The University of Michigan Medical School. Ann Arbor. Michigan 48109 Keven M. Mullane Department of Pharmacology. New York Medical College. Valhalla. New York 10595 THE MEANS OF LIMITING INFARCT SIZE In the early 1970s Maroko, Braunwald, and others demonstrated the im­ portance of myocardial oxygen supply and demand as a major determinant of the extent of myocardial injury 0-3). A variety of agents that reduced myocar­ dial oxygen demand, B-adrenoceptor antagonists and calcium channel blockers for example, were shown to be beneficial in animal models of myocardial ischemia. The time for clinical testing of agents that improve myocardial oxygenation was said to have come (4). A decade later, however, the limited clinical results have been far from exciting. This approach to reducing isch­ emia-induced myocardial injury suffers from three major problems. Implicit in the concept of salvaging ischemic myocardium by altering myocardial oxygen supply and demand is the assumption that myocardial tissue injury results solely from an inability of the coronary vasculature to deliver necessary oxygen and nutrients to maintain myocyte viability. However, we believe that other pathophysiologic processes contribute to irreversible myocar­ dial damage. It is also assumed that the restoration http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Annual Review of Pharmacology and Toxicology Annual Reviews

Leukocytes and Ischemia-Induced Myocardial Injury

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Publisher
Annual Reviews
Copyright
Copyright 1986 Annual Reviews. All rights reserved
Subject
Review Articles
ISSN
0362-1642
eISSN
1545-4304
DOI
10.1146/annurev.pa.26.040186.001221
pmid
3521455
Publisher site
See Article on Publisher Site

Abstract

Benedict R. Lucchesi Department of Pharmacology. The University of Michigan Medical School. Ann Arbor. Michigan 48109 Keven M. Mullane Department of Pharmacology. New York Medical College. Valhalla. New York 10595 THE MEANS OF LIMITING INFARCT SIZE In the early 1970s Maroko, Braunwald, and others demonstrated the im­ portance of myocardial oxygen supply and demand as a major determinant of the extent of myocardial injury 0-3). A variety of agents that reduced myocar­ dial oxygen demand, B-adrenoceptor antagonists and calcium channel blockers for example, were shown to be beneficial in animal models of myocardial ischemia. The time for clinical testing of agents that improve myocardial oxygenation was said to have come (4). A decade later, however, the limited clinical results have been far from exciting. This approach to reducing isch­ emia-induced myocardial injury suffers from three major problems. Implicit in the concept of salvaging ischemic myocardium by altering myocardial oxygen supply and demand is the assumption that myocardial tissue injury results solely from an inability of the coronary vasculature to deliver necessary oxygen and nutrients to maintain myocyte viability. However, we believe that other pathophysiologic processes contribute to irreversible myocar­ dial damage. It is also assumed that the restoration

Journal

Annual Review of Pharmacology and Toxicology – Annual Reviews

Published: Apr 1, 1986

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