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Excitation-contraction coupling in hypothermic ischemic myocardium

Excitation-contraction coupling in hypothermic ischemic myocardium sarcoplasmic reticulum; myofibrils; glycogen continues to be a cornerstone of myocardial preservation during periods of surgically induced, global ischemia (15). Although much work has been done since Proctor et al. (17) stated that virtually nothing was known of the physiology biochemistry of the myocardium at 4”C, a complete understing of the of the hypothermic ischemic myocardium is not yet available. Deep hypothermia (5°C) has been shown to be well tolerated but is still associated with anatomical alterations that include glycogen depletion T-tube mitochondrial distortion in the canine myocardium after 60 minutes of global ischemia (1). In clinical biopsies, Engedal et al. (4) found that myocardial HYPOTHERMIA H336 preservation with only hypothermia was still associated with intracellular edema, myelin figures, myofibrillar lysis. These electron micrographic observations of T-tube distortion myofibrillar lysis in the global ischemic hypothermic myocardium would tend to incriminate a defect in the system involved in the regulation of the myocardial contractility, i.e., the excitation-contraction coupling system. Intracellularly, excitation-contraction coupling proceeds when the action potential causes the regenerative release of calcium from the sarcoplasmic reticulum (7). The increase in intracellular calcium concentration in turn is preferentially bound by the thin-filament protein troponin, calcium-troponin interaction results in cross-bridge http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png AJP - Heart and Circulatory Physiology The American Physiological Society

Excitation-contraction coupling in hypothermic ischemic myocardium

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Publisher
The American Physiological Society
Copyright
Copyright © 1981 the American Physiological Society
ISSN
0363-6135
eISSN
1522-1539
Publisher site
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Abstract

sarcoplasmic reticulum; myofibrils; glycogen continues to be a cornerstone of myocardial preservation during periods of surgically induced, global ischemia (15). Although much work has been done since Proctor et al. (17) stated that virtually nothing was known of the physiology biochemistry of the myocardium at 4”C, a complete understing of the of the hypothermic ischemic myocardium is not yet available. Deep hypothermia (5°C) has been shown to be well tolerated but is still associated with anatomical alterations that include glycogen depletion T-tube mitochondrial distortion in the canine myocardium after 60 minutes of global ischemia (1). In clinical biopsies, Engedal et al. (4) found that myocardial HYPOTHERMIA H336 preservation with only hypothermia was still associated with intracellular edema, myelin figures, myofibrillar lysis. These electron micrographic observations of T-tube distortion myofibrillar lysis in the global ischemic hypothermic myocardium would tend to incriminate a defect in the system involved in the regulation of the myocardial contractility, i.e., the excitation-contraction coupling system. Intracellularly, excitation-contraction coupling proceeds when the action potential causes the regenerative release of calcium from the sarcoplasmic reticulum (7). The increase in intracellular calcium concentration in turn is preferentially bound by the thin-filament protein troponin, calcium-troponin interaction results in cross-bridge

Journal

AJP - Heart and Circulatory Physiology – The American Physiological Society

Published: Mar 1, 1981

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