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Hearse DJ. Ischemia at the crossroads?. Cardiovasc Drugs Ther. 1988;2(1):9-15doi: 10.1007/BF00054247.
Hearse, D. J. (1988). Ischemia at the crossroads?. Cardiovascular drugs and therapy, 2(1), 9-15. https://doi.org/10.1007/BF00054247
Hearse, D J. "Ischemia at the crossroads?." Cardiovascular drugs and therapy vol. 2,1 (1988): 9-15. doi: https://doi.org/10.1007/BF00054247
Hearse DJ. Ischemia at the crossroads?. Cardiovasc Drugs Ther. 1988 May;2(1):9-15. doi: 10.1007/BF00054247. PMID: 3154700.
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Cardiovasc Drugs Ther. 1988 May;2(1):9-15. doi: 10.1007/BF00054247.

Ischemia at the crossroads?.

Cardiovascular drugs and therapy

D J Hearse

Affiliations

  1. Rayne Institute, St. Thomas' Hospital, London, United Kingdom.

PMID: 3154700 DOI: 10.1007/BF00054247

Abstract

Understanding and controlling the consequences of myocardial ischemia requires us to acknowledge that we are dealing with a complex, dynamic, and highly variable process. The severity and progression of ischemic injury is not solely determined by the extent of oxygen deprivation, but by many other factors, including the accumulation of toxic metabolites. It may not be justified to assume that injury to the myocyte necessarily determines the survival of the organ; other components, such as the endothelium and the conducting system, may play a crucial role. Many factors can influence the severity and evolution of ischemic injury, perhaps the most important being the extent of residual (or collateral) flow to the affected tissue. If the ischemia is relatively mild, then the myocardium may survive for some long time, and drugs and other interventions may be used to further extend this period. However, reperfusion and the establishment of an adequate level of coronary flow is an absolute prerequisite for sustained tissue survival. The more severe the ischemia, the earlier must be the reperfusion. However, reperfusion of previously ischemic tissue is not without hazard, and it may precipitate potentially lethal events such as arrhythmias. Reperfusion may possibly result in the death of cells that were potentially viable in the moments before reflow was established, and there is good evidence that manipulation of reperfusion conditions may accelerate and possibly enhance recovery from ischemia. Much remains to be learned about myocardial ischemia and reperfusion, and in doing this we should perhaps put some of the older, yet well established, concepts behind us.

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