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Cited by 7,812

The DOI matches its Crossref record; 2 of the 2 references it cites were found in a registry or an index.

Preconditioning with ischemia: a delay of lethal cell injury in ischemic myocardium.

Open access
Murry, C E, Jennings, R B, Reimer, K A·1986·Circulation
DOI 10.1161/01.cir.74.5.1124
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Abstract

We have previously shown that a brief episode of ischemia slows the rate of ATP depletion during subsequent ischemic episodes. Additionally, intermittent reperfusion may be beneficial to the myocardium by washing out catabolites that have accumulated during ischemia. Thus, we proposed that multiple brief ischemic episodes might actually protect the heart from a subsequent sustained ischemic insult. To test this hypothesis, two sets of experiments were performed. In the first set, one group of dogs (n = 7) was preconditioned with four 5 min circumflex occlusions, each separated by 5 min of reperfusion, followed by a sustained 40 min occlusion. The control group (n = 5) received a single 40 min occlusion. In the second study, an identical preconditioning protocol was followed, and animals (n = 9) then received a sustained 3 hr occlusion. Control animals (n = 7) received a single 3 hr occlusion. Animals were allowed 4 days of reperfusion thereafter. Histologic infarct size then was measured and was related to the major baseline predictors of infarct size, including the anatomic area at risk and collateral blood flow. In the 40 min study, preconditioning with ischemia paradoxically limited infarct size to 25% of that seen in the control group (p less than .001). Collateral blood flows were not significantly different in the two groups. In the 3 hr study, there was no difference between infarct size in the preconditioned and control groups. The protective effect of preconditioning in the 40 min study may have been due to reduced ATP depletion and/or to reduced catabolite accumulation during the sustained occlusion. These results suggest that the multiple anginal episodes that often precede myocardial infarction in man may delay cell death after coronary occlusion, and thereby allow for greater salvage of myocardium through reperfusion therapy.

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Metadata

Authors
Murry, C. E., Jennings, R. B., & Reimer, K. A.
Venue
Circulation
Publisher
Ovid Technologies (Wolters Kluwer Health)
Published
1986-11
Volume
74
Issue
5
Pages
1124-1136
ISSN
  • 0009-7322 (ISSN-L)
  • 1524-4539
DOI
10.1161/01.cir.74.5.1124
OpenAlex
W2146217294
Cited by
7,812
References
2
FWCI
5.29
Type
journal article
Language
en
Open access
bronze

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