Time course of endothelial dysfunction and myocardial injury during myocardial ischemia and reperfusion in the cat.

@article{Tsao1990TimeCO,
  title={Time course of endothelial dysfunction and myocardial injury during myocardial ischemia and reperfusion in the cat.},
  author={Philip S. Tsao and Nobuo Aoki and David J. Lefer and G. Johnson and Allan M. Lefer},
  journal={Circulation},
  year={1990},
  volume={82 4},
  pages={
          1402-12
        }
}
Myocardial ischemia and reperfusion have been shown to impair coronary vasorelaxation to endothelium-dependent vasodilators. To examine the time course of this dysfunction, occlusion of the left anterior descending (LAD) coronary artery (90 minutes) was followed by reperfusion for 0, 2.5, 5, 20, 180, or 270 minutes. Coronary arterial rings from the ischemic LAD and control left circumflex (LCx) arteries were tested for responsiveness to the endothelium-dependent receptor-mediated vasodilator… Expand
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References

SHOWING 1-10 OF 56 REFERENCES
Reperfusion after acute coronary occlusion in dogs impairs endothelium-dependent relaxation to acetylcholine and augments contractile reactivity in vitro.
TLDR
The hypothesis that reperfusion of ischemic myocardium augments reactivity to vasoconstrictor agents by causing endothelial cell damage, excessive calcium influx, and loss of modulating vasodilator function is supported. Expand
Impaired Canine Coronary Vasodilator Response to Acetylcholine and Bradykinin After Occlusion‐ Reperfusion
TLDR
It is suggested that coronary reperfusion impairs coronary vasodilator reserve in intact dogs, and indomethacin or verapamil are not effective in modifying the reperfusions-related impairment of coronary vasODilators reserve. Expand
Reduction of reperfusion injury in the canine preparation by intracoronary adenosine: importance of the endothelium and the no-reflow phenomenon.
TLDR
It is suggested that intracoronary administration of adenosine after reperfusion significantly reduces infarct size and improves regional ventricular function in the ischemic zone in the canine preparation. Expand
Enhancement of recovery of myocardial function by oxygen free-radical scavengers after reversible regional ischemia.
TLDR
Improved recovery of function obtained with SOD and CAT suggests that oxygen-free radicals play an important role in the genesis of myocardial dysfunction after a brief episode of regional ischemia. Expand
Attenuated coronary relaxation after reperfusion: effects of superoxide dismutase and TxA2 inhibitor U 63557A.
TLDR
Cor coronary occlusion followed by reperfusion attenuates the relaxation of canine coronary artery rings in response to LTD4 as well as acetylcholine (ACh), suggesting loss of endothelium-dependent coronary reactivity. Expand
Role of leukocytes in response to acute myocardial ischemia and reflow in dogs.
TLDR
The significant participation of granulocytes in the unfavorable responses of flow, edema formation, and arrhythmias to the 1st h of myocardial ischemia is demonstrated and their role in the no-reflow phenomenon is document. Expand
Coronary vascular reactivity after acute myocardial ischemia.
TLDR
It is indicated that altered responses to thrombin in coronary arteries with damaged endothelium may play an important role in the pathogenesis of coronary vasospasm. Expand
Failure of superoxide dismutase to limit size of myocardial infarction after 40 minutes of ischemia and 4 days of reperfusion in dogs.
TLDR
The results suggest that superoxide anions that are accessible to the infused SOD are not a major cause of myocyte death caused by 40 min of severe ischemia followed by reperfusion, and allopurinol, a xanthine oxidase inhibitor, did not limit infarct size in this same experimental preparation. Expand
Can superoxide dismutase alter myocardial infarct size?
TLDR
The available preclinical studies involving SOD and the rationale for its use during acute myocardial infarction are reviewed to review the available conflicting results in laboratory animals. Expand
Reduction in experimental infarct size by recombinant human superoxide dismutase: insights into the pathophysiology of reperfusion injury.
TLDR
Analysis of the relationship between infarct size and collateral flow measured during ischemia in the two groups indicated that protection by h-SOD was greatest in animals with the lowest collateral flows, supporting the concept that reperfusion of ischemic myocardium results in a separate component of cell damage. Expand
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