Is calcium a mediator of infarct size reduction with preconditioning in canine myocardium?

@article{Przyklenk1997IsCA,
  title={Is calcium a mediator of infarct size reduction with preconditioning in canine myocardium?},
  author={K. Przyklenk and Katsuya Hata and Robert A. Kloner},
  journal={Circulation},
  year={1997},
  volume={96 4},
  pages={
          1305-12
        }
}
BACKGROUND The cellular mechanisms by which brief episodes of ischemia protect or "precondition" the heart and limit infarct size caused by a later period of sustained coronary artery occlusion remain unresolved. We propose that calcium may be an important mediator in eliciting this cardioprotection. METHODS AND RESULTS To test this hypothesis, anesthetized dogs received a 15-minute intracoronary infusion of 20 mmol/L CaCl2 or saline before undergoing 1 hour of coronary occlusion and 4 hours… 

Exercise Preconditioning of Myocardial Infarct Size in Dogs Is Triggered by Calcium

The protective effect of exercise preconditioning on myocardial infarct size is triggered, at least in part, by calcium inflow increase to the cell during exercise and, during the early window, is mediated by NADPH oxidase activation.

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Cardiac sodium/calcium exchanger preconditioning promotes anti-arrhythmic and cardioprotective effects through mitochondrial calcium-activated potassium channel.

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Cardiac preconditioning with 4-h, 17°C ischemia reduces [Ca2+]i load and damage in part via KATP channel opening

It is found that IPC before 4 h moderate hypothermia improved myocardial perfusion, contractility, and relaxation during normothermic reperfusion, and protection was associated with markedly reduced diastolic [Ca2+] loading throughout both hypothermic storage and reperfusions.

Opening of Ca2+-activated K+ channels is involved in ischemic preconditioning in canine hearts.

Ischemic preconditioning prior to aortic cross-clamping protects high-energy phosphate levels, glucose uptake, and myocyte contractility.

It is concluded that regional ischemic preconditioning prior to prolonged ischemia protects myocardial glucose uptake and myocyte contractile function and the beneficial effects on glucose metabolism suggest that preconditionsing may have sustained protective effects on cell metabolism.

Non Ischemic Myocardial Preconditioning by Tachycardia and Exercise

The results suggest that the protective effect of tachycardia and probably that of exercise may be partly due to a decrease in the cytosolic Ca2+ overload produced by ischemia.

Protection of the myocardium during ischemia and reperfusion : Na(+)/H(+) exchange inhibition versus ischemic preconditioning.

A comparison of the efficacy of Na+/H+ exchange inhibition versus ischemic preconditioning in limiting infarct size in dog hearts subjected to regional ischemia and reperfusion in vivo is reported.

Preconditioning-induced cardioprotection and release of the second messenger inositol (1,4,5)-trisphosphate are both abolished by neomycin in rabbit heart

Results demonstrate that myocardial Ins( 1,4,5)P3 content is increased in response to brief preconditioning ischemia and are consistent with the concept that Ins(1,4-5) P3 may be a potential mediator of infarct size reduction with preconditionsing in isolated rabbit heart.
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