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

  title={Is calcium a mediator of infarct size reduction with preconditioning in canine myocardium?},
  author={K. Przyklenk and Katsuya Hata and Robert A. Kloner},
  volume={96 4},
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.

Inhibition of the Na(+)/H(+) exchanger confers greater cardioprotection against 90 minutes of myocardial ischemia than ischemic preconditioning in dogs.

Although IPC and NHE-1 inhibition provide comparable protection against 60 minutes of myocardial ischemia, NHE -1 inhibition is more efficacious than IPC at protecting against a 90-minute ischemic insult.

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

It is concluded that pretreatment with E4031 reduces infarct size and produces anti-arrhythmic effect via stimulating the reverse-mode NCX, and that the mitoKCa channels mediate the protective effects.

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.



Does ischemic preconditioning trigger translocation of protein kinase C in the canine model?

The hypothesis that translocation of PKC, triggered by preconditioning ischemia, is an important mechanism for the reduction in infarct size seen with preconditionsing in the dog model is fail to support.

Reversibly Injured, Postischemic Canine Myocardium Retains Normal Contractile Reserve

It is demonstrated that stunned myocardium in this model retains a normal contractile reserve in response to calcium, suggesting that the mechanism responsible for postischemic contractile dysfunction involves calcium.

Myocardial Protection by Na+-H+ Exchange Inhibition in Ischemic, Reperfused Porcine Hearts

This study was undertaken to determine whether inhibition of Na+-H+ exchange limits infarct size and improves regional systolic shortening in regional ischemia and reperfusion in intact pigs.

A comparison of adenosine-induced cardioprotection and ischemic preconditioning in dogs. Efficacy, time course, and role of KATP channels.

A 10-minute intracoronary infusion of adenosine exhibits the same efficacy as ischemic preconditioning in reducing myocardial necrosis in dogs and supports the hypothesis that endogenousAdenosine released during ischemia is an important mediator of preconditionsing.

Infarct size-limiting effect of ischemic preconditioning is blunted by inhibition of 5'-nucleotidase activity and attenuation of adenosine release.

Increases in ectosolic 5'-nucleotidase activity and adenosine release are primarily responsible for the infarct size-limiting effect of ischemic preconditioning.

Intramyocardial injections and protection against myocardial ischemia. An attempt to examine the cardioprotective actions of adenosine.

It was concluded that fluid injection did not itself cause appreciable necrosis and speculated that muscle was protected in the vicinity of the injection site, and evidence for myocyte protection via a stretch-activated mechanism was found.

Preconditioning protects ischemic rabbit heart by protein kinase C activation.

Activation of protein kinase C with 4 beta-phorbol 12-myristate 13-acetate (PMA) or with 1-oleyl-2-acetyl glycerol (OAG) mimicked preconditioning in buffer-perfused hearts, which blocked protection from ischemic preconditionsing in isolated heart.

Postischemic changes in cardiac sarcoplasmic reticulum Ca2+ channels. A possible mechanism of ischemic preconditioning.

The modifications of cardiac ryanodine receptors/sarcoplasmic reticulum Ca2+ release channels occurring in ischemic preconditioning and the injury produced by 30 minutes of global ischemia was reduced by preexposure to three 3-minute periods of globalIschemia (preconditioning ischemIA).