Lack of both oxygen and glucose contributes to I/R-induced changes in cardiac SR function.

Although ischemia-reperfusion (I/R) has been shown to depress cardiac performance and sarcoplasmic reticulum (SR) function, the mechanisms underlying these alterations are poorly understood. Because lack of oxygen and substrate deprivation are known to occur during the ischemic phase, we examined the effects of reperfusion on cardiac performance and SR function in hearts subjected to hypoxia and substrate lack. For this purpose, isolated rat hearts were perfused with hypoxic and/or glucose-free medium for 30 min and then reperfused with normal medium for 1 h; the SR vesicles were isolated for studying the Ca(2+)-transport activities.

Ca2+-overload inhibits the cardiac SR Ca2+-calmodulin protein kinase activity.

There is increasing evidence to suggest that Ca2+-calmodulin dependent protein kinase (CaMK) regulates the sarcoplasmic reticulum (SR) function and thus plays an important role in modulating the cardiac performance. Because intracellular Ca2+-overload is an important factor underlying cardiac dysfunction in a heart disease, its effect on SR CaMK was examined in the isolated rat heart preparations. Ca2+-depletion for 5 min followed by Ca2+-repletion for 30 min, which is known to produce intracellular Ca2+-overload, was observed to attenuate cardiac function as well as SR Ca2+-uptake and Ca2+-release activities.

Blockade of 5-HT(2A) receptors by sarpogrelate protects the heart against myocardial infarction in rats.

Background: It has been shown that serotonin (5-hydroxytryptamine, 5-HT) is involved in exacerbating vascular abnormalities; however, its role in mediating changes in cardiac function due to myocardial injury has yet to be established. This study examined the effect of sarpogrelate, a 5-HT(2A) receptor blocker, in preventing cardiac dysfunction due to myocardial infarction (MI).

Methods And Results: Rats were treated 3 days before surgery with or without 5 mg x kg(-1) x day(-1) sarpogrelate, and the left coronary artery was ligated for 3 weeks to induce MI.

Preconditioning prevents alterations in cardiac SR gene expression due to ischemia-reperfusion.

We have previously shown that ischemic preconditioning (IP) improves cardiac performance and sarcoplasmic reticulum (SR) function in hearts subjected to ischemia-reperfusion (I/R). In this study, we examined the effect of IP on I/R-induced changes in gene expression for SR proteins such as the Ca(2+) release channel, Ca(2+) pump ATPase, phospholamban, and calsequestrin in the isolated rat heart. Normal isolated rat hearts exposed to three brief cycles of IP (5-min ischemia and 5-min reperfusion) exhibited a significant decrease in the transcript levels of SR genes.