K_ATP channels are common mediators of ischemic and calcium preconditioning in rabbits

Abstract

Calcium preconditioning (CPC), like ischemic preconditioning (IPC), reduces myocardial infarct size in dogs and rats. ATP-sensitive potassium (KATP) channels induce cardioprotection of IPC in these animals. To determine whether KATP channels mediate both IPC and CPC, pentobarbital sodium-anesthetized rabbits received 30 min of coronary artery occlusion followed by 180 min of reperfusion. IPC was elicited by 5 min of occlusion and 10 min of reperfusion, and CPC was elicited by two cycles of 5 min of calcium infusion with an interval period of 15 min. Infarct size expressed as a percentage of the area at risk was 38 ± 3% (mean ± SE) in controls. IPC, CPC, and pretreatment with a KATP channel opener, cromakalim, all reduced infarct size to 13 ± 2, 17 ± 2, and 12 ± 3%, respectively ( P < 0.01 vs. controls). Glibenclamide, a KATP channel blocker administered 45 min (but not 20 min) before sustained ischemia, attenuated the effects of IPC and CPC (31 ± 4 and 41 ± 6%, respectively). Thus KATP channel activation appears to contribute to these two types of cardioprotection in rabbits.

Inhibition of cardiac contractility by 5-hydroxydecanoate and tetraphenylphosphonium ion: a possible role of mitoKATP in response to inotropic stress

“…In fact, this is the case. Calcium preconditioning has been well known for a decade (12,19,21); considerable literature supports the concept that ␣ 1 -receptor stimulation is cardioprotective (1,2,28), and preliminary studies have shown ouabain to be cardioprotective (22). Moreover, each of these modes of protection has been shown to involve K ATP channels.…”

Altered NADH and improved function by anesthetic and ischemic preconditioning in guinea pig intact hearts

“…Also, giving a K ATP antagonist with a volatile anesthetic reduced the preconditioning effects despite a similar temporary depression of function in both groups (24). On the other hand, a temporary increase in extracellular calcium, which induces a positive inotropic effect, has been shown to precondition hearts (26). In contrast, brief exposure to a volatile anesthetic decreased intracellular Ca 2ϩ transients (35).…”

Exercise training alters an anoxia-induced, glibenclamide-sensitive current in rat ventricular cardiocytes

“…Importantly, there has been considerable speculation that I K ATP may play a cardioprotective role in various preconditioning and I/R settings (6,10,21,27,38,44). Interestingly, perhaps depending on the experimental setting, both I K ATP activation (6, 28) and I K ATP attenuation (19,36,47) have been associated with cardioprotection and/or improved recovery after I/R challenge.…”