Thiopentone does not block ischemic preconditioning in the isolated rat heart

Purpose: Ischemic preconditioning protects the heart against subsequent pro longed ischemia by opening of adenosine triphosphate-sensitive potassium (K -ATP) channels. Thiopentone blocks K-ATP channels in isolated cells. Theref ore, we investigated the effects of thiopentone on ischemic preconditioning . Methods: Isolated nat hearts (n = 56) were subjected to 30 min of global no -flow ischemia, followed by 60 min of reperfusion. Thirteen hearts underwen t the protocol without intervention (control, CON) and in I I hearts (preco nditioning, PC), ischemic preconditioning was elicited by two five-minute p eriods of ischemia. In three additional groups, hearts received I (Thio 1, n = 11), 10 (Thio 10, n = 11) or 100 mug.mL(-1) (Thio 100, n = 10) thiopent one for five minutes before preconditioning. Left ventricular (LV) develope d pressure and creatine kinase (CK) release were measured as variables of m yocardial performance and cellular injury, respectively. Results: Recovery of LV developed pressure was improved by ischemic precond itioning (after 60 min of reperfusion, mean SID: PC, 40 +/- 19% of baseline ) compared with the control group (5 +/- 6%, P < 0.01) and this improvement of myocardial function was not altered by administration of thiopentone (T hio 1, 37 +/- 15%; Thio 10, 36 +/- 16%; Thio 100, 38 +/- 16%, P=0.87-0.99 v s PC). Total CK release over 60 min of reperfusion was reduced by precondit ioning (PC, 202 +/- 82 U.g(-1) dry weight) compared with controls (CON, 383 +/- 147 U.g(-1), P < 0.01) and this reduction was not affected by thiopent one (Thio 1, 213 <plus/minus> 69 U.g(-1); Thio 10, 211 +/- 98 U.g(-1); Thio 100, 258 +/- 128 U.g(-1), P=0.62-1.0 vs PC). Conclusion: These results indicate that thiopentone does not block the card ioprotective effects of ischemic preconditioning in an isolated rat heart p reparation.