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ur de rat isolé]


* From the Departments of Anaesthesiology, and Physiology,
Institut I Heinrich-Heine-Universität Düsseldorf Germany.
Address correspondence to: Dr. W. Schlack, Klinik für Anaesthesiologie Heinrich-Heine-Universität Postfach, 101007, 40001 Düsseldorf, Germany. Phone: +49-211-811-8669; Fax: +49-211-811-6253; E-mail: wolfgang{at}herzkreis.uni-duesseldorf.de
Purpose: Ischemic preconditioning protects the heart against subsequent prolonged ischemia by opening of adenosine triphosphate-sensitive potassium (KATP) channels. Thiopentone blocks KATP channels in isolated cells. Therefore, we investigated the effects of thiopentone on ischemic preconditioning.
Methods: Isolated rat hearts (n=56) were subjected to 30 min of global no-flow ischemia, followed by 60 min of reperfusion. Thirteen hearts underwent the protocol without intervention (control, CON) and in 11 hearts (preconditioning, PC), ischemic preconditioning was elicited by two five-minute periods of ischemia. In three additional groups, hearts received 1 (Thio 1, n=11), 10 (Thio 10, n=11) or 100 µgmL1 (Thio 100, n=10) thiopentone for five minutes before preconditioning. Left ventricular (LV) developed pressure and creatine kinase (CK) release were measured as variables of myocardial performance and cellular injury, respectively.
Results: Recovery of LV developed pressure was improved by ischemic preconditioning (after 60 min of reperfusion, mean ± SD: 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 (Thio 1, 37 ± 15%; Thio 10, 36 ± 16%; Thio 100, 38 ± 16%, P=0.870.99 vs PC). Total CK release over 60 min of reperfusion was reduced by preconditioning (PC, 202 ± 82 Ug1 dry weight) compared with controls (CON, 383 ± 147 Ug1, P <0.01) and this reduction was not affected by thiopentone (Thio 1, 213 ± 69 Ug1; Thio 10, 211 ± 98 Ug1; Thio 100, 258 ± 128 Ug1, P=0.621.0 vs PC).
Conclusion: These results indicate that thiopentone does not block the cardioprotective effects of ischemic preconditioning in an isolated rat heart preparation.
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