Abstract
OBJECTIVE: To investigate the role of adenosine triphosphate-regulated potassium (KATP) channels in the propofol-induced changes in the contractile function of hypercholesterolemic rabbit hearts.
METHODS: This study was carried out in the Department of Pharmacology Laboratory, Faculty of Medicine, Dokuz Eylul University, Izmir, Turkey during the period January to December 2003. Twenty-two isolated rabbit hearts were grouped into 4. Group I (n=6) were infused with 50 uM propofol during a 60 minutes perfusion. Group II (n=6) were also infused with 100 uM propofol over the same period. Group III (n=5) was perfused with solutions containing 10 uM glybenclamide and group IV (n=5) 100 uM diazoxide for 5 minutes before and during a 60 minutes infusion with 100 uM propofol.
RESULTS: The 50 uM propofol infusion decreased left ventricular pressure (LVP) significantly (p<0.05) but it did not change dP/dtmax and dP/dtmin. The 100 uM propofol infusion caused a significant increase in LVP at 20 minutes. Furthermore, a 100 uM propofol infusion resulted in a significant increase in maximal positive left ventricular pressure (dP/dtmax) and maximal negative left ventricular pressure (dP/dtmin) compared to baseline (p<0.05). The increase in dP/dtmax and dP/dtmin induced by 100 uM propofol was inhibited by glybenclamide (p<0.05), a KATP channel blocker, but was not affected by diazoxide (p>0.05), a KATP channel opener.
CONCLUSION: The activation of KATP channels seems to be one of the mechanisms by which propofol induced beneficial effect on contractility of myocardium in hypercholesterolemic rabbit hearts.
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