Kalkan Sule, Eminoglu Ozlem, Akgun Aylin, Guven Hulya, Tuncok Yesim
Department of Pharmacology, Dokuz Eylul University School of Medicine, Balcova, Izmir 35340, Turkey.
Saudi Med J. 2007 May;28(5):701-6.
To investigate the role of adenosine triphosphate-regulated potassium (KATP) channels in the propofol-induced changes in the contractile function of hypercholesterolemic rabbit hearts.
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 microM propofol during a 60 minutes perfusion. Group II (n=6) were also infused with 100 microM propofol over the same period. Group III (n=5) was perfused with solutions containing 10 microM glybenclamide and group IV (n=5) 100 microM diazoxide for 5 minutes before and during a 60 minutes infusion with 100 microM propofol.
The 50 microM propofol infusion decreased left ventricular pressure (LVP) significantly (p<0.05) but it did not change dP/dt max and dP/dt min. The 100 microM propofol infusion caused a significant increase in LVP at 20 minutes. Furthermore, a 100 microM propofol infusion resulted in a significant increase in maximal positive left ventricular pressure (dP/dt max) and maximal negative left ventricular pressure (dP/dt min) compared to baseline (p<0.05). The increase in dP/dtmax and dP/dt min induced by 100 microM 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.
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.