[Is isoflurane a calcium antagonist?]

The vasodilating and myocardial depressant effects of isoflurane have been allocated to calcium channel blockade. The present study aimed to test this hypothesis by assessing the effect of isoflurane on the contractile response to potassium stimulation of vascular smooth muscle. Seventy two left anterior descending and circumflex coronary artery rings were removed in twelve dogs and mounted in organ chambers filled with Krebs-Ringer bicarbonate solution and aerated with 95% O2-5% CO2. Rings were pretreated with either 3.8% isoflurane (2.5 MAC in the dog) or 10(-8) mol.l-1 nifedipine, a calcium entry blocker. They were stimulated by addition of 10 to 150 mmol.l-1 potassium chloride. At 70 mmol.l-1 K+, the tension generated by the untreated rings was 119 +/- 4.25% of control, while in the isoflurane treated group the tension was 99 +/- 2.4% of control. In the opposite, the tension was 25 +/- 7.11% in the nifedipine treated rings. Likewise, when isoflurane was added to rings preconstricted with 40 mmol.l-1 potassium chloride, no relaxation occurred, while nifedipine produced relaxation. Isoflurane, unlike nifedipine, had a weak effect on ring tension. The calcium-entry blockade effect of isoflurane appeared weak, dose-dependent and virtually absent at clinical concentrations. Therefore, the vasodilation seen with clinical concentrations of isoflurane is mediated by mechanisms other than calcium-entry blockade.