Influence of halothane and isoflurane on the contractile responses to potassium and prostaglandin F_2α in isolated human pial arteries

SUMMARY

Volatile anaesthetics may modulate cerebrovascular resistance, but their direct actions on human cerebral arteries are unknown. In the present study, we have evaluated the effects of halothane and isoflurane at different MAC (0.4, 1.0 and 2.0) on contractions induced by depolarization (potassium) or receptor stimulation (prostaglandin F_2α) in isolated ring segments of human pial arteries. Neither halothane nor isoflurane had significant effects on potency (unaffected EC₅₀ value) or the maximum response (Emax) in potassium-contracted arteries, even though there was a general tendency to attenuation of Emax. Similarly, the potency of prostaglandin F_2α was unchanged (unaffected EC₅₀ value). However, the Emax value for prostaglandin F_2α at normocapnia (mean Pco₂ 4.3 (SEM 0.1) kPa, pH 7.41 (0.01)) and addition of halothane (0.4, 1.0 and 2.0 MAC) was significantly attenuated to 96 (2) %, 91 (3)% and 84 (4) % at the respective MAC concentrations. Isoflurane at 2 MAC and normocapnia also reduced Emax to 94 (3) %. During hypocapnia (Pco₂ 2.7 (0.1) kPa, pH7.64 (0.01)), the vasodilator effect of halothane was reduced, whereas isoflurane at 0.4 and 1.0 MAC enhanced the contraction induced by prostaglandin F_2α. (Br. J. Anaesth. 1994; 72: 581–586)