Halothane does not protect against vascular injury in isolated cerebral and mesenteric arteries

This study was designed to examine regional differences in the vascular injury induced by hydrogen peroxide (H2O2) and to determine its modulation by halothane in canine basilar and mesenteric arteries.

Rings of canine basilar and mesenteric arteries with intact endothelium were mounted in Krebs bicarbonate solution for isometric tension recording. The relaxation responses to substance P (10(-8) M) and sodium nitroprusside (SNP; 10(-8) to 10(-5) M) were examined before and after exposure to H2O2 (1 mM) for eight minutes in the presence or absence of halothane (2%), to evaluate the effects of oxidative injury on the endothelium-dependent and -independent relaxation. The contractile responses to KCl (30 mM) and prostaglandin (PG) F(2alpha) (3 x 10(-6) M) were also compared in rings with and without exposure to H2O2.

After exposure to H2O2 the relaxant responses to substance P were significantly inhibited in basilar arteries (P < 0.01), but not in mesenteric arteries. Exposure to H2O2 also attenuated SNP-induced relaxation in basilar (P < 0.05), but not in mesenteric arteries. The attenuation of the contractile responses to KCl and PGF(2alpha) after H2O2 exposure was observed only in basilar arteries (P < 0.01). Simultaneous exposure to halothane did not affect the attenuation of these relaxant and contractile responses. Scanning electron microscopy revealed that H2O2 resulted in marked disruption of the endothelial layer in basilar arteries, compared to almost no morphological changes in mesenteric arteries.

These results indicate that the endothelium and vascular smooth muscle of the basilar artery are more susceptible to oxidative stress than those of the mesenteric artery. Halothane, at clinically relevant concentrations, exerts no significant influence on this vascular injury.