Isoflurane does not further impair microvascular vasomotion in a rat model of subarachnoid hemorrhage

PURPOSE: Since isoflurane is known to attenuate endothelium-dependent dilation (EDD) in normal cerebral arterioles, we examined whether the anesthetic has a similar effect and further impairs EDD in vessels exposed to SAH. METHODS: Autologous blood was introduced in the subarachnoid space and the parietal lobe harvested. Control animals were sacrificed without introduction of blood. The response of microvessles to the endothelium-dependent dilator adenosine diphosphate (ADP) 10(-9)-10(-4) M, the endothelium-independent dilator nitroprusside 10(-9)-10(-4) M, and ET-1 10(-13)-10(-8) M was measured by videomicroscopy in the presence of 0-2 minimum alveolar concentration (MAC) of isoflurane. RESULTS: Isoflurane attenuated EDD to ADP in control vessels 66 +/- 5% (control) vs 27 +/- 11% (2 MAC) dilation to ADP 10(-4) M, P < 0.05]. Although SAH was associated with reduced dilation to ADP, exposure to isoflurane did not further impair dilation to ADP after SAH 26 +/- 3% (SAH) vs 21 +/- 5% (SAH/2 MAC) dilation to ADP 10(-4) M, P = NS]. Dilation to nitroprusside was not affected by isoflurane or SAH. Constriction to ET-1 was reduced by 2 MAC of isoflurane 21 +/- 1% (control) vs 13 +/- 5% (2 MAC) constriction to ET-1 10(-8) M, P < 0.05], but not by 1 MAC of isoflurane in control vessels. Constriction to ET-1 was greatly attenuated by 1 or 2 MAC of isoflurane after SAH 32 +/- 5% (SAH) vs 18 +/- 4% (SAH/2 MAC) constriction to ET-1 10(-8) M, P < 0.05]. CONCLUSION: In rats, isoflurane does not further impair EDD after SAH and modulates the constrictive response to ET-1. Such an effect of isoflurane would not predispose the SAH-exposed vessels to vasospasm.