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

[L'isoflurane ne produit pas d'altération subséquente sur la vasomotricité microvasculaire d'un modèle d'hémorragie sous-arachnoïdienne chez le rat]

Kyung W. Park, MD^*, Hai B. Dai, MD, Caroline Metais, MD, Mark E. Comunale, MD^* and Frank W. Sellke, MD

^* From the Departments of Anesthesia and Critical Care and
Surgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusettes, USA.

Dr. Kyung W. Park, Department of Anesthesia and Critical Care Group, Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brookline Avenue, Boston, MA 02215, USA. Phone: 617-754-2678; Fax: 617-754-2677; E-mail: kpark{at}caregroup.harvard.edu

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.