Cerebrovascular reactivity to hypercapnia during sevoflurane or desflurane anesthesia in rats.

Background: Hypercapnia dilates cerebral vessels and increases cerebral blood flow, resulting in increases in intracranial pressure. Sevoflurane is reported to preserve cerebrovascular carbon dioxide reactivity. However, the contribution of inhaled anesthetics to vasodilatory responses to hypercapnia have not been clarified. Moreover, the cerebrovascular response to desflurane under hypercapnia has not been reported. We examined the effects of sevoflurane and desflurane on vasodilatory responses to hypercapnia in rats.

Methods: A closed cranial window preparation are used to measure the changes in pial vessel diameters. To evaluate the cerebrovascular response to hypercapnia and/or inhaled anesthetics, the pial vessel diameters were measured in the following states: under without inhaled anesthetics at normocapnia (control values) and hypercapnia, under inhaled end-tidal 0.5 minimal alveolar concentration (MAC) or 1.0 MAC of either sevoflurane or desflurane at normocapnia, and under 1.0 MAC of sevoflurane or desflurane at hypercapnia.

Results: Under normocapnia, 1.0 MAC, but not 0.5 MAC, of sevoflurane or desflurane dilated pial arterioles and venules. In addition, under both 1.0 MAC of sevoflurane and 1.0 MAC of desflurane, hypercapnia significantly dilated pial arteriolar and venular diameters compared to their diameters without inhaled anesthetics. The amounts of vasodilation were similar for desflurane and sevoflurane under both normocapnia and hypercapnia.

Conclusions: Desflurane induces cerebrovascular responses similar to those of sevoflurane. Desflurane can be used as safely as sevoflurane in neurosurgical anesthesia.