Background: Mild hypothermia has been proposed as a means of providing cerebral protection after traumatic brain injury. However, hypothermia has been shown to alter not only physiologic but also pharmacologic responses. The purpose of this study was to investigate whether mild hypothermia (3-4 degrees C temperature reduction) could alter cerebral vasodilation induced by inodilators, which are characterized by having an inotropic effect in addition to a vasodilatory effect. Isoproterenol (a beta-adrenergic receptor agonist), colforsin dapropate (an adenylate cyclase stimulant), and amrinone (a phosphodiesterase inhibitor) were chosen as inodilators.
Methods: The cranial window technique, combined with microscopic video recording, was used. Forty-eight cats were randomly assigned to either a normothermic or a hypothermic group (33 degrees C). Isoproterenol, colforsin dapropate, or amrinone was topically applied in the cranial window and the diameter of pial arterioles was measured.
Results: Topical administration of isoproterenol, colforsin dapropate, and amrinone produced a significant dilation in a dose-dependent manner during normothermia. The vasodilation induced by these inodilators was not affected by mild hypothermia.
Conclusion: The vasodilation induced by topical administration of isoproterenol, colforsin dapropate, and amrinone was not affected by mild hypothermia.
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