Abstract
Histamine is a mediator of cerebrovascular response; however, it has not yet been confirmed as a modulator for cerebral vascular responses either in physiological or pathological states. In this paper, an experimental study on the reactivity of the cerebral artery to histamine was performed as a preliminary study to evaluate alterations in the reactivity of histamine receptors of the cerebral artery in cerebral vasospasm. The bovine basilar arteries were isolated from the brain stem immediately after the animals were slaughtered. Arterial strips (2 × 20 mm) were prepared and the isometric tension development of the vascular response to histamine and related agents was measured in a heated tissue bath (37°C) containing aerated modified Krebs-Ringer solution.
Histamine and 2, 2-pyridylethylamine (PEA, H1 receptor agonist) produced dose-dependent vasoconstriction of the cerebral artery, whereas dimaprit (H2 receptor agonist) did not induce any vascular response. With pretreatment of tripelennamine (H1 receptor antagonist), the dose-response curves of the bovine basilar arteries to histamine were shifted parallel to the right. The slope of the regression line in Schild's plot for tripelennamine on the response of histamine was 0.904 and pA2 value was 8.76. The antagonistic effect of tripelennamine on the vascular response to histamine was competitive. The histamine-induced vasoconstriction of cerebral arteries was not influenced by cimetidine, α- or β-blockers; however, it was influenced by the phospholipase C inhibitor. No significant differences were found in histamine-induced vasoconstriction of cerebral arteries either with or without removal of endothelium.
The results indicate that the contractile response of the cerebral artery to histamine is induced by activation of H1 receptors. In the bovine basilar artery, H2 receptors are few or entirely absent. It is also suggested that histamine-induced vasoconstriction is mediated by an increase of intracellular Ca2+ through the activation of phospholipase C after direct action of histamine on H1 receptors of the cerebral artery. Further study will be carried out to examine alterations in the reactivity of the histamine receptor of the cerebral arteries in experimental cerebral vasospasm.
