In vivo effects of alpha-adrenoceptor agonists and antagonists on pial veins of cats.

Abstract

Cerebral blood volume and intracranial pressure may be modified by influences on cerebral veins. The known adrenergic innervation of cerebral veins and their sensitivity to norepinephrine raised the question, whether pial veins can be selectively influenced through adrenoceptors in vivo. Therefore, alpha 1 and alpha 2 adrenoceptor agonists and antagonists were locally injected into the perivascular space of pial veins using the microapplication technique. The alpha 1 and alpha 2 adrenoceptor antagonists, prazosin and yohimbine, had only minor effects on pial veins. Both antagonists blocked constrictions induced by norepinephrine (10(-5)M) in a concentration dependent manner (10(-7)-10(-4)M). The alpha 1 adrenoceptor agonist phenylephrine caused significant (10(-7)-10(-3)M) constriction of pial veins, with a maximum of 11.6% of initial diameter at 10(-3)M. Oxymetazoline, an alpha 2 receptor agonist, induced a significant constriction only at 10(-3)M (5.1%). Since both alpha 1 and alpha 2 adrenoceptor agonists are less potent constrictors of pial veins than norepinephrine in vivo, a preferential use of alpha 1 or alpha 2 adrenoceptor agonists cannot be recommended from these experiments, if a therapeutic reduction of intracranial pressure or blood volume is desired.

Dexmedetomidine for Neurological Surgery

“…Surgery under these conditions is particularly difficult, often requiring considerable retraction for adequate operative field exposure. ␣ 2 -Agonists are more potent vasoconstrictors on the venous than on the arteriolar side of the cerebral vasculature (87). Because the venous compartment comprises most of the cerebral blood volume, ␣ 2 -agonists could presumably decrease ICP without greatly increasing arteriolar cerebrovascular resistance.…”

Uso de dexmedetomidina em neurocirurgia

“…Em hemorragias subaracnóideas, o incremento de catecolaminas na circulação e a descarga simpática maciça têm sido fatores contribuintes para o fenômeno de vasoespasmo encefálico, e o bloqueio desse efeito adrenérgico pode ser protetor. Em espécies animais, verifica-se que os α 2agonistas são vasoconstritores venosos mais potentes que arteriais na vasculatura encefálica 39 . Pelo fato de o compartimento venoso compreender a maior parte do volume sangüíneo encefálico, os α 2 -agonistas podem, presumivelmente, diminuir a pressão intracraniana (PIC) sem grandes aumentos na resistência arteriolar encefálica.…”

“…In subarachnoid hemorrhage, the increase in circulating cathecolamines and the massive sympathetic discharge contribute to the cerebral vasospasm, and the blockade of this adrenergic effect can be protective. In animals, α 2 -adrenergic agonists are more potent venous vasoconstrictors than arterial in the brain vasculature 39 . Since the venous compartment encompasses most of the cerebral blood volume, α 2 -adrenergic agonists could, probably, reduce intracranial pressure (ICP) without increasing significantly the cerebral arteriolar resistance.…”

Hypocapnia Enhances the Pressor Effect of Phenylephrine During Isoflurane Anesthesia in Monkeys

“…This is especially true in light of in-vivo evidence of dosedependent a-agonist effects on pial veins. 12 In our study, as cardiac output and venous pressure were not measured, we could not determine whether the enhanced pressor effect of phenylephrine with hypocapnia can be entirely attributed to increased systemic vascular resistance or a combination of physiologic factors. Measurement of cerebral blood flow, cardiac output, and venous pressure would have increased the clinical relevance of our study.…”