Responses of the Internal Carotid Artery to Different Endogenous Vasoconstrictor Substances

Abstract

In order to study the action of serotonin (5-HT), noradrenaline (NA), hypertensin (HT), prostaglandins A_1, B₁ and E₂ (PGA_1, PGB₁ and PGE₂) and vasopressin (VP), internal carotid arteries were isolated in situ from both cerebral and general circulation and perfused continuously with oxygenated Ringers’ bicarbonate solution. The order of potencies of the vasoactive substances when administered intra-arterially was: 5-HT > HT > PGE₂- > PGB₁ > NA. The relative duration of the constrictor effects was: 5-HT < PGA₁^- < HT and PGE₂ < PGB₁ and NA < VP. The relaxation index of these substances on the vascular wall was: 5-HT < PGE₂ < HT < PGB₁^- < NA < PGA¹ < VP. Some of these substances, specifically PGB₁ PGE₂ and VP, frequently caused a residual constriction of the smooth muscle following their dilator effect. The role of these vasoactive substances in the development of vasospasm is discussed.

The Nature of Cerebral Vasospasm

“…The cerebrovascular effects of these substances have been widely investigated [e.g., 9,21,30,47,49,50], Serotonin exerts the strongest vasocon strictor effect upon the cerebral arteries with out any evidence of habituation towards its repeated or prolonged action [10,30,31], Thus serotonin may cause cerebral vaso spasm if it is continuously affecting the ar terial walls (e.g., when an increased amount of the substance is circulating in blood, or originates inside, or adjacent to, the arterial walls). The vasoactive effect of some prosta glandins (E2, F2J is somewhat smaller than that of serotonin, but relaxation of arterial walls is delayed and even residual contrac tion (characteristic of vasospasm) may be ob served [31]. The prolongation of vasocon strictor effects of active amines may be caused by inhibition of monoamine oxidase in the arterial walls [27], Some vasoactive substances (in particular catecholamines, prostaglandins and vaso pressin) have the property, essential for spasm development, of changing specifically vascular reactivity.…”

“…This would potentiate the vasoconstrictor response and delay of relax ation. Under these circumstances even the normal vasoconstrictor stimuli (during regu lation of CBF) may induce a sustained vaso spastic constriction of the arteries [27,31].…”