Effect of Moderate Endothelial Damage on the in vivo Reactivity of Pial Arteries to Norepinephrine and Serotonin

Abstract

Most of the information on the role of the endothelium for the vascular reactivity comes from in vitro experiments on noncerebral vessels. Few studies address the contribution of the endothelium to the cerebrovascular reactions in vivo. In the present study, arterial cerebral air embolism was employed to induce endothelial damage in anesthetized cats. The endothelial injury was verified by scanning electron microscopy: air embolism induced obvious damage to the endothelial layer, consisting of flattening, superficial peeling and/or fissures within and between endothelial cells. Cell debris and small platelet and erythrocyte aggregations were also observed. The present study concerns the effect of endothelial damage on the reactivity to the vasoconstrictor substances serotonin (10^–10–10^-4M) and norepinephrine (10^–9–10^–3M) in vivo. The reactions of the same pial arteries to these substances were tested using the microapplication method before and after air embolism. In contrast to the abolition of the vasodilatation to carbachol found in a previous study, the constriction of pial arteries to serotonin and norepinephrine was preserved after air embolism, although it was diminished in the case of norepinephrine. These results are consistent with the hypothesis that the endothelium may be less important for vasoconstriction than for vasodilatation in cerebral vessels.

Critical Role of Endothelial Nitric Oxide Synthase and Cyclooxygenase in Response of Rabbit Basilar Artery to Serotonin

“…In the latter case, the response to 5-HT varied in relation to the vessel diameter, the smaller arterioles /arteries dilating and the larger ones constricting. However, another study on cat pial arteries in situ did not confirm the existence of such a relationship or such dilatory responses (9). A recent study on human intracortical arterioles showed a biphasic response to the 5-HT1B/D agonist sumatriptan, the small relaxation at low concentration being abolished by nitric oxide synthase inhibition (10).…”

Endothelium-derived relaxing factor modulates noradrenergic constriction of cerebral arterioles in rabbits.

“…A recent study 9 reported that norepinephrine dilates pial arterioles at low concentrations but produces vasoconstriction at high concentrations in cats. The authors observed that constrictor responses to norepinephrine were preserved after injury to arteriolar endothelium produced by air embolism.…”