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. 1995 Mar;114(6):1303-9.
doi: 10.1111/j.1476-5381.1995.tb13347.x.

The effect of nitric oxide donors on haemodynamics and blood flow distribution in the porcine carotid circulation

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The effect of nitric oxide donors on haemodynamics and blood flow distribution in the porcine carotid circulation

E M van Gelderen et al. Br J Pharmacol. 1995 Mar.

Abstract

1. The role of nitric (NO) in the regulation of capillary and arteriovenous anastomotic blood flow was evaluated in the carotid circulation of the pig. For this purpose, the effect of intracarotid (i.c.) infusions of saline and two NO donors, nitroprusside sodium (NPR) and S-nitroso-N-acetylpenicillamine (SNAP) in concentrations of 3-100 micrograms min-1 was studied on systemic haemodynamics and carotid blood flow and its distribution in anaesthetized pigs with low arteriovenous anastomotic blood flow, by use of the radioactive microsphere method. 2. Apart from heart rate, which increased after both NPR and SNAP, no major changes in systemic haemodynamic variables were observed. In contrast to saline, both NPR and SNAP increased common carotid blood flow, vascular conductance and vascular pulsations dose-dependently. 3. The distribution of the carotid artery blood flow over capillary and arteriovenous anastomotic fraction remained stable after saline infusions. Both NPR and SNAP enhanced total capillary blood flow and conductance. In contrast to NPR, arteriovenous anastomotic blood flow and conductance were increased by SNAP. 4. At the tissue level, capillary blood flow increases following NPR or SNAP were reflected by an increase in both extracerebral and dural blood flow without changes in total brain blood flow. 5. These results indicate that both NO donors cause arteriolar dilatation together with enhanced vascular pulsations in the carotid circulation of the pig. Probably by way of a 'steal' phenomenon, this pronounced arteriolar dilatation limits the effect of NO donors on arteriovenous anastomoses. 6. The results of the present investigation support the contention that dilatation of intra- and extra cranial arteries and arteriovenous anastomoses leads to increased vascular pulsations, which (rather than increased blood flow) could, at least in part, be responsible for the headache caused by nitro vasodilators.

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