Effect of salbutamol on regional cerebral oxygen consumption, flow and capillary and arteriolar perfusion

This study quantitatively determined the effect of salbutamol (1 μg kg^-1), a β₂-adrenoceptor agonist, on the perfusion of the brain microvasculature, cerebral O₂ consumption, O₂ extraction and cerebral blood flow (CBF) in conscious rat. Indices of arteriolar and capillary structure and the percentage of the total cerebral microvascular volume/mm³ (% V(v)) and number/mm² (% N(a)) perfused were determined. These parameters were obtained from the perfused microvessels, identified by the presence of fluorescein isothiocyanate (FITC)-dextran, and compared with the entire microvascular bed, identified by alkaline phosphatase stain. Cerebral O₂ extraction was determined microspectrophotometrically and CBF was determined using ¹⁴[C]iodoantipyrine in another group of salbutamol-treated rats. The acute administration of salbutamol did not alter systemic arterial blood pressure. Significant tachycardia was noted in the salbutamol-treated rats. Salbutamol resulted in a significant increase in the percentage of arterioles perfused. Average percentage perfused capillary N(a) increased significantly from 46 ± 2 to 88 ± 1%; % V(v) increased significantly and similarly in the arteriolar and capillary beds in all brain regions examined. Average cerebral O₂ consumption increased significantly from 3.0 ± 0.2 to 7.4 ± 0.7 ml O₂ min^-1 100 g^-1 with salbutamol, while cerebral O₂ extraction was unchanged. Average CBF increased from 50 ± 2 to 142 ± 9 ml min^-1 100 g^-1 with salbutamol. Salbutamol may increase the perfusion of the regional microvasculature by increasing cerebral O₂ consumption (metabolic vasodilation) and CBF and microvascular perfusion secondarily, although a direct effect of salbutamol on cerebral microvessels cannot be ruled out.