Effect of topical amosulalol on tissue circulation in the optic nerve head. The effect of topical 0.1% amosulalol on tissue circulation in the albino rabbit optic nerve head (ONH) was investigated using a laser speckle tissue circulation analyzer. Amosulalol was administered into one eye twice daily for 20 days, and vehicle was administered into the other eye in a masked, randomized manner . Intraocular pressure (IOP) was measured every 5 days. The normalized blur value (NB), a quantitative index of tissue blood flow velocity in the ONH, was measured before treatment and 2 hours after the last instillation on day 20. The IOP was also measured at 5-day intervals. Amosulalol decreased IOP by approximately 2 mmHg in the treated eyes (P < 0.01). There was no significant difference in NB between
treatment increased the number of monocytes adherent to the vascular endothelium. This increase was abrogated by injection of glucose with insulin. Amosulalol, an α-1 and β-adrenoreceptor antagonist, suppressed monocyte adhesion to endothelium and levels of adhesion molecules (intercellular adhesion molecule-1 and vascular cell adhesion molecule-1) in the endothelial surface, which had been enhanced
Effects of amosulalol on the electrical responses of guinea-pig vascular smooth muscle to adrenoceptor activation. The effects of amosulalol, a newly synthesized sulphonamide-substituted phenylethylamine derivative, on electrical responses of smooth muscle cells of the guinea-pig vascular tissues to noradrenaline, isoprenaline and perivascular nerve stimulation were investigated. Amosulalol (10 (-10) -10(-5)M) did not alter the resting membrane potential of smooth muscle cells of the mesenteric artery, the mesenteric vein, the main pulmonary artery and the portal vein. In the mesenteric artery, main pulmonary artery and portal vein, but not in the mesenteric vein, membrane depolarizations produced by noradrenaline were antagonized by amosulalol. In the portal vein, membrane
Beneficial effect of amosulalol and phentolamine on post-hypoxic recovery of contractile force and energy metabolism in rabbit hearts. 1. The effects of phentolamine, an alpha-adrenoceptor blocking agent and amousulalol, an alpha 1 and beta-adrenoceptor antagonist on hypoxia-induced impairment in cardiac function and metabolism were examined using the isolated heart Langendorff preparation kinase from the heart. 3. Treatment of hypoxic hearts with either 83 microM phentolamine or 45 microM amosulalol resulted in a suppression of the rise in resting tension, the tissue calcium accumulation and the release of creatine kinase and ATP metabolites during hypoxia. This treatment also elicited significant recovery of cardiac contractile force, restoration of myocardial high-energy phosphates