Aim: 

The present study was aimed to assess the in vivo rat pial microvascular responses induced by Diosmin during brain hypoperfusion-reperfusion injury.

Methods: 

Pial microcirculation of male Wistar rats was visualized by fluorescence microscopy through a closed cranial window. Hypoperfusion was induced by bilateral common carotid artery occlusion (BCCAO); thereafter, pial microcirculation was observed for 60 min. Arteriolar diameter, permeability increase, leukocyte adhesion to venular walls, perfused capillary length (PCL) and capillary red blood cell velocity (VRBC) were investigated by computerized methods. Pial arterioles were classified by Strahler scheme. Diosmin (50 or 70 mg/kg b.w.) was intravenously administered before BCCAO and at beginning of reperfusion.

Results: 

In control group, BCCAO caused decrease in order 2 arteriole diameter by 17.5 ± 3.0% of baseline, reduced by 11.8±1.2% of baseline at the end of reperfusion (RE). Microvascular permeability and leukocyte adhesion were marked. PCL and capillary VRBC decreased. At the end of BCCAO, Diosmin dose-dependently prevented order 2 arteriolar diameter decrease; at RE Diosmin caused an increase in order 2 arteriolar diameter by 10 ± 2 % of baseline. Microvascular leakage and leukocyte adhesion were reduced. Inhibition of endothelial nitric oxide synthase (NOS) prior to Diosmin significantly reduced Diosmin-induced effects; inhibition of inducible and neuronal NOS prior to Diosmin did not affect the Diosmin's effects.

Conclusions: 

Diosmin protects the pial microcirculation during ischemia-reperfusion, prevents vasoconstriction, microvascular permeability and adhesion of leukocytes promoting endothelial nitric oxide release.