Catechin is an antioxidant polyphenol abundant in green tea and exhibits biological and pharmacological properties. Several studies have demonstrated the long term consumption of catechin prevents dyslipidemia, improves the cerebral blood flow and reduces the inflammatory response and the neuronal damage during cerebral ischemia. The aim of the present study was to assess the in vivo dose-dependent effects of catechin on rat pial microcirculation during hypoperfusion and reperfusion injury. Male Wistar rats were anesthetized with alpha-chloralose (50 mg/Kg b.w. intraperitoneally administered), tracheotomized and intubated. Pial microcirculation of male Wistar rats was observed by fluorescence microscopy through a closed cranial window. Hypoperfusion was induced by bilateral common carotid artery occlusion (BCCAo) for 30 min; thereafter, pial microcirculation was observed for 60 min. Arterioles were classified according to Strahler’s ordering scheme. Arteriolar diameter was determined by computer assisted-method as well as permeability increase, leukocyte adhesion, perfused capillary length (PCL) and capillary red blood cell velocity (VRBC). Neuronal damage was evaluated by TTC staining. Catechin (2 – 4 mg/kg b.w.) or L-N5-(1-Iminoethyl) Ornithine Hydrochloride (L-NIO: 15 mg/Kg b.w.) prior to catechin were intravenously administered before BCCAo and at beginning of reperfusion. In ischemic rats, BCCAo caused decrease in order 2 arteriole diameter, reduced by 13.7 ± 2.0 % of baseline at the end of reperfusion (RE). Microvascular permeability and leukocyte adhesion were marked. PCL and VRBC decreased at RE. At the end of BCCAo, catechin dose-dependently reverted order 2 arteriolar diameter decrease, causing vasodilation at RE. Microvascular leakage and leukocyte adhesion were prevented as well as the cortex and striatum neuronal loss in both hemispheres at RE. L-NIO prior to catechin abolished the catechin-induced effects. Western blotting showed that endothelial nitric oxide synthase (eNOS) protein concentration significantly increased in rats treated with cathechin at RE. In conclusion, catechin administration prevents pial microvascular damage induced by hypoperfusion and reperfusion reducing vasoconstriction, microvascular permeability, leukocyte adhesion, capillary blockade and neuronal loss. It is reasonable to suggest that catechin’s effects are mainly due to nitric oxide release and to free radical scavenger activity.