The effect of inducible nitric oxide synthase inhibitor on microvascular permeability after cerebral ischemia/reperfusion

Our objective was to study the effect of inducible nitric oxide synthase (iNOS) inhibitor aminoguanidine (AG) on microvascular permeability after cerebral ischemialreperfusion (IIR) injury. Cerebral IIR injury was produced by occlusion of both the carotid arteries for 60 min with restitution of blood flow for 60 min. AG (200 mg/kg) was intraperitoneally, administrated 5 min before the onset of ischemia and again 5 mill before reperfusion. Microvascular permeability was evaluated by 0.75% sodium fluorescein (FINa) extravasation during early 300 s. Cerebral IIR injury increased the permeability of microvessel to fluorescein and the concentration of fluorescein outside of microvessels was significantly higher than that in microvessels after 110 s. However, after AG administration. FINa extravasation appears much faster. From 80 s oil. the fluorescence intensity outside is higher. IIR increased microvascular permeability. Nitric oxide defined from iNOS may maintain microvascular permeability at the early stage after IIR. (c) 2005 Pious Science. All rights reserved.