The effects of acute nitric oxide synthase inhibition on systemic circulation and organ blood flow

Nitric oxide (NO) is known as an important mediator in vasorelaxation and blood pressure regulation. NO is produced from nitric oxide synthase (NOS) by converting amino acid L-arginine to amino acid L-citruine and NO. The reduction of NO synthesis by inhibiting NOS activities causes vasoconstriction and hypertension and affects on microvascular blood perfusion. This study aimed to evaluate the effects of NOS activity on organ blood flow distribution by an acute blocking in a hamster dorsal skin fold window chamber model. The inhibition of NOS activities was performed by an intravenous infusion of N(G)-nitro-L-arginine methyl ester (L-NAME). The organ blood flow distribution was assessed with different color fluorescent microspheres over three hours of study. The preliminary results showed that L-NAME significantly increased systemic mean arterial pressure but it decreased heart rate. Venular diameters significantly increased over observation time when treated with L-NAME. Blood flow relative to mean flow increased in vital organs such as heart and brain after L-NAME infusion but not kidneys. In conclusion, the impairment of nitric oxide production on cardiovascular system in this model evidently demonstrated that NO is an important mediator and potentially affects on organ blood flow distribution by reducing blood flow.