Protective Role of Selective Nitric Oxide Synthase Inhibitor for Treatment of Decompensated Hemorrhagic Shock in Normotensive and Hypertensive Rats

Introduction: different vasoactive factors can modulatecardiovascular adaptation to hemorrhagic shock including nitricoxide (no). in this study we investigated the effect of the nosynthase inhibitor for treatment of decompensated hemorrhagicshock in normotensive and hypertensive rats.methods: twenty?four male wistar rats were divided into twogroups: the normotensive and hypertensive groups. hypertensionwas induced by the doca?salt method for eight weeks. then, theanimals were given hemorrhagic shock by continuously withdrawingblood until the mean arterial pressure (map) reached to 40 mmhg.the animals were maintained in the shock state for 120 minutes.subsequently, they were randomly assigned to l?name?treatedand non?treated groups and monitored for 60 minutes. the survivaltime was recorded. blood samples were taken before and after theshock and 60 minutes after l?name administration.results: infusion of l?name caused a significant increase inmap in normotensive animals, however, slightly increased mapin hypertensive animals. the heart rate did not significantly alter.hemorrhage caused a marked increase in serum nitrite levels inboth groups (p < 0.05). l?name treatment significantly reduced theserum nitrite concentration in the normotensive group (p < 0.05),without any change in the hypertensive group. all animals whoreceived l?name treatment survived at the end of experiment.fifty percent of the hypertensive animals died four hours after theexperiment. the 72?hour survival rate was similar in the l?nametreated groups.conclusion: l?name infusion during decompensatedhemorrhagic shock plays a protective role in the improvementof hemodynamic responses and short?term survival rate innormotensive animals.