The role of nitric oxide and prostaglandin E2 in prolonged hemorrhagic shock

Abstract

It is suggested that NO has played a major role in our model of prolonged hemorrhagic shock. The detrimental effects of NO might be further worsen when coupled with prostaglandin E2, a known vasodilator, in prolong hemorrhagic shock. Nitric oxides being a vasodilator might be responsible for the loss of vascular hyporesponsiveness in the presence of a potent vasoconstrictor, angiotensin II, in our model of prolonged hemorrhagic shock. The deleterious effect of NO is also shown in our combine model of prolonged hemorrhagic shock and fluid percussion injury. Our studies showed that the selective inhibitor, AG, maybe beneficial as a potentially useful therapeutic agent in our model of prolonged hemorrhagic shock and the combine model of prolonged hemorrhagic shock and fluid percussion injury.