[The role of nitric oxide in hemorrhagic shock]

The continuous release of nitric oxide (NO) from the constitutive, endothelial isoform of nitric oxide synthase (e-NOS) serves mainly to keep the vasculature in a continuous state of active vasodilation. Although it has been suggested that NO production from e-NOS might also be affected by hemorrhagic shock (HS), this relationship is still controversial. Therefore, the roles of NO in the pathophysiology in hemorrhagic shock were reviewed. According to the previous reports, NO might play an important role in the pathophysioliogy of HS. In the early phase of HS, it may be possible that NO delivered from e-NOS serves a cytoprotective function in preventing shock-induced organ injury. This opinion suggests that endothelial NO production has a significant modulatory effect on vascular tone during hemorrhage, and that inhibition of NO production permits greater vasconstrictor influences leading to organ injury. NO production in the late phases of HS has an adverse effect on survival rate in the HS model. Moreover, the findings from an animal study of prolonged periods of HS suggest that excessive NO formation, including those produced from i-NOS, induces vascular hypoactivity and they have suggested that NOS inhibitors may improve the therapeutic outcome for patients suffering from HS. Therefore, it may be suggested that NO might play a biphasic role, cytoprotective during the early phase and cytotoxic late in HS.