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Although nitric oxide is essential in tumoricidal and bactericidal functions of macrophages, overproduction of nitric oxide has been implicated in septic/cytokine-induced circulatory shock in humans through the activation of guanylate cyclase. This mechanism is responsible for profound hypotension in postoperative patients whose recovery is complicated by bacterial infections that produce endotoxins. Hypotension in these patients is often refractory to treatment with conventional vasoconstrictor medicines. Therapeutic intervention by NOS inhibitors is being examined in inflammatory diseases of the gastrointestinal tract, such as pancreatitis and ulcerative colitis, and in arthritis.

The endothelial isoform of nitric oxide synthase, eNOS or NOS 3, is thought to play a critical role in maintaining a basic vasotonus in hemodynamic regulation such that an imbalance in the production of nitric oxide could result in hypertension, thrombosis, or atherosclerosis. On the other hand, direct application of nitric oxide gas may also be beneficial in the treatment of pulmonary hypertension. Following reports of the administration of inhaled nitric oxide in the laboratory and to elder’s patients with primary pulmonary hypertension, its clinical utility was determined. In selected populations of patients, for example, hypoxic children and elder’s, inhaled nitric oxide has been shown to improve arterial oxygenation and reduce pulmonary arterial hypertension. It has been used in newborn patients with hypoxic respiratory failure to reduce the need for extracorporeal membrane oxygenation, which is both expensive and invasive. Inhaled nitric oxide has also been used to treat acute respiratory distress syndrome, resulting in nitric oxide induced pulmonary vasodilation, decreased pulmonary arterial pressure and increased cardiac index.