Avontuur J A, Biewenga M, Buijk S L, Kanhai K J, Bruining H A
Department of Surgery, University Hospital Rotterdam, The Netherlands.
Shock. 1998 Jun;9(6):451-4. doi: 10.1097/00024382-199806000-00010.
It has been suggested that inhibitors of nitric oxide synthesis are of value in the treatment of hypotension during sepsis. In this pilot study, we examined the effects of inhibition of nitric oxide synthesis by continuous infusion of N(omega)-nitro-L-arginine methyl ester (L-NAME) at 1.5 mg/kg/h in a patient with severe septic shock. L-NAME produced a rise in mean arterial blood pressure and systemic vascular resistance; catecholamine infusion could be reduced. Parallel to these findings, there was a 50% reduction in cardiac output and a 5-fold rise in pulmonary vascular resistance, which resulted in severe pulmonary hypertension after 3 h of L-NAME infusion, for which the infusion had to be stopped. Following the termination of L-NAME infusion, pulmonary artery pressure and blood pressure returned to baseline values, although pulmonary and systemic vascular resistance remained elevated for several hours. We conclude that nitric oxide appears to play a role in the cardiovascular derangements during human sepsis. Inhibition of nitric oxide synthesis with L-NAME can increase blood pressure and systemic vascular resistance. However, reduced cardiac output and pulmonary hypertension are possible side effects of continuous NO synthase inhibition. These side effects necessitate careful monitoring and may hinder the clinical application of NO synthase inhibitors.
有人提出，一氧化氮合成抑制剂在治疗脓毒症期间的低血压方面具有价值。在这项初步研究中，我们对一名严重脓毒性休克患者以1.5毫克/千克/小时的速度持续输注N（ω）-硝基-L-精氨酸甲酯（L-NAME），以研究抑制一氧化氮合成的效果。L-NAME使平均动脉血压和全身血管阻力升高；儿茶酚胺输注量可减少。与这些发现同时出现的是，心输出量降低了50%，肺血管阻力升高了5倍，在输注L-NAME 3小时后导致严重的肺动脉高压，为此不得不停止输注。L-NAME输注终止后，肺动脉压和血压恢复到基线值，尽管肺血管阻力和全身血管阻力在数小时内仍保持升高。我们得出结论，一氧化氮似乎在人类脓毒症期间的心血管紊乱中起作用。用L-NAME抑制一氧化氮合成可升高血压和全身血管阻力。然而，心输出量降低和肺动脉高压可能是持续抑制一氧化氮合酶的副作用。这些副作用需要仔细监测，并且可能会阻碍一氧化氮合酶抑制剂的临床应用。
