Driscoll W, Thurin S, Carrion V, Steinhorn R H, Morin F C
Department of Pediatrics, University of Buffalo, New York, USA.
J Pediatr. 1996 Dec;129(6):904-8. doi: 10.1016/s0022-3476(96)70036-7.
Excess nitric oxide is a mediator of the hypotension in septic shock. Nitric oxide dilates vascular smooth muscle through activation of soluble guanylate cyclase. We report the increase in blood pressure caused by methylene blue (MB), a soluble guanylate cyclase inhibitor, in five neonates with presumed septic shock unresponsive to colloids, inotropic agents, and corticosteroids. MB was given intravenously at a dose of 1 mg/kg during a 1-hour period. MB increased blood pressure in each patient (average, 33% +/- 20%). Blood pressure subsequently decreased to near baseline values in three patients, who then received a second infusion of MB. Blood pressure again increased in these patients. Three of five patients were weaned from inotropic support within 72 hours. Three of five patients survived and were discharged home. We suggest that MB increased blood pressure in these neonates with refractory hypotension.
过量的一氧化氮是脓毒性休克低血压的介质。一氧化氮通过激活可溶性鸟苷酸环化酶使血管平滑肌舒张。我们报告了亚甲蓝(MB),一种可溶性鸟苷酸环化酶抑制剂,在五名对胶体、血管活性药物和皮质类固醇无反应的疑似脓毒性休克新生儿中引起血压升高的情况。MB以1mg/kg的剂量在1小时内静脉给药。MB使每位患者的血压升高(平均升高33%±20%)。随后,三名患者的血压降至接近基线值,之后他们接受了第二次MB输注。这些患者的血压再次升高。五名患者中有三名在72小时内停用了血管活性药物支持。五名患者中有三名存活并出院回家。我们认为MB使这些难治性低血压的新生儿血压升高。