Henderson J L, Statman R, Cunningham J N, Cheng W, Damiani P, Siconolfi A, Horovitz J H
Department of Surgical Research, Maimonides Medical Center, Brooklyn, NY.
Arch Surg. 1994 Dec;129(12):1271-4; discussion 1275. doi: 10.1001/archsurg.1994.01420360061007.
To determine the effect of the inhibition of nitric oxide (NO) on selective organ blood flow in endotoxin-induced sepsis.
Nonrandomized, controlled experiment.
Animal research facility in Brooklyn, NY.
Eleven mongrel dogs.
Eleven dogs were divided into one of two groups: a control group (n = 5) and an endotoxin-treated group (n = 6). The animals were anesthetized, and electromagnetic and ultrasonic flow probes were placed on the distal aorta, right internal carotid artery, superior mesenteric artery, and left renal artery. Sepsis was induced with a 60-mg/kg intravenous injection of Escherichia coli endotoxin. When the arterial blood pressure decreased to less than 60 mm Hg despite adequate fluid resuscitation, NO synthesis was inhibited with a 25-mg/kg intravenous administration of NG-monomethyl-L-arginine. After 15 minutes of inhibition, a 400-mg/kg intravenous administration of L-arginine, the substrate of NO synthase enzyme, was given. Physiologic measurements were continued for 15 minutes thereafter.
Heart rate, blood pressure, central venous pressure, pulmonary artery pressure, pulmonary capillary wedge pressure, cardiac output, hematocrit, arterial and venous blood gas values, and blood flow measurements of right internal carotid artery, superior mesenteric artery, left renal artery, and distal aorta.
Control animals did not demonstrate a significant (P > .05) decrease in blood flow in the internal carotid artery, superior mesenteric artery, and distal aorta after the administration of NG-monomethyl-L-arginine. The endotoxin-treated group showed a significant (P < .05) decrease in organ perfusion when treated with the NO synthase inhibitor, NG-monomethyl-L-arginine.
Inhibition of NO production in the treatment of sepsis caused a significant decrease in blood flow to all vascular beds in vivo. The role, if any, of the inhibition of NO in the treatment of sepsis is questioned.
确定抑制一氧化氮（NO）对内毒素诱导的脓毒症中选择性器官血流的影响。
非随机对照实验。
纽约布鲁克林的动物研究设施。
11只杂种犬。
11只犬被分为两组之一：对照组（n = 5）和内毒素治疗组（n = 6）。动物被麻醉，电磁和超声血流探头分别置于腹主动脉远端、右颈内动脉、肠系膜上动脉和左肾动脉上。通过静脉注射60mg/kg大肠杆菌内毒素诱导脓毒症。当尽管进行了充分的液体复苏但动脉血压仍降至低于60mmHg时，静脉注射25mg/kg NG-单甲基-L-精氨酸以抑制NO合成。抑制15分钟后，静脉注射400mg/kg NO合酶底物L-精氨酸。此后继续进行15分钟的生理测量。
心率、血压、中心静脉压、肺动脉压、肺毛细血管楔压、心输出量、血细胞比容、动脉和静脉血气值，以及右颈内动脉、肠系膜上动脉、左肾动脉和腹主动脉远端的血流测量。
给予NG-单甲基-L-精氨酸后，对照组动物颈内动脉、肠系膜上动脉和腹主动脉远端的血流未出现显著（P > 0.05）下降。内毒素治疗组在用NO合酶抑制剂NG-单甲基-L-精氨酸治疗时，器官灌注出现显著（P < 0.05）下降。
在脓毒症治疗中抑制NO生成导致体内所有血管床的血流显著减少。对抑制NO在脓毒症治疗中的作用（如果有）提出质疑。
