Lobo Suzana M, Soriano Francisco G, Barbeiro Denise F, De Backer Daniel, Sun Qinghua, Tu Zizhi, Dimopoulos George, Preiser Jean-Charles, Vray Bernard, Vercruysse Vincent, Vincent Jean-Louis
Department of Medicine, Division of Intensive Care Medicine, Faculdade de Medicina de Sao Jose do Rio Preto, Sao Paulo, Brazil.
Med Sci Monit. 2009 Feb;15(2):BR37-42.
Dobutamine is the agent of choice for increasing cardiac output during myocardial depression in humans with septic shock. Studies have shown that beta-adrenoceptor agonists influence nitric oxide generation, probably by modulating cyclic adenosine monophosphate. We investigated the effects of dobutamine on the systemic and luminal gut release of nitric oxide during endotoxic shock in rabbits.
MATERIAL/METHODS: Twenty anesthetized and ventilated New Zealand rabbits received placebo or intravenous lipopolysaccharide with or without dobutamine (5 micro g/kg/min). Ultrasonic flow probes placed around the superior mesenteric artery and the abdominal aorta continuously estimated the flow. A segment from the ileum was isolated and perfused, and serum nitrate/nitrite levels were measured in the perfusate solution and the serum every hour.
The mean arterial pressure decreased with statistical significance in the lipopolysaccharide group but not in the lipopolysaccharide/dobutamine group. The abdominal aortic flow decreased statistically significantly after lipopolysaccharide administration in both groups but recovered to baseline in the lipopolysaccharide/dobutamine group. The flow in the superior mesenteric artery was statistically significantly higher in the lipopolysaccharide/dobutamine group than in the lipopolysaccharide group at 2 hours. The serum nitrate/nitrite levels were higher in the lipopolysaccharide group and lower in the lipopolysaccharide/dobutamine group than those in the control group. The gut luminal perfusate serum nitrate/nitrite level was higher in the lipopolysaccharide group than in the lipopolysaccharide/dobutamine group.
Dobutamine can decrease total and intestinal nitric oxide production in vivo. Those effects seem to be inversely proportional to the changes in blood flow.
多巴酚丁胺是用于增加感染性休克患者心肌抑制期间心输出量的首选药物。研究表明,β-肾上腺素能激动剂可能通过调节环磷酸腺苷来影响一氧化氮的生成。我们研究了多巴酚丁胺对内毒素休克家兔全身和肠腔一氧化氮释放的影响。
材料/方法:20只麻醉并通气的新西兰兔接受安慰剂或静脉注射脂多糖,同时给予或不给予多巴酚丁胺(5μg/kg/分钟)。将超声流量探头置于肠系膜上动脉和腹主动脉周围,持续估计血流量。分离一段回肠并进行灌注,每小时测量灌注液和血清中的硝酸盐/亚硝酸盐水平。
脂多糖组平均动脉压显著降低,而脂多糖/多巴酚丁胺组未降低。两组给予脂多糖后腹主动脉血流量均显著下降,但脂多糖/多巴酚丁胺组恢复至基线水平。2小时时,脂多糖/多巴酚丁胺组肠系膜上动脉血流量显著高于脂多糖组。脂多糖组血清硝酸盐/亚硝酸盐水平高于对照组,脂多糖/多巴酚丁胺组低于对照组。脂多糖组肠腔灌注液血清硝酸盐/亚硝酸盐水平高于脂多糖/多巴酚丁胺组。
多巴酚丁胺可降低体内一氧化氮的总量和肠道生成量。这些作用似乎与血流量的变化成反比。