Morelli Andrea, Rocco Monica, Conti Giorgio, Orecchioni Alessandra, De Gaetano Andrea, Coluzzi Flaminia, Vernaglione Enrico, Pelaia Paolo, Pietropaoli Paolo
Department of Anesthesiology and Intensive Care, University of Rome La Sapienza, Rome, Italy.
Anesthesiology. 2004 Sep;101(3):576-82. doi: 10.1097/00000542-200409000-00005.
Inadequate splanchnic perfusion in septic shock is associated with increased morbidity and mortality. As result of splanchnic ischemia, mucosal permeability increases. Considering the implication of improved mucosal perfusion in terms of maintenance of mucosal barrier integrity, dopamine-1 receptor stimulation could be helpful in septic shock. The goal of the current study was to determine the effects of fenoldopam on systemic hemodynamic parameters and gastric mucosal perfusion in patients with septic shock. Furthermore, the authors tested the hypothesis that the addition of fenoldopam (0.1 microg x kg(-1) x min(-1)) to a combination of norepinephrine and dobutamine (5 microg x kg(-1) x min(-1)) may improve gastric mucosal perfusion in septic shock.
Patients with septic shock were randomized to a double-blind 2-h infusion of fenoldopam (n = 20) or placebo (n = 20). Each group received dobutamine (5 microg x kg(-1) x min(-1)), and the dosage of norepinephrine was adjusted to achieve a mean arterial pressure between 70 and 80 mmHg. A laser-Doppler probe and tonometer were introduced into the gastric lumen.
A significant increase in gastric mucosal perfusion, detected by laser-Doppler flowmetry, was observed in the group treated with fenoldopam (P < 0.05). In addition, this increase in microcirculatory flow occurred despite the fact that systemic flow remained unchanged. Differences in gastroarterial partial pressure of carbon dioxide values were not statistically significant in the fenoldopam and placebo groups.
The study showed that, for the same mean arterial pressure, short-term fenoldopam infusion increased gastric mucosal perfusion in patients with septic shock.
感染性休克时内脏灌注不足与发病率和死亡率增加相关。由于内脏缺血,黏膜通透性增加。考虑到改善黏膜灌注对维持黏膜屏障完整性的意义,刺激多巴胺-1受体可能有助于治疗感染性休克。本研究的目的是确定非诺多泮对感染性休克患者全身血流动力学参数和胃黏膜灌注的影响。此外,作者检验了以下假设:在去甲肾上腺素和多巴酚丁胺(5μg·kg⁻¹·min⁻¹)联合用药基础上加用非诺多泮(0.1μg·kg⁻¹·min⁻¹)可能改善感染性休克患者的胃黏膜灌注。
感染性休克患者被随机分为两组,分别接受为期2小时的双盲非诺多泮输注(n = 20)或安慰剂输注(n = 20)。每组均接受多巴酚丁胺(5μg·kg⁻¹·min⁻¹),并调整去甲肾上腺素剂量以维持平均动脉压在70至80 mmHg之间。将激光多普勒探头和张力计插入胃腔。
通过激光多普勒血流仪检测发现,接受非诺多泮治疗的组胃黏膜灌注显著增加(P < 0.05)。此外,尽管全身血流保持不变,但微循环血流仍出现了这种增加。非诺多泮组和安慰剂组的胃动脉二氧化碳分压值差异无统计学意义。
研究表明,在相同平均动脉压下,短期输注非诺多泮可增加感染性休克患者的胃黏膜灌注。