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多巴酚丁胺可代偿血管加压素在内毒素休克时对内脏区域产生的有害血流动力学和代谢效应。

Dobutamine compensates deleterious hemodynamic and metabolic effects of vasopressin in the splanchnic region in endotoxin shock.

作者信息

Martikainen T J, Uusaro A, Tenhunen J J, Ruokonen E

机构信息

Department of Anesthesiology and Intensive Care, Kuopio University Hospital, Finland.

出版信息

Acta Anaesthesiol Scand. 2004 Sep;48(8):935-43. doi: 10.1111/j.0001-5172.2004.00435.x.

Abstract

BACKGROUND

Vasopressin is a potent vasopressor in septic shock, but it may impair splanchnic perfusion. We compared the effects of vasopressin alone and in combination with dobutamine on systemic and splanchnic circulation and metabolism in porcine endotoxin shock.

METHODS

Twelve pigs were randomized to receive either vasopressin (VASO, n = 6) or vasopressin in combination with dobutamine (DOBU, n = 6) during endotoxin shock (E. coli endotoxin infusion). Endotoxin infusion rate was increased to induce hypotension after which vasoactive drugs were started. We aimed to keep systemic mean arterial pressure (MAP) >70 mmHg by vasopressin; the goal of dobutamine infusion was to prevent decrease in cardiac output often associated with vasopressin infusion. Regional blood flows, oxygen delivery and consumption, arterial and regional lactate concentrations were measured.

RESULTS

Mean arterial pressure >70 mmHg was achieved in both the VASO and DOBU groups. After the primary decrease of cardiac output by vasopressin, systemic blood flow remained stable in vasopressin-treated animals. However, vasopressin as a monotherapy decreased portal venous blood flow. This was prevented by dobutamine. Vasopressin also induced splanchnic lactate release and arterial hyperlactatemia, which were not observed when dobutamine was combined with vasopressin.

CONCLUSION

Dobutamine prevents adverse hemodynamic and metabolic effects of vasopressin in septic shock.

摘要

背景

血管加压素是感染性休克中一种强效的血管升压药,但它可能会损害内脏灌注。我们比较了单独使用血管加压素以及血管加压素与多巴酚丁胺联合使用对猪内毒素休克时全身和内脏循环及代谢的影响。

方法

12头猪在内毒素休克(输注大肠杆菌内毒素)期间被随机分为接受血管加压素组(VASO,n = 6)或血管加压素联合多巴酚丁胺组(DOBU,n = 6)。在内毒素输注速率增加以诱导低血压后开始使用血管活性药物。我们旨在通过血管加压素使全身平均动脉压(MAP)>70 mmHg;多巴酚丁胺输注的目标是防止通常与血管加压素输注相关的心输出量下降。测量局部血流量、氧输送和消耗、动脉和局部乳酸浓度。

结果

VASO组和DOBU组均实现了平均动脉压>70 mmHg。在血管加压素使心输出量首次下降后,血管加压素治疗的动物全身血流保持稳定。然而,单独使用血管加压素会降低门静脉血流量。多巴酚丁胺可防止这种情况。血管加压素还会诱导内脏乳酸释放和动脉血乳酸水平升高,而多巴酚丁胺与血管加压素联合使用时未观察到这种情况。

结论

多巴酚丁胺可预防血管加压素在感染性休克中的不良血流动力学和代谢效应。

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