Brander Lukas, Jakob Stephan M, Knuesel Rafael, Savolainen Hannu, Widmer Matthias K, Schmidli Juerg, Takala Jukka
Department of Intensive Care Medicine, University Hospital-Inselspital, Bern, Switzerland.
Shock. 2006 Apr;25(4):402-13. doi: 10.1097/01.shk.0000217813.50104.5d.
Low cardiac output impairs the hepatic arterial buffer response (HABR). Whether this is due to low abdominal blood flow per se is not known. Dobutamine is commonly used to increase cardiac output, and it may further modify hepatosplanchnic and renal vasoregulation. We assessed the effects of isolated abdominal aortic blood flow changes and dobutamine on hepatosplanchnic and renal blood flow. Twenty-five anesthetized pigs with an abdominal aorto-aortic shunt were randomized to 2 control groups [zero (n = 6) and minimal (n = 6) shunt flow], and 2 groups with 50% reduction of abdominal blood flow and either subsequent increased abdominal blood flow by shunt reduction (n = 6) or dobutamine infusion at 5 and 10 microg kg(-1) min(-1) with constant shunt flow (n = 7). Regional (ultrasound) and local (laser Doppler) intra-abdominal blood flows were measured. The HABR was assessed during acute portal vein occlusion. Sustained low abdominal blood flow, by means of shunt activation, decreased liver, gut, and kidney blood flow similarly and reduced local microcirculatory blood flow in the jejunum. Shunt flow reduction partially restored regional blood flows but not jejunal microcirculatory blood flow. Low-but not high-dose dobutamine increased gut and celiac trunk flow whereas hepatic artery and renal blood flows remained unchanged. Neither intervention altered local blood flows. The HABR was not abolished during sustained low abdominal blood flow despite substantially reduced hepatic arterial blood flow and was not modified by dobutamine. Low-but not high-dose dobutamine redistributes blood flow toward the gut and celiac trunk. The jejunal microcirculatory flow, once impaired, is difficult to restore.
低心输出量会损害肝动脉缓冲反应（HABR）。这是否归因于低腹部血流量本身尚不清楚。多巴酚丁胺常用于增加心输出量，它可能会进一步改变肝内脏和肾血管调节。我们评估了孤立的腹主动脉血流变化和多巴酚丁胺对肝内脏和肾血流的影响。将25只带有腹主动脉 - 主动脉分流的麻醉猪随机分为2个对照组[零（n = 6）和最小（n = 6）分流流量]，以及2组腹部血流量减少50%的组，其中一组随后通过减少分流增加腹部血流量（n = 6），另一组在恒定分流流量下以5和10μg·kg⁻¹·min⁻¹的剂量输注多巴酚丁胺（n = 7）。测量区域（超声）和局部（激光多普勒）腹内血流量。在急性门静脉闭塞期间评估HABR。通过激活分流维持低腹部血流量，同样降低了肝脏、肠道和肾脏的血流量，并减少了空肠的局部微循环血流量。减少分流流量部分恢复了区域血流量，但空肠微循环血流量未恢复。低剂量而非高剂量的多巴酚丁胺增加了肠道和腹腔干血流量，而肝动脉和肾血流量保持不变。两种干预均未改变局部血流量。尽管肝动脉血流量大幅减少，但在持续低腹部血流量期间HABR并未消失，且未被多巴酚丁胺改变。低剂量而非高剂量的多巴酚丁胺使血流重新分布至肠道和腹腔干。一旦受损，空肠微循环血流很难恢复。
