Takala Jukka, Booke Michael, Westphal Martin, Hinder Frank, Traber Lillian D, Traber Daniel L
*Department of Anesthesiology, Klinikum des Main-Taunus-Kreises GmbH, Bad Soden am Taunus, Germany; †Department of Anesthesiology and Intensive Care, University of Münster, Münster, Germany; and ‡Department of Anesthesiology, University of Texas Medical Branch, Galveston, Texas.
Anesth Analg. 2003 Apr;96(4):1122-1128. doi: 10.1213/01.ANE.0000052516.86497.B6.
The origin of cerebral dysfunction in patients with sepsis is still unclear. However, altered cerebral perfusion may play an important role in its pathogenesis. Using an established, chronic model of hyperdynamic ovine sepsis, we examined cerebral perfusion in 20 sheep subjected to a continuous infusion of live Pseudomonas aeruginosa. After 24 h of sepsis, the hypotensive sheep (reduction in mean arterial blood pressure by 16%; P < 0.05) received the nitric oxide synthase inhibitor N(G)-mono-methyl-L-arginine (L-NMMA; 7 mg. kg(-1). h(-1); n = 7), norepinephrine (NE; n = 7), or normal saline (control; n = 6). NE infusion was individually targeted to achieve the same increase in mean arterial blood pressure as that observed in matched sheep of the L-NMMA group. Regional perfusion was measured by using colored microspheres. Although L-NMMA caused a significant increase in systemic vascular resistance index (1167 +/- 104 versus 793 +/- 59 dyne. cm(-5). m(2); P < 0.05), it caused a change neither in cerebrovascular resistance nor in cerebral blood flow. When related to systemic blood flow, a redistribution of blood flow to the brain became obvious. The NE-associated increase in systemic blood pressure (98 +/- 5 versus 83 +/- 5; P < 0.05) was accompanied by an increase in cardiac output (7.8 +/- 0.5 versus 6.7 +/- 0.6; P < 0.05) and, hence, systemic perfusion. However, blood flow to the brain remained unaffected. Although detrimental vasoconstrictive effects of NE and L-NMMA, including cerebral hypoperfusion, are discussed, neither drug had any effect on cerebral perfusion during experimental hyperdynamic sepsis.
Cerebral dysfunction is often found in septic patients. In this regard, it is debated whether vasopressor drugs, such as norepinephrine and L(G)-mono-methyl-L-arginine, have harmful effects on the cerebral circulation. During experimental hyperdynamic sepsis, however, neither drug altered cerebral vascular resistance or cerebral blood flow.
脓毒症患者脑功能障碍的起源仍不清楚。然而，脑灌注改变可能在其发病机制中起重要作用。我们使用已建立的慢性高动力羊脓毒症模型，对20只持续输注活铜绿假单胞菌的绵羊的脑灌注进行了研究。脓毒症24小时后，低血压绵羊（平均动脉血压降低16%；P<0.05）接受一氧化氮合酶抑制剂N(G)-单甲基-L-精氨酸（L-NMMA；7mg·kg(-1)·h(-1)；n=7）、去甲肾上腺素（NE；n=7）或生理盐水（对照组；n=6）。NE输注的目标是使平均动脉血压升高幅度与L-NMMA组配对绵羊中观察到的相同。使用彩色微球测量局部灌注。虽然L-NMMA导致全身血管阻力指数显著增加（1167±104对793±59达因·cm(-5)·m(2)；P<0.05），但它既未引起脑血管阻力改变，也未引起脑血流量改变。当与全身血流量相关时，脑血流重新分布变得明显。NE使全身血压升高（98±
