Bellomo Rinaldo
Department of Intensive Care and Medicine, Austin & Repatriation Medical Centre, Melbourne, Australia.
Heart Lung Circ. 2003;12 Suppl 2:S42-8. doi: 10.1046/j.1443-9506.2003.t01-7-.x.
Septic shock, systemic inflammation and pharmacological vasodilatation are often complicated by systemic hypotension despite aggressive fluid resuscitation and an increased cardiac output. If the physician wishes to restore arterial pressure to higher levels (> 80-85 mmHg), with the aim of sustaining cerebral and coronary perfusion pressure, the administration of systemic vasopressor agents, such as norepinephrine (noradrenaline), becomes necessary. However, because norepinephrine (NE) induces vasoconstriction in many vascular beds (visibly in the skin), it may decrease renal and visceral blood flow, impairing visceral organ function. This unproven fear deters clinicians from using NE more consistently. Vasodilated states, however, are often associated with impaired peripheral vascular responsiveness. In such states, unlike under normal circulatory conditions, NE may actually improve visceral organ blood flow by selectively increasing organ perfusion pressure. Data available from animal studies show that the increased organ perfusion pressures achieved with NE results in improved GFR and renal blood flow. In fact, recent sophisticated physiological analysis of its effects on the kidney shows that, even after controlling for the pressure effect, NE therapy is associated with an increase in renal blood flow after endotoxin administration. In particular, the renal Pzf (pressure at which there is no further blood flow) is decreased such that, at a constant pressure, renal blood flow increases after NE. There are no controlled human data to define the effects of NE on the kidney in the clinical context. However, many patient series have now been reported. They show a seemingly positive effect of NE administration on GFR and urine output. Our clinical experience in septic patients and cardiac patients with inflammatory or pharmacological vasodilatation is also positive. We have demonstrated a positive effect on coronary blood flow. There is no reason to fear the effect of NE. If it is used to support a vasodilated circulation after adequate intravascular filling has occurred and after a normal or increased cardiac output has been established, it is likely to be a friend not a foe.
尽管积极进行液体复苏且心输出量增加，但脓毒性休克、全身炎症反应和药物性血管扩张常伴有系统性低血压。如果医生希望将动脉压恢复到较高水平（>80 - 85 mmHg），以维持脑和冠状动脉灌注压，则有必要使用全身性血管升压药，如去甲肾上腺素。然而，由于去甲肾上腺素（NE）会在许多血管床（如在皮肤中明显可见）诱导血管收缩，它可能会减少肾和内脏血流，损害内脏器官功能。这种未经证实的担忧使临床医生不太愿意持续使用NE。然而，血管扩张状态通常与外周血管反应性受损有关。在这种状态下，与正常循环条件下不同，NE实际上可能通过选择性增加器官灌注压来改善内脏器官血流。动物研究的数据表明，NE使器官灌注压升高可导致肾小球滤过率（GFR）和肾血流量增加。事实上，最近对其对肾脏作用的复杂生理分析表明，即使在控制压力效应后，内毒素给药后NE治疗仍与肾血流量增加有关。特别是，肾零流量压力（Pzf）降低，使得在恒定压力下，给予NE后肾血流量增加。目前尚无对照的人体数据来确定NE在临床环境中对肾脏的影响。然而，现在已经报道了许多患者系列研究。这些研究表明给予NE对GFR和尿量似乎有积极作用。我们在脓毒症患者以及伴有炎症或药物性血管扩张的心脏病患者中的临床经验也是积极的。我们已经证明其对冠状动脉血流有积极作用。没有理由害怕NE的作用。如果在充分的血管内补液后以及建立了正常或增加的心输出量后使用它来支持血管扩张的循环，它很可能是有益而非有害的。
