Intrarenal blood flow distribution in hyperdynamic septic shock: Effect of norepinephrine
Intrarenal blood flow distribution in hyperdynamic septic shock: Effect of norepinephrine
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DOI：
10.1097/01.ccm.0000084842.66153.5a
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发表时间：
2003-10-01
影响因子：
8.8
通讯作者：
Bellomo, R
中科院分区：
文献类型：
--
作者：
Di Giantomasso, D;Morimatsu, H;Bellomo, R
目标。测量实验性高动力脓毒症期间髓质和皮质肾血流的变化以及随后输注去甲肾上腺素对此类血流的影响。设计：实验动物研究。设置。大学附属生理研究所动物实验室。课题。十八只麻醉的美利奴羊。干预：将通过时间流量探针放置在左肾动脉周围。通过显微操作将激光多普勒血流探针插入左肾髓质和皮质，以测量局部肾内血流的变化。测量和主要结果。连续测量体循环压力、心输出量、肾血流量和肾内血流量。静脉内给予大肠埃希氏菌（7.5 x 10(9) 菌落形成单位）以诱导高动力脓毒症。高动力脓毒症发作后，所有动物被随机分配到去甲肾上腺素（0.4 mug(.)kg(-1.)min(-1)，持续30分钟）或随机观察30分钟。大肠杆菌注射导致平均动脉压显着降低（102.2 +/- 15.2 mm Hg 至 74.3 +/- 16.1 mm Hg，p < .05），平均心输出量增加（4.60 +/- 1.62 L/min 至 5.93 +/- 1.18 L/min，p < .05）。然而，尽管肾电导增加了 30%（3.27 +/- 1.52 至 4.13 +/- 2.01 mL(.)min(-1.)mm Hg-1，p < .05），但肾血流量没有显着变化（326.4 +/- 139.4 mL/min 至 293.1 +/- 117.5 mL/min，不显着）。脓毒症期间皮质血流量减少 15%（不显着），髓质血流量减少 5%（不显着），但个体变化是不可预测的。另一方面，输注去甲肾上腺素可显着改善平均动脉压（74.3 +/- 16.1 至 105.7 +/- 17.7 mm Hg，p < .05），并进一步增加心输出量（5.93 +/- 1.18 至 7.13 +/- 1.52 L/min，p < .05）。尽管肾电导率降低（4.13 +/- 2.01 至 3.73 +/- 1.91 mL(.)min(-1.)mm Hg-1，p < .05），但平均肾血流量也增加（293.1 +/- 117.5 至 384.5 +/- 168.1 mL/min，p < .05）。与基线相比，输注去甲肾上腺素显着增加了髓质血流量 35% (p < .05)，与未经治疗的脓毒症相比增加了 54% (p < .05)，而皮质血流量的增加（分别为 16% 和 53%）并不显着。 结论：高动力脓毒症引起肾血管舒张，但对局部肾内血流影响有限。脓毒症期间去甲肾上腺素输注（0.4 mug(.)kg(-1.)min(-1)）显着增加肾肾全血流量和肾髓质血流量，并使肾血管张力恢复至正常水平，但不高于正常水平。
Objectives. To measure changes in medullary and cortical renal blood flow during experimental hyperdynamic sepsis and the effect of subsequent norepinephrine infusion on such flows.Design: Experimental animal study.Setting. Animal laboratory of university-affiliated physiology institute.Subjects. Eighteen anesthetized merino sheep.Interventions: A transit-time flow probe was placed around the left renal artery. Laser Doppler flow probes were inserted in the left renal medulla and cortex by micromanipulation to measure changes in regional intrarenal blood flow.Measurements and Main Results. Systemic pressures, cardiac output, renal, and intrarenal blood flows were measured continuously. A bolus of Escherichia coli (7.5 x 10(9) colony forming units) was given intravenously to induce hyperdynamic sepsis. After the onset of hyperdynamic sepsis, all animals were randomly allocated to either norepinephrine (0.4 mug(.)kg(-1.)min(-1) for 30 mins) or observation for 30 mins in random order. E. coli injection induced a significant decrease in mean arterial pressure (102.2 +/- 15.2 mm Hg to 74.3 +/- 16.1 mm Hg, p < .05) and an increase in mean cardiac output (4.60 +/- 1.62 L/min to 5.93 +/- 1.18 L/min, p < .05). However, renal blood flow did not change significantly (326.4 +/- 139.4 mL/min to 293.1 +/- 117.5 mL/min, not significant) despite a 30% increase in renal conductance (3.27 +/- 1.52 to 4.13 +/- 2.01 mL(.)min(-1.)mm Hg-1, p < .05). Cortical blood flow decreased by 15% (not significant) and medullary flow by 5% (not significant) during sepsis, but individual changes were unpredictable. On the other hand, norepinephrine infusion caused a significant improvement in mean arterial pressure (74.3 +/- 16.1 to 105.7 +/- 17.7 mm Hg, p < .05) and a further increase in cardiac output (5.93 +/- 1.18 to 7.13 +/- 1.52 L/min, p < .05). Mean renal blood flow also increased (293.1 +/- 117.5 to 384.5 +/- 168.1 mL/min, p < .05) despite decreased renal conductance (4.13 +/- 2.01 to 3.73 +/- 1.91 mL(.)min(-1.)mm Hg-1, p < .05). Infusion of norepinephrine significantly increased medullary blood flow by 35% compared with baseline (p < .05) and by 54% compared with untreated sepsis (p < .05), whereas the increases in cortical blood flow (16 and 53%, respectively) were not significant.Conclusions: Hyperdynamic sepsis caused renal vasodilation but had limited effects on regional intrarenal blood flow. Norepinephrine infusion (0.4 mug(.)kg(-1.)min(-1)) during sepsis significantly increased global and medullary renal blood flow and restored renal vascular tone toward but not above normal.