Vital organ blood flow during hyperdynamic sepsis
Vital organ blood flow during hyperdynamic sepsis
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DOI：
10.1378/chest.124.3.1053
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发表时间：
2003-09-01
期刊：
影响因子：
9.6
通讯作者：
Bellomo, R
中科院分区：
文献类型：
--
作者：
Di Giantomasso, D;May, CN;Bellomo, R
目的：建立一种非致死性高动力性脓毒症模型，并在此环境下测量重要器官的血流量。设计：随机交叉动物研究。设置：大学附属生理学研究所动物实验室。受试者：七只美利奴杂交羊。干预措施：手术植入矢状窦和回旋冠状动脉、上级肠系膜动脉和左肾动脉周围的渡越时间血流探头，以及一个电磁流量探针。恢复后，随机分配至正常条件下观察6小时（对照）或诱导高动力非致死性脓毒症（脓毒症）后观察6小时，每只动物在2周间隔后交叉至另一种治疗。测量和主要结果：大肠杆菌注射致5 ~ 6 h内非致死性高动力性脓毒症伴低血压（平均动脉压[+/- SD]，85 +/- 7 mm Hg vs 69 +/- 8 mm Hg），心输出量增加（4.0 +/- 0.9 L/min vs 7.2 +/- 1.2 L/min）、心动过速（60 +/- 10次/min vs 160 +/- 15次/min）、发热、少尿和呼吸急促。与对照动物相比，高动力性脓毒症增加了肾（330 +/- 101 mL/min vs 214 +/- 75 mL/min）、肠系膜（773 +/- 370 mL/min vs 516 +/- 221 mL/min）和冠状动脉（54 +/- 24 mL/min vs 23 +/- 10 mL/min）血流量（p < 0.05）。矢状窦血流无明显变化。尽管冠状动脉血流增加，心肌收缩力降低（800 +/- 150 L/min/s vs 990 +/- 150 L/min/s）。尽管肠系膜和肾脏血流量增加，但仍有高乳酸血症（0.5 ± 0.1 mmol/L vs 1.9 ± 0.3 mmol/L）;尽管肾血流量增加，所有实验动物均获得少尿（160 +/- 75.3 mL/2 h vs 50.2 +/- 13.1 mL/2 h）和升高的血清肌酐水平（0.07 +/- 0.02 mmol/L vs 0.11 +/- 0.02 mmol/L）。在这种高动力性脓毒症期间，流向心脏、肠道和肾脏的血流量显著增加;然而，器官功能障碍发展。我们推测，全脑缺血可能不是高动力性脓毒症重要器官功能障碍的主要机制。
Objectives: To develop a nonlethal model of hyperdynamic sepsis, and to measure vital organ blood flows in this setting.Design: Randomized crossover animal study.Setting: Animal laboratory of university-affiliated physiology institute.Subjects: Seven Merino cross sheep.Interventions: Surgical implantation of transit-time flow probes around sagittal sinus and circumflex coronary, superior mesenteric, and left renal arteries, and of an electromagnetic flow probe around the ascending aorta. After recovery, randomization to either 6 h of observation under normal conditions (control) or 6 h of observation after the induction of hyperdynamic nonlethal sepsis (sepsis), with each animal crossing over to the other treatment after a 2-week interval.Measurements and main results: Injection of Escherichia coli induced nonlethal hyperdynamic sepsis within 5 to 6 h with hypotension (mean arterial pressure [+/- SD], 85 +/- 7 mm Hg vs 69 +/- 8 mm Hg), increased cardiac output (4.0 +/- 0.9 L/min vs 7.2 +/- 1.2 L/min), tachycardia (60 +/- 10 beats/min vs 160 +/- 15 beats/min), fever, oliguria, and tachypnea. Compared to control animals, hyperdynamic sepsis increased renal (330 +/- 101 mL/min vs 214 +/- 75 mL/min), mesenteric (773 +/- 370 mL/min vs 516 +/- 221 mL/min), and coronary (54 +/- 24 mL/min vs 23 +/- 10 mL/min) blood flow (p < 0.05). There was no significant change in sagittal sinus flow. Despite increased coronary flow, myocardial contractility decreased (800 +/- 150 L/min/s vs 990 +/- 150 L/min/s). Despite increased mesenteric and renal blood flow, there was hyperlactatemia (0.5 +/- 0.1 mmol/L vs 1.9 +/- 0.3 mmol/L); despite increased renal blood flow, all experimental animals acquired oliguria (160 +/- 75.3 mL/2 h vs 50.2 +/- 13.1 mL/2 h) and increased serum creatinine levels (0.07 +/- 0.02 mmol/L vs 0.11 +/- 0.02 mmol/L).Conclusions: Injection of E coli induced hyperdynamic nonlethal sepsis. During such hyperdynamic sepsis, blood flow to heart, gut, and kidney was markedly increased; however, organ dysfunction developed. We speculate that global ischemia may not be the principal mechanism of vital organ dysfunction in hyperdynamic sepsis.