OBJECTIVE: To test the hypothesis that persistent villi hypoperfusion explains intramucosal acidosis after endotoxemic shock resuscitation. DESIGN: Controlled experimental study. SETTING: University-based research laboratory. SUBJECTS: A total of 14 anesthetized, mechanically ventilated sheep. INTERVENTIONS: Sheep were randomly assigned to endotoxin (n = 7) or control groups (n = 7). The endotoxin group received 5 microg/kg endotoxin, followed by 4 microg x kg(-1) x hr(-1) for 150 mins. After 60 mins of shock, hydroxyethylstarch resuscitation was given to normalize oxygen transport for an additional 90 mins. MEASUREMENTS AND MAIN RESULTS: Endotoxin infusion decreased mean arterial blood pressure, cardiac output, and superior mesenteric artery blood flow (96 +/- 10 vs. 51 +/- 20 mm Hg, 145 +/- 30 vs. 90 +/- 30 mL x min(-1) x kg(-1), and 643 +/- 203 vs. 317 +/- 93 mL x min(-1) x kg(-1), respectively; p < .05 vs. basal), whereas it increased intramucosal-arterial PCO2 (deltaPCO2) and arterial lactate (3 +/- 3 vs. 14 +/- 8 mm Hg, and 1.5 +/- 0.5 vs. 3.7 +/- 1.3 mmol/L; p < .05). Sublingual, and serosal and mucosal intestinal microvascular flow indexes, and the percentage of perfused ileal villi were reduced (3.0 +/- 0.1 vs. 2.3 +/- 0.4, 3.2 +/- 0.2 vs. 2.4 +/- 0.6, 3.0 +/- 0.0 vs. 2.0 +/- 0.2, and 98% +/- 3% vs. 76% +/- 10%; p < .05). Resuscitation normalized mean arterial blood pressure (92 +/- 13 mm Hg), cardiac output (165 +/- 32 mL x min(-1) x kg(-1)), superior mesenteric artery blood flow (683 +/- 192 mL x min(-1) x kg(-1)), and sublingual and serosal intestinal microvascular flow indexes (2.8 +/- 0.5 and 3.5 +/- 0.7). Nevertheless, deltaPCO2, lactate, mucosal intestinal microvascular flow indexes, and percentage of perfused ileal villi remained altered (10 +/- 6 mm Hg, 3.7 +/- 0.9 mmol/L, 2.3 +/- 0.4, and 78% +/- 11%; p < .05). CONCLUSIONS: In this model of endotoxemia, fluid resuscitation corrected both serosal intestinal and sublingual microcirculation but was unable to restore intestinal mucosal perfusion. Intramucosal acidosis might be due to persistent villi hypoperfusion.
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机译：目的：检验内毒素休克复苏后持续绒毛灌注不足可解释粘膜内酸中毒的假说。设计：对照实验研究。地点：大学研究实验室。受试者：总共14只麻醉的机械通风的绵羊。干预措施：将绵羊随机分为内毒素（n = 7）或对照组（n = 7）。内毒素组接受5 microg / kg内毒素，然后在150分钟内接受4 microg x kg（-1）x hr（-1）。休克60分钟后，给予羟乙基淀粉复苏以使氧气传输正常化90分钟。测量和主要结果：内毒素输注降低了平均动脉血压，心输出量和肠系膜上动脉血流量（96 +/- 10 vs. 51 +/- 20 mm Hg，145 +/- 30 vs. 90 +/- 30 mL x min（-1）x kg（-1）和643 +/- 203 vs.317 +/- 93 mL x min（-1）x kg（-1）; p <.05 vs.基础），而它增加了粘膜内动脉PCO2（deltaPCO2）和动脉乳酸盐（3 +/- 3 vs. 14 +/- 8 mm Hg，1.5 +/- 0.5 vs. 3.7 +/- 1.3 mmol / L; p < .05）。舌下，浆膜和粘膜肠微血管流量指数以及灌注回肠绒毛的百分比降低（3.0 +/- 0.1 vs. 2.3 +/- 0.4、3.2 +/- 0.2 vs. 2.4 +/- 0.6、3.0 + / -0.0 vs. 2.0 +/- 0.2，以及98％+/- 3％和76％+/- 10％; p <.05）。复苏标准化的平均动脉血压（92 +/- 13 mm Hg），心输出量（165 +/- 32 mL x min（-1）x kg（-1）），肠系膜上动脉血流量（683 +/- 192） mL x min（-1）x kg（-1）），舌下和浆膜肠微血管流量指数（2.8 +/- 0.5和3.5 +/- 0.7）。尽管如此，deltaPCO2，乳酸，粘膜肠微血管流量指数和灌注回肠绒毛的百分比仍发生变化（10 +/- 6 mm Hg，3.7 +/- 0.9 mmol / L，2.3 +/- 0.4和78％+/- 11％; p <.05）。结论：在这种内毒素血症模型中，液体复苏可纠正浆膜肠和舌下微循环，但无法恢复肠粘膜灌注。粘膜内酸中毒可能是由于持续的绒毛灌注不足所致。
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