Krausz M M, Moriel E, Coronado E
Department of Surgery B, Hadassah University Hospital, Jerusalem, Israel.
Circ Shock. 1989 Jan;27(1):39-50.
Pulmonary insufficiency is a major cause for mortality and morbidity following shock and sepsis. We studied the effect of hemorrhagic shock and retransfusion on endotoxin-induced lung dysfunction. Eighteen unanesthetized sheep with chronic lung lymph fistulae were divided into 3 groups. In Group I (n = 5) hemorrhagic shock of 50 torr was induced by arterial bleeding. Shed blood was retransfused after 4 h, and the animals were observed for 5 h. In Group II (n = 7) 1 microgramg/kg E. coli endotoxin was injected intravenously, and the animals were observed for 5 h. In Group III (n = 6) hemorrhagic shock was induced similarly to Group I. After 2 h of hypotension, E. coli endotoxin was injected similarly to Group II. Blood was retransfused after 4 h. During hemorrhagic shock arterial oxygen tension (PaO2) increased from 78.0 to 94.0 torr (P less than 0.005), lymph flow (QL) decreased from 7.2 to 5.2 ml/h (P less than 0.05) and lymph protein clearance (L/P.QL) from 4.6 to 3.3 ml/h (P less than 0.05). Calculated pulmonary microvascular pressure (Pmv) decreased from 11.1 to 7.0 torr (P less than 0.05). Plasma TXB2 increased from 197 to 967 pg/ml (P less than 0.05) and lymph TXB2 from 272 to 833 pg/ml (P less than 0.05). Endotoxin infusion was followed by a fall in WBC to 2,900/microliters (P less than 0.001), rise in pulmonary artery pressure (Ppl) from 17.5 to 49.7 torr (P less than 0.005), and Pmv from 12.1 to 23.7 torr (P less than 0.01). PaO2 decreased from 78.0 to 61.0 torr (P less than 0.01), QL increased to 36.9 ml/h (P less than 0.001), and L/P.QL to 24.3 ml/h (P less than 0.001). Plasma TXB2 increased to 7,600 pg/ml (P less than 0.005) and 6-Keto PGF1 alpha to 1,519 pg/ml (P less than 0.01). Infusion of endotoxin during hemorrhagic shock was followed by a comparable fall in WBC, pulmonary hypertensive response and hypoxemia, while Pmv increased only to 19.2 torr which was significantly lower than Group II (P less than 0.05). The rise in QL to 17.4 and L/P.QL to 10.6 ml/h in response to endotoxin was also significantly lower than Group II (P less than 0.05 and P less than 0.05, respectively). Plasma and lymph TXB2 and 6-Keto PGF1 alpha were unchanged. It is concluded that hemorrhagic shock reduced endotoxin-induced pulmonary microvascular pressure, pulmonary lymph production and protein flux, while the fall in WBC, early pulmonary hypertensive phase, hypoxemia, and prostanoid production were not altered by the hypotensive insult.
肺功能不全是休克和脓毒症后导致死亡和发病的主要原因。我们研究了失血性休克及再输血对内毒素诱导的肺功能障碍的影响。18只患有慢性肺淋巴瘘的未麻醉绵羊被分为3组。第一组（n = 5）通过动脉放血诱导50托的失血性休克。4小时后回输流出的血液，并对动物观察5小时。第二组（n = 7）静脉注射1微克/千克大肠杆菌内毒素，并对动物观察5小时。第三组（n = 6）以与第一组相似的方式诱导失血性休克。低血压2小时后，以与第二组相似的方式注射大肠杆菌内毒素。4小时后回输血。在失血性休克期间，动脉血氧分压（PaO2）从78.0托升至94.0托（P < 0.005），淋巴流量（QL）从7.2毫升/小时降至5.2毫升/小时（P < 0.05），淋巴蛋白清除率（L/P.QL）从4.6毫升/小时降至3.3毫升/小时（P < 0.05）。计算得出的肺微血管压力（Pmv）从11.1托降至7.0托（P < 0.05）。血浆TXB2从197皮克/毫升升至967皮克/毫升（P < 0.05），淋巴TXB2从272皮克/毫升升至833皮克/毫升（P < 0.05）。输注内毒素后，白细胞降至2900/微升（P < 0.001），肺动脉压力（Ppl）从17.5托升至49.7托（P < 0.005），Pmv从12.1托升至23.7托（P < 0.01）。PaO2从78.0托降至61.0托（P < 0.01），QL升至36.9毫升/小时（P < 0.001），L/P.QL升至24.3毫升/小时（P < 0.001）。血浆TXB2升至7600皮克/毫升（P < 0.005），6 - 酮 - PGF1α升至1519皮克/毫升（P < 0.01）。在失血性休克期间输注内毒素后，白细胞有类似下降，出现肺高血压反应和低氧血症，而Pmv仅升至19.2托，显著低于第二组（P < 0.05）。内毒素引起的QL升至17.4毫升/小时和L/P.QL升至10.6毫升/小时也显著低于第二组（分别为P < 0.05和P < 0.05）。血浆和淋巴TXB2以及6 - 酮 - PGF1α无变化。结论是，失血性休克降低了内毒素诱导的肺微血管压力、肺淋巴生成和蛋白通量，而白细胞减少、早期肺高血压阶段、低氧血症和类前列腺素生成并未因低血压损伤而改变。
