Endotoxemia-induced leukopenia in sheep. Correlation with lung vascular permeability and hypoxemia but not with pulmonary hypertension.
Endotoxemia-induced leukopenia in sheep. Correlation with lung vascular permeability and hypoxemia but not with pulmonary hypertension.
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内毒素血症引起的绵羊白细胞减少症。
DOI：
10.1164/arrd.1983.127.3.306
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发表时间：
1983
期刊：
影响因子：
--
通讯作者：
Brigham,KL
中科院分区：
文献类型：
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作者：
Snapper,JR;Bernard,GR;HinsonJr,JM;Hutchison,AA;Loyd,JE;Ogletree,ML;Brigham,KL
本文研究了内毒素对26只非麻醉绵羊白细胞(WBC)计数、血流动力学、肺液和溶质交换的影响。7只绵羊也在甲氯芬酸酯(5 mg/kg团注+3 mg/kg/h)存在的情况下注射相同剂量的大肠杆菌内毒素。内毒素血症导致肺动脉压开始升高(PPA由18±1扫描电子显微镜升至59±7 cm H2O)。在内毒素血症后4h，淋巴蛋白清除率(淋巴流出时间淋巴/血浆蛋白浓度)增加到内毒素前对照的255.6%±28，肺泡与动脉血氧分压差(Δ)从12±4升至38±3毫米汞柱。WBC数在内毒素反应早期显著下降(内毒素后1h WBC数为基线的29%±6SEM)，但WBC数与早期肺动脉高压的严重程度无关。一些动物的WBC数比其他动物上升得更快，因此在内毒素后4小时，WBC数在1111到12134个/mm3之间。此时，CLP(r=0.5 3，P<0.0 1)和ΔAAPo2(r=0.83，P<0.0 1)均与WBC计数相关。甲氯芬酯能明显减轻早期肺动脉高压，但对内毒素血症所致的白细胞减少无明显影响。我们的结论是，肺白细胞淤滞不是内毒素血症后早期肺动脉高压的原因，但白细胞可能参与了晚期肺血管通透性增加和低氧血症。
The effects of endotoxin on white blood cell (WBC) counts, hemodynamics, and lung fluid and solute exchange were studied in 26 unanesthetized sheep. Seven sheep also received the same dose ofEscherichia coliendotoxin in the presence of meclofenamate (5 mg/kg bolus plus 3 mg/kg/h). Endotoxemia caused an initial increase in pulmonary artery pressure (Ppa from 18 ± 1 SEM to 59 ± 7 cm H2O). At 4 h after endotoxemia, lymph protein clearance (Clp = lymph flow times lymph/plasma protein concentration) had increased to 255.6% ± 28 SEM of the pre-endotoxin control values and the alveolar to arterial oxygen differences (ΔAaPO2) had increased from 12 ± 4 to 38 ± 3 mmHg. The WBC counts dropped dramatically early in the endotoxin reaction (WBC counts = 29% ± 6 SEM of baseline at 1 h after endotoxin), but the WBC counts did not correlate with the severity of the early pulmonary hypertension. The WBC counts rose more rapidly in some animals than in others, so that at 4 h after endotoxin WBC counts ranged between 1,111 and 12,134 cells/mm3. At this time, both Clp (r = 0.53, p < 0.01) and ΔAaPO2(r = 0.83, p < 0.01) correlated with the WBC counts. Meclofenamate markedly attenuated the early pulmonary hypertension, but it had no effect on the leukopenia caused by endotoxemia. We conclude that pulmonary leukostasis does not contribute to the early pulmonary hypertension after endotoxemia but that leukocytes may be involved in the late increase in lung vascular permeability and hypoxemia.