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内毒素休克时的肝脏氧供及血浆乳酸和葡萄糖水平

Hepatic oxygen supply and plasma lactate and glucose in endotoxic shock.

作者信息

Rink R D, Short B L, Pennington C

出版信息

Circ Shock. 1978;5(2):105-13.

PMID:352569
Abstract

Hepatic oxygen supply and selected blood parameters were recorded in fasted male rates given 20--30 mg/kg Escherichia coli endotoxin intraperitoneally. Mortality was 70% within 24 hours. Measurements during the initial eight hours postendotoxin recorded no differences of hematocrit, systemic arterial pressure, or arterial pO2 between survivors and eventual nonsurvivors. However, by the sixth or eighth hour nonsurvivors showed significantly higher plasma lactate, lower plasma glucose and blood pH, and a greater degree of hypocapnea. In addition, a mean hepatic pO2 had decreased from 25.2 mm Hg during the control to 3.8 mm Hg after six hours. A decline of hepatic oxygen supply also occurred in surviving rats but was significantly less severe. Control rats showed a mild degree of respiratory alkalosis but were otherwise stable over eight hours. The relationship of hepatic oxygen supply to differences of plasma lactate and glucose is discussed. Failure of hepatic circulation is cited as the probable cause of extensive liver anoxia and related developments in nonsurviving endotoxic rats.

摘要

对禁食的雄性大鼠腹腔注射20 - 30毫克/千克大肠杆菌内毒素,记录其肝脏氧供应及选定的血液参数。24小时内死亡率为70%。在内毒素注射后的最初8小时内,幸存者和最终非幸存者之间的血细胞比容、体循环动脉压或动脉血氧分压均无差异。然而,到第6或8小时,非幸存者的血浆乳酸显著升高,血浆葡萄糖和血液pH值降低,且低碳酸血症程度更严重。此外,肝脏平均氧分压从对照时的25.2毫米汞柱降至6小时后的3.8毫米汞柱。存活大鼠的肝脏氧供应也出现下降,但程度明显较轻。对照大鼠表现出轻度呼吸性碱中毒,但在8小时内其他方面保持稳定。讨论了肝脏氧供应与血浆乳酸和葡萄糖差异之间的关系。肝脏循环衰竭被认为是内毒素血症死亡大鼠广泛肝脏缺氧及相关病变的可能原因。

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