Endotoxin and prevention of hypoxic pulmonary vasoconstriction.
Endotoxin and prevention of hypoxic pulmonary vasoconstriction.
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内毒素与预防缺氧性肺血管收缩。
DOI：
10.5555/uri:pii:0022214376905205
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发表时间：
1976
期刊：
影响因子：
--
通讯作者：
R. Grover
中科院分区：
文献类型：
--
作者：
E. Weir;J. Mlczoch;J. Reeves;R. Grover
已知内毒素既能刺激前列腺素的产生，又能消除肺血管对缺氧的升压反应。目前的研究表明，两种前列腺素合成抑制剂，甲氨蝶呤和吲哚美辛，防止损失的肺血管收缩时，由于缺氧亚致死剂量的内毒素管理。这表明，内毒素可能刺激产生的扩张剂前列腺素，这将对抗缺氧性血管收缩，但这些抑制剂药物可能发挥作用的其他方式被认为是。内毒素破坏血小板和白细胞，两者都可以形成前列腺素，并可能是扩张剂前列腺素的来源。然而，在这些实验中，内毒素消除了狗的缺氧加压反应，使严重血小板减少的血小板抗血清。这表明血小板不参与其中。在进一步的实验中，来自麻醉狗的血液通过玻璃珠柱循环。灌注后白细胞计数的变化与随后对缺氧的升压反应的变化相关。白细胞可能参与内毒素对缺氧性升压反应的影响。
Endotoxin is known both to stimulate prostaglandin production and to abolish the pulmonary vascular pressor response to hypoxia. The present study demonstrated that two inhibitors of prostaglandin synthesis, meclofenamate and indomethacin, prevent loss of pulmonary vasoconstriction due to hypoxia when sublethal doses of endotoxin are administered. This suggests that endotoxin may stimulate the production of a dilator prostaglandin which would oppose the hypoxic vasoconstriction, but other ways in which these inhibitor drugs might act are considered. Endotoxin damages platelets and leukocytes, both of which can form prostaglandins and could be the source of a dilator prostaglandin. However, in these experiments endotoxin abolished the hypoxic pressor response in dogs rendered severely thrombocytopenic by platelet antiserum. This suggests that platelets are not involved. In further experiments blood from anesthetized dogs was circulated through glass bead columns. Changes in the leukocyte count following perfusion were correlated with changes in the subsequent pressor response to hypoxia. The possibility that leukocytes may be involved in the effect of endotoxin on the hypoxic pressor response is considered.