<原著>エンドトキシンの低酸素性肺血管収縮反応への作用

概要

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Loss of hypoxic pulmonary vasoconstriction (HPV) response might cause hypoxemia in an acute lung injury such as ARDS. The inhibitory effect of cyclooxygenase pathway products on the HPV response induced by the low-dose endotoxin was examined in dogs. The HPV response was investigated by measuring %Q_<LLL> (ratio of the left lower lobe blood flow to the total pulmonary blood flow), P_ao_2 and the pressure-flow curve of the left lower lobe pulmonary vasculature. An endotoxin-induced increase in %Q_<LLL> with the hypoxic gas ventilation was prevented by ibuprofen pretreatment. The increase in %Q_<LLL> was from 3.7±0.7(%) to 15.8±1.0 and was significant, and the decrease was from 4.8±0.6 to 3.1±0.5. Findings of P_ao_2 and the pressure-flow curve indicated the same HPV inhibition. An endotoxin-induced increase in 6-keto-PGF_<1α> was blocked by ibuprofen pretreatment. The expected increase in 6-keto-PGF_<1α> was from 175.5±27.1 (pg/ml) to 332.8±84.1. The block reduced the value from 187.3±37.7 to 217.2±60.4. Decrease in leucocytes counts after endotoxin infusion was observed both in the groups of presence and absence of ibuprofen. These results suggested that prostacyclin release involved with the HPV response inhibition by endotoxin.
近畿大学の論文
1991-06-25