Effect of vasodilators on the hypoxic pulmonary vasoconstriction

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1. Using the separatedly ventilated left lower lung model, effects of vasodilators such as nitoroglycerine (TNG) and prostacyclin (PGI_2) on the hypoxic pulumonary vasoconstfiction (HPV) were investigated in the dogs. The results showed that the both TNG and PGI_2 were considered to cause hypoxemia either by increasing pulmonary ventilation-perfusion unevennes because of non-specific vasodilation with TNG or by inhibiting HPV in a dose-related manner with PGI_2.2. For more precise evaluation of pulmonary vascular tone the new model to measure the vascular pressure-flow curve of the left lower lobe was developed in the dogs in vivo and the effects of inhalation anesthetics such as isofulurane and halothane on HPV were investigated. As the results there were little inhibitory effect of HPV with clinical dose (1-2MAC) of isoflurane and halothane, although both of them inhibited HPV in a dose-related manner when directly inhaled to the hypoxic lobe.3. Using the same pressure-flow cureve model in the dogs, a dosage of prostagiandin E_1 which decrease systemic blood pressure by 30% was showed to result hypoxemia by inhibiting HPV.4. Modulation of HPV in the injured lung such as ARDS was investigated with the same pressure-flow curve model in the dogs. Low dose of endotoxin completely depressed HPV and accompanied with a decrese in stable metabolyte of prostacyclin, 6-keto-PGF_1alpha. This depression of HPV with endotoxin was prevented by pretreating with cyclooxgenase inhibitor, ibuprofen and 6-keto-PGF_1alpha did not decreased. These results indicated that incresed release or production of prostacyclin from the pulmonary endothelial cells were involved with the inhibition of HPV by endotoxin.