The effects of prostaglandins (PGF
2α, E
1) on the pulmonary circulation were studied, with special reference to the influence of hypoxic gas (5.9% O
2, 5.6% CO
2) ventilation and β-blocking agent treatment. Also the comparison was made with the effects of conventional vasoactive agents were studied in the same manner.
The excised lung lobe of the dog was perfused with heparinized autologous blood at a constant flow rate by a pulsatile pump. Pulmonary inflow pressure, pulmonary blood flow, and bronchial pressure were recorded continuously and following results were obtained.
Noradrenaline increased pulmonary inflow pressure. Histamine and PGF
2α increased both pulmonary inflow and bronchial pressure. The elevation in bronchial pressure longer than that in pulmonary inflow pressure.
Elevation in the pulmonary inflow pressure by hypoxia started between 20 seconds and one minute, and its peak was achieved 1 to 3 minute after induction of hypoxia. Hypoxia the increase of mean pulmonary inflow pressure was 2.3mmHg.
More remarkable response to noradrenaline, histamine and PGF
2α were observed during hypoxia than control gas ventilation.
Although propranolol showed no influence on the pulmonary circulation and bronchial system in the control state, the response of the perfused lung lobe to noradrenaline as well as histamine was augmented by propranolol pretreatment. But the effect of PGF
2α was not altered by propranolol.
In the control state, isoproterenol and aminophylline showed a continued reduction both in the pulmonary inflow pressure and bronchial pressure, but no change was induced by PGE
1.
Both the vasoconstriction evoked by hypoxic gas ventilation and the bronchoconstriction induced by room air ventilation were reduced by PGE
1, and the pressor responses to noradrenaline and histamine were also reduced by PGE
1.
Vasodilatory effect of isoproterenol was abolished by propranolol, but not the case of PGE
1.
In conclusion, the mecanism of vasoactivation of PGs seems to be different from that of the other vasoactive agents used here. Therefore futher studies should be required to determine whether PG is mediated by adrenergic receptor or not.
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