Bronchial and cardiovascular actions of prostaglandin endoperoxides and an endoperoxide analogue

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Abstract
Effects of PGG2, PGH2 and the endoperoxide analogue, EPA, on bronchial and vascular smooth muscle were studied in vivo and in vitro. In the cat PGG2, PGH2 and particularly EPA proved potent stimulators of airway resistance, and they were all significantly more active than PGF2α. They also increased pulmonary vascular resistance but EPA alone was more active than PGF2α. In guinea pigs EPA was 90–190 times more active than PGF2α in increasing tracheal insufflation pressure. Human bronchi contracted in response to PGG2, PGH2 and EPA. PGG2 and PGH2 were equiactive with PGF2α and EPA was more than 500 times as potent. PGG2 and PGH2 lowered systemic arterial blood pressure and increased heart rate in cats. They were as active or more active than PGE2. EPA, on the other hand, resembled PGF2α in producing biphasic changes of blood pressure and heart rate or decrease of blood pressure and bradycardia in guinea pig and cat. The results obtained in this study indicate that PGG2, PGH2 and EPA are potent stimulators of bronchial and pulmonary vascular smooth muscle. The data are also consistent with the view that a significant proportion of effects resulting from prostaglandin generation in the lung is due to prostaglandin endoperoxides rather than primary prostaglandins.