6‐Ketoprostaglandin F1αand thromboxane B2in isolated, blood‐perfused lungs from monocrotaline pyrrole‐treated rats

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Abstract
Monocrotaline pyrrole (MCTP) causes pulmonary vascular injury and pulmonary hypertension in rats. Although the mechanism by which MCTP causes pulmonary hypertension is unknown, vasoconstriction may play a role. Thromboxane (Tx) A2 is a vasoconstrictor released from platelets and other blood cells. Following treatment with MCTP in vivo, the release of stable metabolites of TxA2 and prostacyclin [TxB2 and 6‐keto prostaglandin F1α (6‐keto‐PGF1α), respectively] was determined in isolated lungs perfused with blood. Early in the development of pulmonary hypertension, the concentrations of TxB2 and 6‐keto‐PCF1α in the effluent plasma of lungs from treated rats were not different from control rats. When pulmonary hypertension was well established, the concentration of TxB2 was higher in the effluent plasma of lungs from MCTP‐treated rats, although the concentration of 6‐keto‐PCF1α was not affected by treatment.