AN IMBALANCE BETWEEN THE EXCRETION OF THROMBOXANE AND PROSTACYCLIN METABOLITES IN PULMONARY-HYPERTENSION
AN IMBALANCE BETWEEN THE EXCRETION OF THROMBOXANE AND PROSTACYCLIN METABOLITES IN PULMONARY-HYPERTENSION
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DOI:
10.1056/nejm199207093270202
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发表时间:
1992-07-09
影响因子:
158.5
通讯作者:
LOYD, JE
中科院分区:
文献类型:
--
作者:
CHRISTMAN, BW;MCPHERSON, CD;LOYD, JE
Background. Constriction of small pulmonary arteries and arterioles and focal vascular injury are features of pulmonary hypertension. Because thromboxane A2 is both a vasoconstrictor and a potent stimulus for platelet aggregation, it may be an important mediator of pulmonary hypertension. Its effects are antagonized by prostacyclin, which is released by vascular endothelial cells. We tested the hypothesis that there may be an imbalance between the release of thromboxane A2 and prostacyclin in pulmonary hypertension, reflecting platelet activation and an abnormal response of the pulmonary vascular endothelium.Methods. We used radioimmunoassays to measure the 24-hour urinary excretion of two stable metabolites of thromboxane A2 and a metabolite of prostacyclin in 20 patients with primary pulmonary hypertension, 14 with secondary pulmonary hypertension, 9 with severe chronic obstructive pulmonary disease (COPD) but no clinical evidence of pulmonary hypertension, and 23 normal controls.Results. The 24-hour excretion of 11-dehydro-thromboxane B2 (a stable metabolite of thromboxane A2) was increased in patients with primary pulmonary hypertension and patients with secondary pulmonary hypertension, as compared with normal controls (3224+/-482, 5392+/-1640, and 1145+/-221 pg per milligram of creatinine, respectively; P