This preclinical study demonstrates that prostaglandin-like substances and rabbit aorta contracting substance are released directly from platelets during aggregation, contributing to pulmonary pressor responses.
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Does not yet inform clinical practice; leaves open platelet-derived mediators in human pulmonary hypertension.
During pulmonary microembolism subsequent to induced platelet aggregation in vivo, a pressor response is elicited in the lungs due to the release of vasoactive substances. During the prefusion of isolated cat lungs with whole blood, platelet aggregation induced by collagen released prostaglandin-like substances (PG-LS), and a rabbit aorta contracting substance (RCS) as measured by continuous biosassay of the venous effluent. This release occurred in parallel to the pulmonary pressor response. The same amount of PG-LS and RCS was released when the lungs were replaced by a blood filter to trap platelet aggregates. Apparently PG-LS and RCS are released from platelets during their aggregation. As E- and F-type PGs are rapidaly inactivated in the pulmonary circulation, there must either be an equal generation of PGs in the lungs themselves, or rather, the release of PGs from platelets must occur distal to the inactivation mechanism without any additional PG-release from the lungs. The exact role of PGs in the lung responses to intravascular platelet aggregation is not clear.
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Vaage et al. (1975) studied this question.
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