The effect of cooling on in vitro vascular prostacyclin and platelet thromboxane A2 synthesis: relevance to cold-induced pathology.

The effect of cooling (at 27 degrees C) on the synthesis of prostacyclin (PGI2) by rat aortic rings, thromboxane A2 (TXA2) synthesis by human platelets and phosphodiesterase activity in human platelets was investigated. Cooling induced a significant reduction in both PGI2 synthesis by rat aortic rings and TXA2 synthesis by human platelets, but the inhibition of the former was proportionately greater. Platelet phosphodiesterase activity decreased, with a subsequent increase in intraplatelet c-AMP content. Diminished PGI2 synthesis/release associated with the previously described diminution in the sensitivity of platelets to PGI2 after cooling probably contributes to the hyperaggregability of platelets at lower temperatures. This occurs in spite of the potential antiaggregatory effect of diminished TXA2 synthesis by platelets and the increase in intraplatelet c-AMP. These observations are relevant to the pathogenesis of hyperaggregability of platelets in Raynaud's syndrome.