Increased platelet arachidonic acid metabolism in diabetes mellitus.

Platelets obtained from some diabetic patients show enhanced in vitro platelet aggregation. This study sought to determine if platelet obtained from insulin-dependent diabetic subjects synthesize increased quantities of the labile aggregating substance, thromboxane A2 (TXA2), and if it may play a role in the enhanced platelet aggregation. Arachidonic acid (1 mM)-stimulated TXA2 synthesis, as determined via radioimmunoassay of its stable metabolite TXB2, was significantly greater (P less than 0.01, N = 12) in platelet-rich plasma obtained from diabetics compared with matched controls. Arachidonic acid-stimulated TXB2 synthesis in the diabetic platelet-rich plasma was positively correlated with the ambient fasting plasma glucose (r = 0.61, P less than 0.02, N = 15). Platelet aggregation induced by arachidonic acid (0.4-0.8 mM) was inhibited significantly less by 13-azaprostanoic acid (P less than 0.04, N = 14), a competitive antagonist of the actions of prostaglandin H2 or TXA2 on platelets, compared with matched controls. The results support the notion that platelets obtained from some insulin-dependent diabetic subjects manifest increased synthesis of TXA2, which may contribute to the enhanced platelet aggregation.

Incidence of hypertension in infants on extracorporeal membrane oxygenation.

Systemic hypertension has been associated with extracorporeal membrane oxygenation (ECMO) applied in neonatal respiratory failure. To determine the incidence of ECMO-related hypertension, we reviewed blood pressure measurements from indwelling aortic catheters in 31 infants consecutively placed on ECMO. Systemic hypertension (systolic blood pressures greater than 100 mm Hg for 4 or more consecutive hours) developed in 18 of the 31. Causes investigated included the roles of renin secretion, sodium, and colloid loads. There was no evidence of increased plasma renin activities in hypertensive infants (H), when compared with their own pre-ECMO controls or with the nonhypertensive infants (NH). Sodium and colloid loads and their rates of delivery were not different between H and NH. No consistent duration of ECMO was clearly associated with development of hypertension (mean time on ECMO at onset of hypertension, 43.8 +/- 38.5 hours; range, 1 to 142 hours). Demographic information was not statistically significant. Contrary to previous reports, H did not seem predisposed to an increased incidence of intracranial hemorrhage. Development of hypertension during ECMO is not related to increased plasma renin activity, sodium or colloid loads, or their rates of infusion.