SummaryADP-induced platelet aggregation and the breakdown of ADP in platelet-poor plasma of normal and magnesium deficient calves and rats have been studied. There was no statistically significant difference in ADP-induced platelet aggregation between the treated and untreated groups of animals. There was a significant difference in the ADP breakdown in platelet poor plasma of magnesium deficient rats as compared to the untreated animals. The platelet count of the magnesium deficient calves and in the citrated platelet-rich plasma of the magnesium deficient rats was not different from the normal. The thrombin clotting and partial thromboplastin times were significantly shortened in the magnesium deficient calves, but the prothrombin time was not affected. These findings suggest that pathological alterations in the serum magnesium levels that are still compatible with life do not influence adenosine diphosphate-induced platelet aggregation but do affect the breakdown of adenosine diphosphate in the plasma of rats. Just as magnesium administration may produce an anticoagulant effect, so may magnesium depletion produce a procoagulant effect in the blood of animals rendered magnesium deficient by diet. The clinical implications of this are discussed.

The clinical and laboratory features of a case of alphamethyldopa-induced thrombocytopenia are described. This is the second reported case in which the presence of alpha-methyldopa-induced platelet antibodies have been demonstrated.

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Intermittent pneumatic compression of the calf has proven beneficial as prophylaxis for calf vein thrombosis. To define a possible role for the fibrinolytic system, two studies were performed.Two groups of normal male volunteers aged 18-42 years were rested for one half hour; a control blood sample was drawn and one arm or both legs pumped for one half hour using a pneumatic boot inflated intermittently to 50mm Hg (90 sec. on, 90 sec. off; filling time 60 sec.). A second blood sample was obtained. In group one (arm pumped; antecubital vein sample, same side) the euglobulin lysis time decreased 23% (191 to 147 min., n=13, p=.05). In group two (both legs pumped; simultaneous sample from femoral and antecubital veins) there was a 25% reduction in euglobulin lysis (230 to 172 min., n=16, p=.01) in femoral vein blood and an 18% decrease in antecubital vein blood (229 to 188 min., n=16, p=.04). As expected the effect was most pronounced in the local venous effluent and less noticeable in the systemic circulation due to dilution.The possibility that mechanical compression of the calf veins produces chemical changes that might exert a beneficial effect in preventing venous calf thrombosis is consistent with the data.

In an attempt to determine whether compensatory changes in alpha2 macroglobulin occur in patients with thrombotic tendencies, studies were performed by the two dimensional immunoelec-trophoretic technique of Laurell on the plasmas of healthy laboratory workers and patients with possible thrombotic tendencies. A single, broad, asymmetrical peak was noted in 16 of 18 laboratory workers. A slower moving discrete second spike of lesser magnitude was found in 2 of the 18. A pattern with two peaks appeared in 11 of 14 patients on warfarin therapy for recurrent thrombophlebitis (8 of 8), for prophylaxis after artificial heart valve replacement (3 of 3), and coronary revascularization (1 of 3). Antithrombin III patterns studied according to Sas were normal in all but 2 of these patients. A volunteer ingesting warfarin was normal. A single patient with liver disease showed two peaks.Preliminary in vitro incubation of plasma with thrombin, plasmin, or streptokinase failed to create more than one peak.These preliminary data suggest changes in alpha2 macroglobulin may represent in vivo coagulation and might provide another means to identify thrombosis prone individuals.