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Biomedical subjects

R A Vaillancourt

Publications and source records attributed to R A Vaillancourt.

5 recordsLinked to original sources
PubMed1978

The pathogenetic significance of intravascular coagulation in experimental acute renal failure.

Serum and urine fibrin(ogen) degradation products (FDP), FDP clearances, and serum urea nitrogen (SUN) concentrations of rats challenged with glycerol-induced myohemoglobinuria were measured serially over a period of 4 days. The results obtained in animals that developed acute renal failure (ARF) were compared with those obtained in rats made refractory to renal failure by long-term salt loading or recent recovery from prior renal failure. Only the rats susceptible to ARF experienced a major rise in serum FDP concentration. Urine FDP excretion rose most markedly in the same rats but, being elevated in all groups. showed the utilization of fibrinogen whether serum FDP values increased or not. The results obtained might reflect differences in the degree of intravascular coagulation which are pathogenetically important. It is possible, however, that increased serum FDP concentrations found exclusively in rats with ARF are the results rather than the cause of impaired filtration, and that reduced tubular absorption may at least partly account for the high urinary FDP excretion observed in this model of experimental acute renal failure.

Acute Kidney Injury↗
PubMed1978

Activation of the kallikrein system in hyperbetalipoproteinemia.

In 30 patients with hyperlipoproteinemia (19 type II and 11 type IV), the role of the intrinsic coagulation pathway was evaluated by assays of preK, Kl's, and Hageman factor (factor XII). Analysis of the plasma of type II patients suggested activation of the intrinsic pathway characterized by a 40% decrease in preK (p less than 0.01) and a 50% decrease Kl (p less than 0.01); in contrast, analysis of the plasma of type IV patients showed no activation of the intrinsic pathway. In type II patients C-1INH was present in normal concentrations as measured by immunochemical techniques. The findings of normal levels of C-1INH by immunoassay, in association with altered electrophoretic mobility, are suggestive of formation of a kallikrein-C-1INH complex in vivo.

Blood Coagulation↗
PubMed1977

Coagulation abnormalities in women taking oral contraceptives.

Thirteen asymptomatic women taking oral contraceptives (OCs) were compared with normal subjects. Platelet aggregation and serotonin (tagged with carbon 14) release with adenosine diphosphate, epinephrine, and collagen did not differ from controls. Activation of the intrinsic coagulation pathway was evaluated by measurements of factor XII, prekallikrein, and kallikrein inhibitors. Women taking OCs had normal factor XII levels, moderately elevated prekallikrein levels, and decreased kallikrein inhibitor levels, a pattern not consistent with activation of the intrinsic pathway. The concentration of heavy molecular weight fibrinogen derivatives (HMWFD) was significantly elevated (P less than .001). In contrast, fibrin and fibrinogen degradation products in serum were lower than normal (P less than .05). The increased HMWFD concentration may reflect activation of the coagulation system not mediated by factor XII activation nor potentiated by decreased antithrombin III. Thus, plasma coagulation abnormalities rather than platelet changes may be the factor that predisposes women taking OCs to thromboembolic disorders.

Adult↗
PubMed1977

Effect of clofibrate on intravascular coagulation in hyperlipoproteinemia.

Intravascular coagulation (IVC) was evaluated in 19 patients with type II and 11 with type IV hyperlipoproteinemia before and after clofibrate therapy by measurements of soluble fibrin complexes (SFC) in plasma; fibrinolysis was estimated by quantitation of fibrin (ogen) degradation products in serum. Untreated type II and type IV patients had increased SFC (P less than 0.01). The former also had activation of the intrinsic coagulation pathway as evidenced by decreased plasma prekallikrein (P less than 0.001), kallikrein inhibitors (P less than 0.001), and factor XII (P less than 0.02). Although clofibrate treatment of the type II patients did not change plasma lipids, it decreased intravascular coagulation, apparently via decreased factor XII activation and stimulation of fibrinolysis. In contrast, treated type IV patients had unchanged SFC and FDP levels, despite decreased plasma triglycerides (P less than 0.01). Clofibrate-induced changes in blood coagulation are independent of lipid-lowering. Clofibrate therapy decreases intravascular coagulation in type II patients and may help to prevent thromboembolic sequelae.

Antithrombins↗