Biomedical subjects

D C Stump

Publications and source records attributed to D C Stump.

58 records · Page 4Linked to original sources

PubMedDate not supplied

Effects of hydroxyethyl starch on fibrinogen, fibrin clot formation, and fibrinolysis.

The effects of hydroxyethyl starch on the final stages of hemostasis were investigated in vivo and in vitro. When compared to control solutions of either 5 percent albumin or isotonic (0.9%) NaCl, 6 percent hydroxyethyl starch (HES) exerted several effects. Results of in vivo studies were as follows: following infusion of 1 liter of 6 percent HES into healthy subjects, fibrinogen and antithrombin-III concentrations fell slightly due to plasma volume expansion and consequent dilution. Concentrations of fibrin monomer and fibrin-fibrinogen degradation products remained unchanged. Thrombin and reptilase clotting times were shortened to indicate rapid detection (and presumably accelerated formation) of fibrin clots. Urokinase-activated clot lysis times were shortened to suggest rapid fibrinolysis. Results of in vitro studies were similar. Shortened thrombin, reptilase, and urokinase-activated clot lysis times were reproduced in vitro by mixing HES, but not albumin or NaCl, with normal plasma. Although these findings qualitatively are similar to those reported previously for dextran, the molecular mechanisms involved and the clinical importance, if any, of the hemostatic effects remain to be defined. Thus, it would be premature to conclude either that HES or dextran exert identical biological effects on hemostasis or that the two agents possess similar clinical properties. HES has an excellent safety record when it has been used during leukocytapheresis and for plasma volume expansion in recommended doses. Its effects when given in larger doses remain to be defined.

Antithrombin III↗

PubMedDate not supplied

Hydroxyethyl starch accentuates von Willebrand's disease.

A healthy man with previously undiagnosed, mild von Willebrand's disease received one 1 of 6 percent hydroxyethyl starch solution intravenously. Following infusion, the bleeding time lengthened, platelet adhesion decreased, and the partial thromboplastin time was prolonged in association with decreased plasma levels of factor VIII coagulant activity, factor VIII-related antigen, and factor VIII ristocetin cofactor. Abnormalities persisted for days, but overt bleeding did not occur. Care should be taken to screen and possibly reject prospective granulocyte donors with positive personal or family bleeding histories. Caution should be used when administering hydroxyethyl starch as a colloidal plasma volume expanding agent to patients with underlying hemostatic defects.

Adult↗

PubMedDate not supplied

Effects of hydroxyethyl starch on blood coagulation, particularly factor VIII.

The effects of hydroxyethyl starch (HES) on hemostasis were investigated extensively. In order to simulate acute blood loss due to surgery or trauma, one unit (450 ml) of blood was drawn from normal healthy men. This was followed by a 1-liter infusion over 60 minutes of either 6 percent HES, 5 percent albumin, or 0.9 percent sodium chloride (NaCl) as replacement. Coagulation studies were performed before phlebotomy, before infusion and at 0, 4, 20, 27, and 92 hours following infusion. Following infusion of HES and albumin, plasma fibrinogen and antithrombin-III levels fell slightly due to plasma volume expansion and hemodilution. In subjects receiving HES, partial thromboplastin times (PTTs) were significantly (p less than .05) prolonged and factor VIII activities were significantly (p less than .05) decreased when compared to the albumin and NaCl groups. These findings could not be attributed solely to hemodilution. The effects of HES on PTT and factor VIII could not be correlated with plasma HES levels; neither could they be reproduced in vitro by mixing HES with normal plasma. Mean values of the following studies remained normal after infusion of all replacement fluids: prothrombin time, bleeding time, fibrin monomer, fibrin-fibrinogen degradation products, platelet adhesion, circulating platelet aggregates, and platelet count.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMedDate not supplied

Fibrinogen-fibrin transformation in situ in renal cell carcinoma.

The mechanism of coagulation activation in renal cell carcinoma was investigated using immunohistochemical techniques applied to fresh frozen sections of resected primary tumors. Tissue factor antigen was detected in the endothelium of vascular channels within the tumors. Fibrinogen and factor V were distributed diffusely in the perivascular tumor connective tissue. Fibrin was readily detected in a linear pattern along the edges of nodules of viable tumor indicating that thrombin had formed from the interaction of coagulation factors demonstrated previously in renal cell carcinoma tissue. Tissue plasminogen activator was detected in the endothelium of blood vessels in the vicinity of the tumor and urokinase in areas of necrosis but neither were associated with viable tumor cells. These results indicate that thrombin is formed locally in renal cell carcinoma tissue that transforms fibrinogen to fibrin. There also appears to be a net deficit in fibrinolysis in situ in this tumor. We postulate that these conditions might contribute to stabilization and progression of renal cell carcinoma and that clinical trials of antithrombotic agents are justified in this tumor type.

Antibodies↗