Search PubMed⌕ Search

Biomedical subjects

V Gurewich

Publications and source records attributed to V Gurewich.

At least 91 records · Page 5Linked to original sources
PubMed1979

Effects of long-term treatment with suloctidil on blood viscosity, erythrocyte deformability and total fibrinogen plasma levels in diabetic patients.

1-(4-Isopropylthiophenyl)-2-n-octylaminopropanol (suloctidil, Sulocton), a drug introduced into clinical practice for the treatment of cerebral and peripheral vascular insufficiency and its complications, has been shown to decrease blood hyperviscosity after long-term treatment in diabetic patients. Suloctidil was particularly effective in lowering measured blood viscosity at high shear rate (230 s-1). At low shear rate (0.77 s-1) a decreasing effect was also observed but reached a statistically significant level only after one month. Since neither total plasma fibrinogen levels nor red blood cell deformability were modified by suloctidil treatment, its lowering effect on blood hyperviscosity could be due to a hitherto unrecognized mechansim of action.

Adult↗
PubMed1978

Side-to-side portacaval shunt versus nonsurgical treatment of Budd-Chiari syndrome.

Although a side-to-side portacaval shunt will relieve some patients with Budd-Chiari syndrome, distinction between relief as a result of operation and spontaneous recovery may be inexact. A nonshunting operation relieved one of two patients as much as a side-to-side portacaval shunt did. In these two patients and one additional patient, streptokinase therapy may have been beneficial.

Adult↗
PubMed1978

Hemostatic effects of uniform, low-dose subcutaneous heparin in surgical patients.

Two hours before surgery and every 12 hours thereafter 5,000 units of heparin sodium was administered subcutaneously to 100 general surgical patients. Hemostasis was evaluated by a template bleeding time and an activated partial thromboplastin time (PTT). The latter was sensitive to 0.05 units/ml of heparin and gave a straight-line response up to 0.2 units/ml. In the great majority of patients, only a modest elevation of the PTT occurred two and four hours after heparin therapy. However, in 10% to 15% the PTT was prolonged two times or more and in a similar number, PTT after surgery was shorter than baseline values despite heparin. No correlation between PTT prolongation and weight, ponderal index, age, or sex was found. Significant bleeding occurrred in three patients, two from the group of hyperresponders to heparin. Recent aspirin ingestion was implicated in one patient and our evidence indicates that low-dose heparin potentiates aspirin-induced prolongation of bleeding time in certain individuals. Local hematoma formation and discomfort from the injections was not a problem.

Adult↗
PubMed1977

Abnormal fibrinogen heterogeneity and fibrinolytic activity in advanced liver disease.

The present study demonstrates that the fibrinolytic activity is significantly increased and the level of plasminogen antiactivator diminished in the blood of patients with advanced liver cirrhosis and chronic aggressive hepatitis as compared with the values for healthy subjects. Total fibrinogen concentration was similar in patients and controls. However, electrophoresis of plasma with the use of SDS-polyacrylamide gel (3.5%) showed considerable differences in the composition of fibrinogen fractions. Lower molecular weight (LMW and LMW1) clottable protein was significantly (p less than 0.01) increased in the patients. In two out of 22 patients the higher molecular weight (HMW) fraction was virtually absent. In vitro incubation (37 degrees C for 48 hr) of diluted (1:10) plasma from a patient resulted in extensive degradation of a low-solubility fibrinogen fraction (HMW) previously added to the sample. No degradation was observed in any undiluted plasma samples. It is concluded that the increased concentration of lower-molecular-weight forms of clottable protein in the blood of patients with liver disease is probably related to increased in vivo degradation rather than abnormal synthesis. An association rather than a direct correlation with fibrinolytic activity was found.

Adult↗
PubMed1976

The effect of the fibrinogen concentration and the leukocyte count on intravascular fibrin deposition from soluble fibrin monomer complexes.

Fibrin formation from fibrin monomer (FM) complexes was studied in experimental animals utilizing a previously described technique for quantitating fibrin deposition. A uniform thrombin infusion was used to produce FM, fibrinolysis being inhibited by EACA. In vivo complex formation between FM and 125I-fibrinogen was demonstrated chromatographically. A direct correlation was found between blood fibrinogen concentration and fibrin deposition in organs. By contrast, an inverse correlation between fibrinogen concentration and both enzymatic or non-enzymatic fibrin formation was found in vitro. The mechanism by which fibrinogen potentiates FM precipitation in vivo could not be explained by coprecipitation of fibrinogen in the complex which could not be demonstrated. The inhibitory effect of HN2 on fibrin deposition despite the associated hyperfibrinogemia induced by this drug is believed to underscore the importance of leukocytes in certain types of fibrin deposition. A correlation between the leukocyte count and fibrin formation from FM was also found. It was concluded that the risk of intravascular fibrin deposition is increased by a raised fibrinogen level especially when accompanied by leukocytosis.

Animals↗
PubMed1976

Thrombin elaboration in endotoxin-induced intravascular fibrin deposition. A leukocyte dependent process distinct from systemic hypercoagulability.

Intravascular coagulation was induced by two appropriately spaced doses of endotoxin and by infusion of thromboplastin. The resulting fibrin deposition was measured by a previously described quantitative technique. Evidence of thrombin elaboration was obtained indirectly by measurement of fibrin monomer (FM) and by the detection and isolation of a thrombin-induced anticlotting activity. Venous segments were isolated at intervals and examined for thrombus formation following 40 minutes of stasis. Endotoxin triggered thrombin elaboration was not detectable in the circulation for at least one hour and was not accompanied by any thrombosis in isolated venous segments. No thrombin elaboration was found in leukopenic rabbits given endotoxin. In the thromboplastin infused animals, the quantity of fibrin deposited in the organs was comparable to that found after endotoxin. However, thrombin was found in the blood immediately and was associated with thrombosis in the isolatet venous segments. Less thrombin-induced anticoagulant activity was found after thromboplastin than after endotoxin. The findings suggest that endotoxin-induced intravascular coagulation is probably not caused by a mechanism of systemic hypercoagulability due to the release of thromboplastic material into the blood stream. A focal process of thrombin elaboration involving leukocytes is postulated. The study is believed relevant to patients with disseminated intravascular coagulation in whom venous thromboembolism is rarely found despite evidence of extensive microvascular fibrin deposition.

Animals↗
PubMed1976

Semiquantitative determination of soluble fibrin monomer complexes by chromatography and serial-dilution protamine sulfate test.

Plasmas were prepared from blood obtained from rabbits and from healthy individuals and patients with thrombotic disorders. Gel filtration (Sepharose-4B) chromatography and the serial-dilution protamine sulfate (SDPS) test were performed on each sample. For healthy individuals and rabbits, a narrow fibrinogen peak was obtained on chromatogram and was associted with a negative SDPS test. After administration of thrombin or endotoxin to rabbits and in plasmas from patients with intravascular coagulation, major shifts to earlier effluent volumes occurred. These higher-molecular-weight derivatives corresponded to soluble fibrin monomer complexes (FM). Positive SDPS tests were found in these plasmas. There was a highly significant correlation between percentage area occupied by FM on chromatogram and SDPS test titer. It is concluded that the SDPS test is a reliable semiquantitative measure of FM that can be used clinically as well as in experimental animal models.

Animals↗
PubMed1976

Fibrinogen heterogeneity in cancer, in occlusive vascular disease, and after surgical procedures.

Electrophoresis in 3.5% polyacrylamide gel was used to determine the patterns of fibrinogen heterogeneity in healthy subjects, in postoperative patients and in patients with cancer or occlusive vascular disease. Two major and one minor fibrinogen fractions, differing in molecular weight, were identified, and their concentrations in blood determined. The high-molecular-weight (HWM) fraction was found in greatest concentration after operation, during the period of hyperfibrinogenemia, whereas no simultaneous increase of lower-molecular-weight (LMW and LMW') fractions occurred, suggesting that these were derivatives of HMW ("native") fibrinogen. No correlation between the concentrations of the LMW and LMW' fractions and fibrinolytic activity was found, suggesting that direct degradation of HMW fibrinogen by plasmin was unlikely. The high fibrinogen level in cancer patients was related to increased concentrations of HMW and LMW fractions, whereas in the vascular-disease patients it was due exclusively to increased concentrations of LMW and LMW' fibrinogen. Serial observations indicated little fluctuation in the concentration of these fractions, indicating a persistently accelerated rate of conversion of HMW to LMW and LMW' fibrinogen in occlusive vascular disease. Possible pathogenic implications are discussed.

Adult↗
PubMed1976

A study of the large heparin requirements in the generalized Shwartzman reaction.

The heparin requirements necessary to inhibit intravascular fibrin deposition and soluble fibrin monomer (FM) formation in the generalized Shwartzman reaction (GSR) were evaluated. Fibrin deposition was measured by a quantitative technique utilizing 125I-labeled rabbit fibrinogen. FM was measured semiquantitatively by gel exclusion chromatography and by the serial dilution protamine sulfate (SDPS) test. There was a fourfold increase in heparin requirement 5 min after compared with 5 min before the second dose of endotoxin. This increase in heparin requirement was not related to thrombin elaboration, since FM was not found until more than 1 hr after the second dose of endotoxin. Neither was there any evidence of diminished sensitivity to the anticoagulant effect of heparin. The heparin requirements in the GSR rabbits were found to be in excess of those needed to neutralize a defibrinating dose of thrombin. It was concluded that a potent, heparin-resistant clotting activity developed within 5 min of the second endotoxin injection. The mechanism by which the activity caused the gradual elaboration of a thrombin-like enzyme is diffucult to explain on the basis of traditional coagulation reactions. The apparent role of white cells is discussed.

Animals↗