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Biomedical subjects

R E Bettigole

Publications and source records attributed to R E Bettigole.

At least 19 recordsLinked to original sources
PubMed1987

Platelet-collagen adhesion enhances platelet aggregation induced by binding of VWF to platelets.

Ristocetin-induced platelet aggregation (RIPA) was evaluated in the presence of platelet-collagen adhesion. RIPA of normal donor platelet-rich plasma (PRP) demonstrated a primary wave of aggregation mediated by the binding of von Willebrand factor (VWF) to platelets and a secondary aggregation wave, due to a platelet-release reaction, initiated by VWF-platelet binding and inhibitable by acetylsalicylic acid (ASA). An enhanced RIPA was observed in PRP samples to which collagen had been previously added. These subthreshold concentrations of collagen, which by themselves were insufficient to induce aggregation, caused measurable platelet-collagen adhesion. Subthreshold collagen did not cause microplatelet aggregation, platelet release of [3H]serotonin, or alter the dose-responsive binding of 125I-labeled VWF to platelets, which occurred with increasing ristocetin concentrations. However, ASA inhibition of the platelet release reaction prevented collagen-enhanced RIPA. These results demonstrate that platelet-collagen adhesion altered the platelet-release reaction induced by the binding of VWF to platelets causing a platelet-release reaction at a level of VWF-platelet binding not normally initiating a secondary aggregation. These findings suggest that platelet-collagen adhesion enhances platelet function mediated by VWF.

Blood Platelets↗
PubMed1986

Platelet-collagen interaction: inhibition by ristocetin and enhancement by von Willebrand factor-platelet binding.

The contribution of von Willebrand factor (vWF)-platelet binding to platelet-collagen interaction was examined in vitro. The binding of vWF to platelets was mediated and regulated by ristocetin. Subthreshold concentrations of ristocetin (less than or equal to 1 mg/mL), insufficient to cause ristocetin-induced platelet aggregation (RIPA), were added to platelet-rich plasma (PRP) prior to the addition of collagen. The collagen-induced platelet aggregation (CIPA) was modified by ristocetin and the degree of alteration was dependent on the ristocetin concentration. Response as a function of ristocetin concentration was designated the Collagen-Platelet Aggregation Response (CoI-PAR). In normal PRP the CoI-PAR was a progressive inhibition followed by decreasing inhibition and then an enhanced response. The enhanced response occurred over a narrow range of ristocetin concentrations (0.8 to 1.0 mg/mL). In the absence of vWF (severe von Willebrand's disease, Type I, vWF less than 1%) the CoI-PAR was a progressive, eventually complete inhibition with no enhanced response (with ristocetin concentrations up to 3.0 mg/mL). With addition of vWF to this PRP an enhanced response was observed at a ristocetin concentration inversely proportional to the vWF level. PRP from a patient with severe Hemophilia A showed a response within the normal range. Subthreshold ristocetin did not cause plasma protein precipitation or platelet release of 3H-serotonin, nor induce micro platelet aggregate formation. Digestion of platelet membrane glycoproteins (GP(s] with chymotrypsin demonstrated that upon removal of GPI, RIPA was absent, CIPA retained and the CoI-PAR was progressive inhibition, with no enhancement. With removal of GPs I, II, and III, RIPA, CIPA, and the CoI-PAR were absent. A dose-response 125I-vWF-platelet binding occurred with increasing ristocetin concentrations which was unchanged by the addition of collagen. These results demonstrated that ristocetin-platelet association inhibited CIPA, and vWF-platelet binding enhanced platelet-collagen adhesion and platelet aggregation. The in vitro-enhanced CIPA represents a vWF-dependent aggregation of sufficient magnitude to overcome the inhibitory effect of ristocetin. These studies demonstrate an influential interaction of ristocetin, vWF, and collagen with the platelet membrane and imply an important hemostatic contribution of vWF-platelet binding in platelet-collagen interaction.

Blood Platelets↗
PubMed1981

Diagnosis of myeloproliferative disease by analysis of the platelet volume distribution.

Analysis of platelet volume distribution curves was performed on whole blood specimens from patients with myeloproliferative disease, reactive thrombocytosis, and a control group. Estimates of the mean platelet volume and megathrombocyte index were made using either the maximum height or the area under the curve. Also, a lognormal curve was fitted to the data, providing a measure of the dispersion and another estimate of the mean platelet volume. An index expression the breadth of the distribution was derived from the ratio of megathrombocyte index to estimated mean volume. The control and reactive thrombocytosis groups were indistinguishable except for mean platelet count. The mean platelet volume and megathrombocyte index did not provide a useful separation of the myeloproliferative disease group from the other, however their ratios, when considered together with the dispersion of the distribution, enabled a distinction to be made in most cases. Thus, analysis of the platelet volume distribution is useful in detecting the presence of myeloproliferative disease.

Acute Disease↗
PubMed1980

Haemoglobin E trait and probable alpha-thalassaemia in a black American family: a family study.

This is a report of haemoglobin E trait in a black American family with no known Asian ancestory. The father appears to be heterozygous for both haemoglobin E and alpha-thalassaemia. The mother is normal both clinically and haematologically. These children carry Hb E trait alone. The youngest son has a normal haemoglobin pattern and appears to have alpha-thalassaemia.

Black People↗
PubMed1979

Coronary bypass in a patient with hemophilia B, or Christmas disease. Case report.

A 40-year-old patient with moderate factor IX deficiency (Christmas disease) underwent quadruple saphenous vein coronary bypass grafts for angina and severe coronary atherosclerosis involving the left and right main, left anterior descending, and circumflex coronary arteries. Excessive bleeding was prevented by infusion of factor IX concentrates during and after the operation. The surgical procedure and total body perfusion were carried out in the same manner as in patients without a hemorrhagic disorder. The patient was discharged after 13 days of hospitalization. He is doing well at the time of this publication and has returned to work.

Adolescent↗
PubMed1978

Fibrinogen kinetics in patients with neoplastic disease.

Fibrinogen half-life was determined in 30 patients with active or inactive malignancies by monitoring survival of administered 125I-labeled autologous fibrinogen. Six patients had no evidence of active disease and served as controls having fibrinogen levels and half-lives within the normal range reported in the literature. Twenty-six studies were conducted on 24 patients with various active malignancies. Significantly shorter fibrinogen half-lives were found in patients with active malignancies. The fractional catabolic rates calculated from both the plasma data and the urinary isotope excretion were significantly increased in patients in this group. Although there is some evidence that exposure to intensive chemotherapy may further shorten fibrinogen survival, there is no significant difference between treated and untreated or responding and nonresponding groups. The major determinant of fibrinogen survival appears to be the presence of active malignant disease, in addition to the specific type of malignancy involved.

Adult↗
PubMed1977

Use of 125I-fibrinogen kinetic data to detect disseminated intravascular coagulation and deposition of fibrin in patients with metastatic cancer.

A technique using computerized data handling for following the fate of 125I-fibrinogen through various physiological compartments is presented. Its use in detecting fibrin build up in patients with metastatic tumors and cancer-caused DIC is explained. An increase in j3u (fractional catabolic rate as seen in the urine data) throughout the course of a study was found to be an important indicator of extravascular fibrin build up.

Disseminated Intravascular Coagulation↗
PubMed1975

Fibrinogen survival in cirrhosis: improvement by "low dose" heparin.

The effect of "low dose" heparin therapy on fibrinogen survival in patients with cirrhosis was studied in six patients. Survival of I-125 radiolabeled fibrinogen was measured using both autologous and homologous material. Average fibrinogen half-life before heparin therapy was 52 hours and after 3000 units of intravenous heparin every 6 hours was 101.8 hours. Median survival before heparin therapy was 56 hours and after therapy was 91 hours. In every instance fibrinogen survival was improved by heparin administration. These data indicate that "low dose" heparin improves fibrinogen survival in cirrhosis and suggest that disseminated intravascular coagulation is a primary process in the defibrination syndrome associated with cirrhosis.

Disseminated Intravascular Coagulation↗