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Biomedical subjects

V H Donaldson

Publications and source records attributed to V H Donaldson.

At least 55 records · Page 3Linked to original sources
PubMed1982

Some molecular and functional changes in high molecular weight kininogen induced by plasmin and trypsin.

When purified human HMW-kininogen was digested by plasmin, its specific antigenic properties were initially enhanced and then gradually destroyed, but its clot-promoting activity (Fitzgerald factor activity) was only slightly decreased. When endogenous serum plasminogen was activated by streptokinase, similar alterations in specific HMW-kininogen antigens and Fitzgerald factor activity occurred. In contrast, trypsin induced increased antigenic properties initially, but readily destroyed the Fitzgerald factor activity and less readily destroyed the specific HMW-kininogen antigenic properties in purified HMW-kininogen and in normal human serum. When normal serum was treated with streptokinase, the antigenic properties shared by HMW and LMW-kininogens were in Sephadex G-200 fractions of lower molecular weight than in the case of untreated serum, but the elution volumes of specific HMW-kininogen antigens and Fitzgerald factor activity were not significantly altered. When prekallikrein-deficient serum was subjected to the same G-200 gel filtration process, there was a broad overlap in the elution volumes of antigens shared by both HMW and LMW-kininogens with specific HMW-kininogen antigenic and coagulant properties, which remained after streptokinase treatment of the serum. Depsite the disparate rates of destruction of the antigenic and clot-promoting portion of HMW-kininogen by proteases these properties did not separate from one another during ion exchange chromatography.

Blood Coagulation Factors↗
PubMed1981

Reduced titers of Hageman factor (factor XII) in Orientals.

Hageman factor (factor XII) is a procoagulant upon which the surface-mediated generation of fibrinolytic activity and kinin formation depends. We found that the clotpromoting activity and antigenic properties of Hageman factor were present in lower levels in the plasma of a small group of Oriental subjects than in that of American whites, whereas the levels of plasma prekallikrein (Fletcher factor), high-molecular-weight kininogen (Fitzgerald factor), and plasma thromboplastin antecedent (factor XI) in plasma samples from Oriental subjects did not significantly differ from those from normal white subjects. In one family, there was an excess of plasma Hageman factor antigens with respect to functional activity. These findings stress the importance of defining the racial characteristics of subjects used to establish standards for clotting assays.

Adult↗
PubMed1980

Rapid fibrinolysis, augmented Hageman factor (factor XII) titers, and decreased C1 esterase inhibitor titers in women taking oral contraceptives.

The use of OCAs has been associated with multiple hemostatic abnormalities and an increased risk of thromboembolic disease. These changes have been attributed to increased synthesis of various clotting factors and decreased titers of antithrombin III. Paradoxically, enhanced in vitro fibrinolytic activity is also found in plasmas of women using OCAs. The present study demonstrates marked elevation of both procoagulant and antigenic HF titers in plasmas of women using OCAs, accompanied by a simultaneous decrease in plasma C-1-INH concentration. Titers of plasma prekallikrein, HMW kininogen, PTA, and alpha 2-Pl were unchanged. The rate of kaolin-assisted fibrinolysis was related directly to the titer of HF and inversely to C-1-INH concentration. Further, the addition of human HF to normal plasma enhanced fibrinolytic activity to a degree similar to that observed in plasmas of women taking OCAs. These data suggest that the increase in plasma HF concentration may participate in the phenomenon of enhanced in vitro fibrinolysis associated with OCA use, possibly augmented by diminished inhibitory control by C-1-INH. The relationship of these phenomena to the increased incidence of thrombosis is not known.

Adult↗
PubMed1978

Remissions induced in hereditary angioneurotic edema with an attenuated androgen (danazol): correlation between concentrations of C1-inhibitor and the forth and second components of complement.

Serum concentrations of antigenic and functional C1-INH increased in patients in whom remissions from attacks of HANE were induced with danazol. The levels of C4 were directly related to serum concentrations of C1-INH antigens up to a concentration of about half the C1-INH found in normal plasma; at this point, the C4 concentrations were in the normal range and no longer correlated well with C1-INH concentration. Serum C2 levels correlated less well with C1-INH concentration. In normal serum there was a poor correlation between C1-INH, C4, and C2 levels, suggesting that C1-INH is normally present in excess of the amount needed for normal C4 levels. The increments in serum C1-INH were related to the dose of danazol.

Angioedema↗
PubMed1977

Prekallikrein deficiency in a kindred with kininogen deficiency and Fitzgerald trait clotting defect. Evidence that high molecular weight kininogen and prekallikrein exist as a complex in normal human plasma.

Plasma from an individual with a hereditary deficiency of kininogens is deficient in kininogen antigens; heterozygous relatives are partially deficient in plasma kininogen antigens. In addition, plasma from the proband is partially deficient in functional and antigenic properties of a plasma prekallikrein, and the relatives heterozygous for kininogen deficiency are also partially deficient in the plasma prekallikrein. It is possible that the defects are both inherited and that the inheritance of a deficiency of prekallikrein is genetically linked to the inheritance of a deficiency of kininogen. Alternatively, it is possible that the deficiency of prekallikrein may be due to its hypercatabolism which could be a consequence of a deficiency of high molecular weight kininogen that may stabilize the prekallikrein in plasma. Evidence to support this possibility is presented by the fact that prekallikrein and high molecular weight kininogen apparently exist as a complex in normal plasma, because monospecific antiserum to kininogen removed both high molecular weight kininogen and prekallikrein from plasma, and vice versa. Moreover, prekallikrein was not adsorbed from kininogen-deficient plasma by antiserum to kininogen unless high molecular weight kininogen was first added to the plasma. Low molecular weight kininogen did not participate in these reactions.

Blood Coagulation↗
PubMed1976

Kininogen deficiency in Fitzgerald trait: role of high molecular weight kininogen in clotting and fibrinolysis.

Plasma from an asymptomatic person with defects in blood coagulation, release of kinin, and evolution of fibrinolytic activity upon contact with a foreign surface was deficient in kininogen. The coagulation defect was identified as "Fitzgerald trait." A preparation of high molecular weight kininogen repaired the defects in clotting, kinin release and fibrinolysis, but a preparation of low molecular weight kininogen did not. Therefore, Fitzgerald factor appears to be a high molecular weight kininogen. The site of action of the kininogen appears to be after that of activated Hageman factor and kallikrein in the generation of clot-promoting activity through activation of plasma thromboplastin antecedent (PTA).

Adult↗