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Featured researches published by Duncan P. Thomas.


American Heart Journal | 1968

Humoral factors in massive pulmonary embolism: An experimental study

Victor Gurewich; Marsha L. Cohen; Duncan P. Thomas

Abstract Alterations in central venous pressure (CVP) were measured in response to embolization with standardized autologous venous thrombi. Platelets were counted before and after embolization and their accretion on the embolus was determined microscopically at autopsy. The rise in CVP could be blocked by heparin but only at sufficient doses to prevent the platelet accretion, or by aging the thrombus prior to embolization. conversely, the postembolic rise in CVP and mortality rates were augmented by an inhibitor of monoamine oxidase whose effect in turn was nullified by a serotonin antagonist. It is concluded that the release of biogenic amines from platelets, triggered by thrombin on the embolus, plays a significant role in the animals response to thromboemboli. Both in vivo and in vitro evidence is presented demonstrating that the dose requirements of heparin necessary to inhibit these events is greater than that generally used in treating pulmonary embolism. Certain clinical observations relating to these experimental findings are reviewed and the therapeutic implications discussed.


Circulation | 1963

Bronchoconstriction in the Presence of Pulmonary Embolism

Victor Gurewich; Duncan P. Thomas; Myron Stein; Stanford Wessler

In a group of seven patients with pulmonary embolism, evidence of bronchoconstriction was found. Heparin appeared to relieve partially the observed airway obstruction. A possible common mechanism for the initiation of intravascular coagulation and the production of bronchoconstriction was considered. When other causes can be eliminated, the detection of bronchoconstriction may serve as a useful index for the early recognition of pulmonary emboli.


The New England Journal of Medicine | 1966

Pulmonary Embolism after Ligation of the Inferior Vena Cava

Victor Gurewich; Duncan P. Thomas; Keith R. Rabinov

THE rationale for venous ligation in pulmonary embolic disease is based on its assumed ability to prevent subsequent emboli from reaching the lungs. The level of the inferior vena cava is now gener...


The New England Journal of Medicine | 1966

Platelet Adherence to Thromboemboli in Relation to the Pathogenesis and Treatment of Pulmonary Embolism

Duncan P. Thomas; Victor Gurewich; Thomas P. Ashford

THE mechanisms by which pulmonary thromboemboli produce pulmonary hypertension, increased airway resistance, pulmonary edema and even sudden death have not been satisfactorily explained solely by m...


Experimental Biology and Medicine | 1966

Activation of Intravascular Coagulation by Collagen.

Stefan Niewiarowski; R. Kenneth Stuart; Duncan P. Thomas

Summary The activation of Factor XII (Hageman Factor) by bovine collagen has been studied in vitro and in vivo. Alkaline eluates obtained from collagen exposed to human and rabbit plasma contained Factors XII and XI, and were found to shorten markedly the whole blood clotting time of rabbits in vivo and in vitro. Formation of stasis thrombi could also be demonstrated in rabbits following injection of collagen eluates. The possible significance of collagen-induced Factor XII activation in the mechanism of hemostasis and thrombosis is discussed.


Circulation Research | 1964

Stasis Thrombi Induced by Bacterial Endotoxin

Duncan P. Thomas; Stanford Wessler

1. In normal rabbits, single intravenous doses of E. coli and Salmonella endotoxin produce an immediate, transient, hypercoagulable state. Venous stasis occurring during such a state allows the formation of massive red thrombi at sites of obstructed blood flow. The duration of stasis required to produce thrombi following endotoxin administration depends in part on the preinfusion silicone clotting time of the rabbit. 2. E. coli endotoxin shortens the recalcification time of platelet-poor plasma obtained from normal subjects and from patients with heredofamilial coagulation defects of Factor XII (Hageman) and Factor IX (plasma thromboplastin component). In contrast, the recalcification time of platelet-poor plasma obtained from patients with Factor XI (plasma thromboplastin antecedent) deficiency is lengthened by endotoxin. It is suggested that the heat-labile plasma factor known to be required for the platelet-endotoxin interaction may be related to Factor XI.


The New England Journal of Medicine | 1969

Experiment versus Authority

Duncan P. Thomas

IT is generally agreed today that the advent of the controlled clinical trial has been one of the most notable advances in modern medical practice. The type of trial that has evolved over the past ...


The New England Journal of Medicine | 1947

Venous Thrombosis and Pulmonary Embolism

Michael Hume; Simon Sevitt; Duncan P. Thomas


Nature | 1969

Platelet Factor 4 and Adenosine Diphosphate Release during Human Platelet Aggregation

Stefan Niewiarowski; Duncan P. Thomas


The New England Journal of Medicine | 1967

Platelet Aggregation in Patients with Laennec's Cirrhosis of the Liver

Duncan P. Thomas; V.Jane Ream; R. Kenneth Stuart

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Victor Gurewich

Beth Israel Deaconess Medical Center

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V.Jane Ream

Lemuel Shattuck Hospital

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Arthur A. Sasahara

Brigham and Women's Hospital

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Henry N. Wagner

Penn State Cancer Institute

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