Red Clots Research Articles

The influence of the velocity gradient on in vitro blood coagulation and artificial thrombosis

Blood coagulation was studied in a cone-in-cone viscometer. Seventeen cases were used for this investigation, covering such a variety of diseases as myocardial infarction, thrombocytopenia, thrombocythaemia, polycythaemia, multiple myeloma, anaemia, and macroglobulinaemia. Blood coagula formed in the viscometer were studied by microscopic techniques. A general pattern emerges in which an artificial white thrombus is formed at high rates of shear, while a red clot is obtained at low rates of shear. The degree of aggregation of platelets increases as the velocity gradient increases. This function is illustrated by means of an exponential equation. One of the parameters of this equation is related to the adhesiveness of the platelets and is specific to the individual samples of blood studied. The coagulation time decreases as the velocity gradient increases. In all cases the coagulation times determined by means of the viscometer are lower than the values obtained by means of Lee-White test. It is suggested that this new method may be more relevant to the physiological conditions than some currently employed methods of investigation of blood coagulation and thrombosis.

Pulmonary arteriosclerosis due to serotonin.

HITHERTO, experimental pulmonary arteriosclerosis has been induced in rabbits by the intravenous injection of fragmented blood clots prepared from their own blood or from that of another animal; either red blood clots or fibrin clots can be used1–3. Arteriosclerosis can also be produced by repeated injections of oxygen, nitrogen, argon or air4,5. We report here the production of pulmonary arteriosclerosis by serotonin.

PLATELET THROMBOSIS IN HUMAN HEMOSTASIS A HISTOLOGIC STUDY OF SKIN WOUNDS IN NORMAL AND PURPURIC INDIVIDUALS

Abstract The histologic appearance of human skin puncture wounds obtained at biopsy, after measurement of the local bleeding times, has been studied in serial section in 3 patients with normal hemostasis and in 4 patients with idiopathic thrombocytopenic purpura. It is found that agglutinated platelets arrest hemorrhage in normal skin by rapidly sealing the mouths of all cut vessels larger than capillaries. Such platelet thrombi can resist the effective blood pressure in a cut arteriole of 55 micra. The puncture tract is normally filled with red cell-fibrin clot into which the platelet thrombi protrude. The red clot seals the mouth of the few opened capillaries which can be identified. Other capillaries may be sealed by endothelial agglutination. Fibrin does not enter or form within the injured vessels. Platelet thrombosis does not occur in idiopathic thrombocytopenic purpura. When larger arterioles and venules are cut the bleeding time is greatly prolonged and fibrin fails to form within the wound because of the speed of blood flow. When smaller vessels are cut in purpura the bleeding time is moderately prolonged, but the cut vessels are eventually sealed by fibrin alone. In thrombocytopenic purpura the bleeding time is normal if only capillaries are cut, since these are normally sealed by fibrin. The similarity of the histologic appearance of human puncture wounds to that described after experimental vascular injury in other mammals, suggests considerable similarity in mammalian hemostatic mechanisms. Clinical bleeding time tests vary greatly in depth of puncture and in the caliber and number of the vessels cut. Sufficient volume of hemorrhage during the first minute is thought to be the best guide to an adequate test of the entire hemostatic mechanism.

A Case of Pedunculated Papilloma of the Stomach

Three years ago, a male patient suddenly vomited more than a pint of clear fluid mixed with dark red blood. He was admitted to the Alloa Hospital and the vomiting stopped on the day of admission. At the same time bleeding piles, which had been troubling him at times for several years, began to bleed more severely whenever his bowels moved. He passed bright red blood and darker clots. He was in hospital for a week. On discharge he was very weak, and rested at home for a month. There was no further vomiting, but the piles continued to bleed. Weakness continued after he returned to work. He was eating well but losing weight. As he was not improving, he was admitted to the Royal Infirmary, Edinburgh and was treated with liver for six weeks.

STUDIES IN EXPERIMENTAL EXTRACORPOREAL THROMBOSIS

The effects of environmental temperature on thrombosis in circulating blood were tested in the extracorporeal loop by the method previously described. Cold (7 degrees to 15 degrees C.) about the collodion tube retards the clotting of circulating blood. Obstruction of the arterial cannula occurs after from 15 to 25 minutes. Heat (40 degrees and 55 degrees C.) tends to hasten clotting; obstruction by red clot takes place after from 4 to 6 minutes and from 2 to 4 minutes, respectively. In the latter case no characteristic thrombus structure may be seen. These results were what might be expected. The formation of white thrombi occurs even under the influence of cold, and they continue to form and grow as long as the circulation continues. When the carotid artery is partially occluded and the blood stream slowed, after the injection of the anticoagulant, the blood has a tendency to form red thrombi on the foreign surface of the vascular loop. The thrombi are deposited chiefly in the arterial half of the apparatus, especially at the bottom of the arterial end of the collodion tube, just as in the case of Aschoff's sand experiments. In spite of incoagulability of heparinized blood, red clots, with interwoven fibrin bands, are found. Also very tiny white thrombi may form in other parts of the collodion tube. The effect of complete obstruction of the carotid artery and jugular vein on thrombus formation was studied after the use of anticoagulant. When the carotid artery is obstructed the formation of white thrombi is negligible and sedimentation of erythrocytes and deposition of fibrin appear throughout the apparatus; then the blood, at a standstill, clots very slowly. When the jugular vein is obstructed, dislodgment of platelet thrombi probably results from the pulsating movement, and sedimentation of erythrocytes follows, forming mixed thrombi. The dislodged white thrombi tend to gather in the bottom of the tubes of the widest caliber, especially in the collodion tube.