Accelerated Thromboplastin Generation in Acute Arterial Occlusion Complicating Arteriosclerosis Obliterans

Spittell, John A.; Pascuzzi, Chris A.; Thompson, John H.; Owen, Charles A.

doi:10.7326/0003-4819-55-5-765

Cited by 10 publications

(3 citation statements)

References 12 publications

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“…Thus, Rapaport and Chapman (18) discussed cases of hypofibrinogenemia associated with hypercoagulability presumably caused by thromboplastin released from prostatic tissue. Seldom have such patients been studied by appropriate two-stage techniques, but Graham , Emerson and Anglem (6) reported that plasma obtained from a patient with postoperative hypofibrinogenemia produced a shortening of the clotting time of normal human blood, and Spittell, Pascuzzi, Thompson and Owen (25), using a modified thromboplastin generation test , observed an enhancement of coagulation in a group of patients with acute arterial occlusion. Recently, Skjodt (20) reported on a patient with premature separation of the placenta in whom there was a decrease in concentration of a number of coagulation factors, though an enhancement of coagulation could be demonstrated by the thromboplastin activation test.…”

Section: Discussionmentioning

confidence: 99%

Serum Effects Following Tissue Thromboplastin Infusion

Astrup¹,

Ok²

1969

Thromb Haemost

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SummaryTissue thromboplastin injected into the femoral vein of anesthetized rabbits produced intravascular clotting in the vessels through which the thromboplastin flowed. In the systemic arteries macroscopically visible clots were never observed. No trace of tissue thromboplastin could be demonstrated in blood drawn from the carotid artery following infusion of tissue thromboplastin into the femoral vein. The slight, transient enhancement of coagulation of the arterial blood following tissue thromboplastin infusion was caused by a serum effect. After intravenous injection of serum, enhanced activation of coagulation could be observed for a period of up to 2 hrs. It is concluded that tissue thromboplastin, intravenously injected, is removed from the blood during its passage from the femoral vein to the systemic arteries, probably in the capillaries of the lung. True hypercoagulability appears to be due to a serum effect or caused by partial activation of the intrinsic coagulation system. The levels of coagulation precursors in blood are of minor significance.

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Section: Discussionmentioning

confidence: 99%

Serum Effects Following Tissue Thromboplastin Infusion

Astrup¹,

Ok²

1969

Thromb Haemost

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“…Admittedly this concept is hypothetical. We have been struck by the fact that certain coagulation factors were elevated in disease when reduced levels might have been expected: among these, chronic ulcerative colitis [134] and arteriosclerosis obliterans [216] are examples. This was identified as representing "hypercoagulability" [174].…”

Section: Causes Of Icf Syndromesmentioning

confidence: 99%

“…"Hypercoagulability" is said to be present in some patients with peripheral vascular disease [44,216], and such patients are prone to complications postoperatively [44]. Chronic ICF is often observed with aortic aneurysms [70,202], perhaps because of clotting within the aneurysm [120].…”

Section: Cardiovascular Systemmentioning

confidence: 99%