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Titolo:
Uptake of heparin cofactor II and antithrombin into the aorta wall after adeendothelializing injury in vivo: Comparison with the behaviors of prothrombin and fibrinogen
Autore:
Hatton, MWC; Ross, B; Southward, SMR; Dereske, M; Hoogendoorn, H; Blajchman, MA; Richardson, M;
Indirizzi:
McMasteradaiv, Hlth Sci Ctr, Dept Pathol HSC4N67, Hamilton, ON L8N 3Z5, Can McMaster Univ Hamilton ON Canada L8N 3Z5 C4N67, Hamilton, ON L8N 3Z5, Can
Titolo Testata:
JOURNAL OF LABORATORY AND CLINICAL MEDICINE
fascicolo: 1, volume: 133, anno: 1999,
pagine: 81 - 87
SICI:
0022-2143(199901)133:1<81:UOHCIA>2.0.ZU;2-E
Fonte:
ISI
Lingua:
ENG
Soggetto:
ARTERIAL SMOOTH-MUSCLE; RABBIT AORTA; TISSUE FACTOR; IN-VIVO; SULFATE PROTEOGLYCANS; THROMBIN; SURFACE; INVITRO; INVIVO; SUBENDOTHELIUM;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
29
Recensione:
Indirizzi per estratti:
Indirizzo: Hatton, MWC McMaster Univ, Hlth Sci Ctr, Dept Pathol HSC4N67, 1200 Main StW, Hamilton, McMaster Univ 1200 Main St W Hamilton ON Canada L8N 3Z5 ilton,
Citazione:
M.W.C. Hatton et al., "Uptake of heparin cofactor II and antithrombin into the aorta wall after adeendothelializing injury in vivo: Comparison with the behaviors of prothrombin and fibrinogen", J LA CL MED, 133(1), 1999, pp. 81-87

Abstract

The initiation of a denuding injury to the vascular endothelium rapidly leads to a deposition of platelets and fibrin at the site of injury. We have measured previously the responses of rabbit fibrinogen, prothrombin, and antithrombin to a deendothelializing balloon-catheter injury to the rabbit aorta in vivo. In this study, rabbit iodine 125-labeled HCII and iodine 125-labeled AT were coinjected intravenously into anesthetized rabbits 5 minutesbefore deendothelialization of the thoracic aorta. The rabbit was exsanguinated at 5 to 60 minutes after injury, the aorta was excised, and the accumulation of each radiolabeled protein in each layer of aorta wall was determined relative to the concentration of the respective native protein in circulating blood at exsanguination. The maximum flux rates into the aorta wall(ie, platelet layer and intima-media) in the first minute after injury were calculated from the uptake data; approximately 2.8 molecules of AT accumulated for each HCII molecule. By comparison with previous measurements, themaximum flux rate of AT was similar to that of prothrombin. further, the molar ratio of accumulated prothrombin/AT + HCII) in the aorta wall was 0.75. Detergent extracts of the injured aorta intima-media contained unreacted HCII and HCII complexes; the uninjured aorta contained only unreacted HCII. By contrast, high molecular weight AT complexes and unreacted AT were extracted from the uninjured, and in greater quantity from the injured, aorta wall. We conclude that, of the plasma antithrombins, AT accumulated more rapidly than HCII in vivo and appeared to be the more active inhibitor at the site of vascular injury. HCII may play a relatively minor role as an antithrombin and possibly only after injury.

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Documento generato il 02/04/20 alle ore 00:01:54