Literature DB >> 989195

Inhibition of injury induced thromboatherosclerotic lesions by anti-platelet serum in rabbits.

S Moore, R J Friedman, D P Singal, J Gauldie, M A Blajchman, R S Roberts.   

Abstract

We have previously shown that repeated or continuous intimal injury caused by an indwelling aortic catheter causes a variety of lesions in rabbits maintained on a diet unsupplemented by lipid. These include fatty streaks, lipid-free fibrous plaques and lipid-rich raised thromboatherosclerotic plaques. Whether lipid-rich raised lesions are a result of injury or co-existing thrombosis or both is not clear. The present experiment was designed to answer this question. Anti-platelet serum (APS) to washed sonicated rabbit platelets was raised in sheep. PE 60 polyethylene catheters were placed in the aortas of 35 rabbits by way of a femoral artery. The animals were randomly divided into 2 groups. The experimental group (17 rabbits) received an intravascular injection of 1.0 ml of APS followed 8 hours later by a subcutaneous injection of 0.5 ml. Thereafter, 0.5 ml APS was given subcutaneously each day for 13 additional days. The control group (18 rabbits) received no APS. Platelet counts were done prior to surgery, at 5 minutes following surgery, at 4 days, 8 days and just prior to killing. Extent of lesions was estimated by photographing the opened aortas, projecting the photographs on cardboard, cutting out the areas occupied by the different lesions and weighing the cardboard. The mean weight of raised lesions in the control group was 6 to 7 times greater than in the experimental groups. Statistical analysis of this difference based on Welsh's "t" test for unequal variances was highly significant (P less than 0.001). Platelet counts in the experimental groups varied from 0 to 20,000 at 14 days. In animals with platelet counts less than or equal to 1,000 mm3 raised lesions were completely prevented. In a second experiment the effect of APS was compared with normal sheep serum (NSS). A similarly significant inhibition of raised lesions occurred in the APS group. The extent of lesions in the NSS control was similar to that in the No-APS group of the first experiment. These findings indicate that thrombosis is more important than injury in the development of lipid-rich raised lesions.

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Year:  1976        PMID: 989195

Source DB:  PubMed          Journal:  Thromb Haemost        ISSN: 0340-6245            Impact factor:   5.249


  24 in total

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Authors:  M Richardson; M W Hatton; M R Buchanan; S Moore
Journal:  Am J Pathol       Date:  1990-12       Impact factor: 4.307

Review 2.  St Cyres lecture. Endothelium in control.

Authors:  A H Henderson
Journal:  Br Heart J       Date:  1991-03

3.  New mechanism for foam cell generation in atherosclerotic lesions.

Authors:  L K Curtiss; A S Black; Y Takagi; E F Plow
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4.  Release of platelet-derived growth factor from human platelets by arachidonic acid.

Authors:  B L Linder; A Chernoff; K L Kaplan; D S Goodman
Journal:  Proc Natl Acad Sci U S A       Date:  1979-08       Impact factor: 11.205

Review 5.  The vascular endothelium-pathobiologic significance.

Authors:  G Thorgeirsson; A L Robertson
Journal:  Am J Pathol       Date:  1978-12       Impact factor: 4.307

6.  Resistance to arteriosclerosis in pigs with von Willebrand's disease. Spontaneous and high cholesterol diet-induced arteriosclerosis.

Authors:  W Fuster; E J Bowie; J C Lewis; D N Fass; C A Owen; A L Brown
Journal:  J Clin Invest       Date:  1978-03       Impact factor: 14.808

7.  Safety and antithrombotic efficacy of moderate platelet count reduction by thrombopoietin inhibition in primates.

Authors:  Erik I Tucker; Ulla M Marzec; Michelle A Berny; Sawan Hurst; Stuart Bunting; Owen J T McCarty; András Gruber; Stephen R Hanson
Journal:  Sci Transl Med       Date:  2010-06-23       Impact factor: 17.956

8.  Homocystine-induced arteriosclerosis. The role of endothelial cell injury and platelet response in its genesis.

Authors:  L A Harker; R Ross; S J Slichter; C R Scott
Journal:  J Clin Invest       Date:  1976-09       Impact factor: 14.808

9.  Platelet activation releases megakaryocyte-synthesized apolipoprotein J, a highly abundant protein in atheromatous lesions.

Authors:  D P Witte; B J Aronow; M L Stauderman; W D Stuart; M A Clay; R A Gruppo; S H Jenkins; J A Harmony
Journal:  Am J Pathol       Date:  1993-09       Impact factor: 4.307

10.  Focal mesangial proliferative glomerulonephritis in the rat caused by Habu snake venom: the role of platelets.

Authors:  V Cattell
Journal:  Br J Exp Pathol       Date:  1979-04
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