Literature DB >> 3707430

Influence of arterial damage and wall shear rate on platelet deposition. Ex vivo study in a swine model.

L Badimon, J J Badimon, A Galvez, J H Chesebro, V Fuster.   

Abstract

To study the influence of blood flow on platelet interaction with selected biological surfaces, we have developed an ex vivo perfusion chamber system. In the present experiments, deendothelialized pig aorta and collagen Type I bundles from Achilles tendon were exposed to either native or heparinized pig blood for periods of time ranging from 1 to 30 minutes, and for flow rates corresponding to wall shear rates of 106 to 3380 sec-1. On the deendothelialized vessel wall, platelet deposition increased with both exposure time and wall shear rate, reaching a maximum value between 5 and 10 minutes of perfusion. At high shear rates and long exposure time (over 10 minutes), platelet deposition decreased from maximum values, indicating that some platelets were embolized by the flow. Ultrastructure analysis of the specimens showed platelet activation, spreading, and degranulation. Collagen induced a progressive accumulation of platelets following a power type curve of aggregate growth with exposure time without reaching a saturation level, even after long perfusion times (30 minutes) and high wall shear rates (3380 sec-1). In conclusion, the reactivity of the exposed materials and the local shear rate, defined by the blood flow and the patent luminal cross section, regulate platelet deposition to injured vascular wall.

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Year:  1986        PMID: 3707430     DOI: 10.1161/01.atv.6.3.312

Source DB:  PubMed          Journal:  Arteriosclerosis        ISSN: 0276-5047


  20 in total

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Review 5.  Vessel wall-related risk factors in acute vascular events.

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8.  Decreased platelet function in aortic valve stenosis: high shear platelet activation then inactivation.

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9.  Amyloid, thrombosis, and acute myocardial infarction in association with a bicuspid aortic valve.

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10.  Pharmacological prevention of peri-, and post-procedural myocardial injury in percutaneous coronary intervention.

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