Delivery of passivating proteins to sutures during passage through the vessel wall reduces subsequent platelet deposition by blocking fibrinogen adsorption.

Abstract

Intraluminal vascular suture material, which attracts fewer than the expected number of platelets compared with the same biomaterial exposed to blood in vitro, differs from the untreated biomaterial in that it has been passed once through the vessel wall. The mechanism by which this apparently trivial maneuver reduces platelet deposition was investigated. Polypropylene suture (7-0 Prolene) was passed through human arteries (fetal and adult), and platelet deposition to the suture was measured in a standardized perfusion chamber. Single vessel passage of the sutures reduced platelet deposition by 68 ±23%, which contrasts sharply with the power of prostaglandin E, (1 (iM PGE, is sufficient to abolish platelet shape change and aggregation), which inhibited only 11% of platelet deposition to the sutures. Aspirin treatment of the vessel (to prevent PGI 2 formation) or endothelial stripping (to remove the ability to produce nitric oxide) had no effect on the degree of inhibition. Passage of the suture through a vessel analogue (expanded polytetrafluoroethylene) did not inhibit platelet deposition. I-fibrinogen adsorption to the suture after vessel passage was reduced to a degree similar to that of platelet deposition. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis of proteins eluted from vessel-passed sutures revealed bands at 66, 47, and 16 kd. Western blotting indicated the presence of large amounts of albumin and hemoglobin, a moderate amount of haptoglobin, and only trace amounts of fibrinogen. When sutures were exposed to each of these proteins in vitro before perfusion, albumin and hemoglobin were found to reproduce the effect of vessel passage alone on platelet deposition. We conclude that albumin and hemoglobin adsorb to sutures during their passage through the vessel subendothelium. This reduces the subsequent adsorption of fibrinogen from blood, thereby reducing the ability of platelets to attach to the suture. (Arteriosclerosis and Thrombosis 1992;12:727-735)

Estudo experimental do uso de um antagonista do receptor da glicoproteína IIb/IIIa das placentas na prevenção de tromboses em microanastomoses vasculares

“…Although some experiments suggest that the suture material or the disturbances of the flow in the anastomosed area are the main causes for the development of the thrombosis, DICKSON et al (1993) and JOHNSON et al (1992) COOLEY;HANSEN (1985) and GREENBERG et al (1988) (1992) and BRAAM (1995). KOROMPILIAS (1997) A trombose nas microanastomoses sempre se constituiu um desafio, sendo uma complicação presente mesmo quando realizada por microcirurgiões treinados e experientes.…”

“…Embora alguns experimentos sugiram que o tipo de material de sutura ou os distúrbios do fluxo na região anastomosada sejam as causas principais para o desenvolvimento da trombose, DICKSON et al (1993) e JOHNSON et al (1992) demonstram que esses dois fatores são secundários. JOHNSON; BARKER (1992) e HILL; WHITTEN (1997) consideram que as lesões do endotélio, com a exposição do subendotélio, são as responsáveis pela gênese da trombose nas anastomoses, já que a lesão do endotélio ativa a cascata da coagulação e as plaquetas.…”

“…JOHNSON; BARKER (1992) e HILL; WHITTEN (1997) consideram que as lesões do endotélio, com a exposição do subendotélio, são as responsáveis pela gênese da trombose nas anastomoses, já que a lesão do endotélio ativa a cascata da coagulação e as plaquetas.…”

“…A heparina atua potencializando a ação da antitrombina III que inativa a ação da trombina e dos fatores de coagulação XIIa, XIa, IXa e Xa. A administração da heparina pode ser pela via sistêmica, como relatam COOLEY; HANSEN (1985) e GREENBERG et al (1988, ou localmente, cuja eficácia na prevenção de trombos é aumentada quando se adiciona a heparina na solução salina e irriga-se o vaso durante o procedimento da microanastomose vascular, como demonstram ZINBERG (1989), COX (1992) e BRAAM (1995). KOROMPILIAS (1997), em um estudo com heparina de baixo peso molecular (enoxiparina), relatam que não há maiores benefícios na administração sistêmica e tópica com relação à irrigação tópica isolada.…”

“…BRAAM (1995) and COX (1992) (BATES et al, 1991). On the other hand, the experimental model for arterial lesion was so effective that, soon after the pendulum fall, and before the microanastomosis, the thrombosis occurred within 30 minutes when abciximab was not given.…”