Abstract

Damaged arterial surfaces initiate platelet accumulation which leads to thrombus formation. On artificial surfaces, albumin pretreatment inhibits platelet deposition. To investigate albumin pretreatment on damaged vessel surfaces, 16 carotid arteries were obtained from 8 anesthetized dogs (11–15 kg). Each artery was divided into 2 segments. Each segment was mounted in a perfusion system, distended to 100 mmHg, and the middle section damaged. One segment was perfused with Tyrodes solution plus bovine albumin (5 g/100 ml), while the other segment was perfused only with Tyrodes solution. After 120 mins, both segments were perfused with whole citrated blood containing Indium-111 labeled platelets. Without albumin pretreatment, the proximal section contained 11±8 (x ± SEM) percent of total blood radioactivity, while the damaged section contained 53±11 percent (p<0.01). Albumin pretreatment significantly reduced platelet deposition in the damaged section (53±11 versus 9±6 percent, p<0.01). Further, with albumin pretreatment the radioactive counts in the damaged section were not significantly different from the nondamaged proximal section (9±6 vs 8±7 percent, p>.8). Quantitative examination of the scanning electron micrographs demonstrated significantly more platelet and red blood cell coverage of the damaged segments (60±12.8 percent) than of the albumin treated segments (12.9±5 percent). In four additional experiments, we pretreated arterial segments with albumin for varying time intervals. After 15, 30 and 60 mins of albumin pretreatment, each artery was perfused with radiolabeled platelets and whole blood for 5 mins at 100 mm Hg perfusion pressure. Radioactive evidence of platelet deposition on arterial segments treated with albumin for 15, 30, and 60 minutes was also significantly less than control (p<.05). Beneficial effects of albumin were apparent up to 30 mins of blood flow at 100 mm Hg. Our results suggest that albumin may inhibit platelet and red blood cell deposition on damaged arteries. This could be an adjunct therapy for vessel preservation during artery bypass procedures.

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