Low dose ASA (4 mg/kg) peroperatively does not prevent in vivo platelet accumulation at microarterial anastomotic sites. An experimental study in the rabbit.

Twenty microarterial end-to-end anastomoses were performed on the central arteries of the ears in 12 rabbits divided into two groups: Group A (10 anastomoses) served as control and Group B (10 anastomoses) was treated with 4 mg ASA per kg b.w. given as a single intraaortical dose 5 min prior to infusion of 32P-labelled platelets. Two hours later blood-flow was reestablished after end-to-end anastomoses. Anastomotic bleeding-times, qualitative and quantitative differences in platelet accumulation and patency were registered. In addition, platelet aggregability and thromboxane production were studied in 3 rabbits. The bleeding-times (median and quartiles) in group A were 3(+0)-2 min and in group B 3(+2)-0 min. In vivo accumulation of 32P-labelled platelets was somewhat increased initially (p less than 0.05) in the ASA group. Poor patency was registered in two vessels, one in each group, all other vessels having good patency. Aspirin peroperatively in low doses (4 mg/kg) did not markedly affect bleeding-times or patency rates in microarterial anastomoses, but platelet accumulation in vivo was initially increased. The radioactivity values decreased with time in all aspirin cases but only in 50% of the control group vessels, suggesting efficient platelet disaggregation/fibrinolysis. This might favour the view that PGI2 production in the endothelium recovers more rapidly than the pro-aggregatory mechanisms affected by ASA. ASA-treatment led to almost complete inhibition of thromboxane production for at least four hours, but, despite this, a moderate decrease in platelet aggregability occurred only when collagen was used as stimulant.