Effect of Oral Aspirin Dose on Platelet Aggregation and Vascular Prostacyclin (PGI2) Synthesis in Humans and Rabbits

Differential effects of two doses of aspirin on platelet-vessel wall interaction in vivo

“…The different effect exerted by these two doses of ASA is likely related to an alteration of PGI12TXA2 balance. The high dose (150 mg/kg) used in the present study has previously been shown to inhibit PGI2 and TXA2 production in rabbits (5,12). The infusion of exogenous PGI2 into the rabbits treated with 150 mg/kg ASA is consistent with the hypothesis that suppression of local PGI2 production at the damaged vessel wall contributes to massive platelet aggregate accumulation.…”

“…Previous studies in several laboratories have shown that ASA at 10-30 mg/kg selectively inhibits platelet TXA2, while at 150-200 mg/kg it blocks both TXA2 and PGI2-like activities (5,12). To check whether absorption of ASA had occurred, the blood salicylate level (13) was measured 3 h after aspirin administration in two rabbits ofeach group; the mean values were 21 mg/dl, 4.3 mg/dl, and 0 for the 150-mg group, the 30-mg group and the vehicle group, respectively.…”

Acute arterial thrombosis in rabbits: reduced platelet accumulation after treatment with dazoxiben hydrochloride (UK 37,248‐01).

“…Alternatively, vascular cyclooxygenase, not investigated in the present study, may be more resistant to aspirin since PGI2 synthesis still occurred in aortic rings in vitro from rabbits which had received aspirin 30mg/kg orally (Ellis et al, 1980). Higher doses, however, inhibited both platelet and vascular cyclo-oxygenase.…”

Effects of aspirin and prostacyclin on arrhythmias resulting from coronary artery ligation and on infarct size

“…Our aspirin treatment schedules may have abolished all prostaglandin production (1 h pretreatment) or favoured formation of prostacyclin (36 h treatment) (Livio et al, 1978;Korbut & Moncada, 1979;Masotti et al, 1979;Ellis et al, 1980), but regardless of whether such differences in prostaglandin production occurred, treatments had no major effect on responses to ligation of a coronary artery. Arrhythmias were reduced (in accord with other workers findings), but not to a statistically significant degree, with both aspirin treatments, 'S-T' segment changes were also reduced after aspirin although there were no changes in either occluded or infarct zone sizes.…”

“…Aspirin regimens have previously been used to manipulate endogenous prostacyclin levels preferentially (Livio, Villa & de Gaetano, 1978;Korbut & Moncada, 1979; Masotti, Poggesi, Galanti, Abbate & Neri Sereni, 1979;Ellis, Wright, Jones, Richardson & Ellis, 1980) and aspirin has also been shown to be antiarrhythmic in the rat (Coker & Parratt, 1981a; Lepran, Koltai & Szekeres, 1981). However, the salicylate ion alone is also antiarrhythmic in the dog (Regan, Moore, Bakth, Moschos & Oldewurtal, 1980).…”