REDUCTION OF EXPERIMENTAL MYOCARDIAL INFARCT SIZE BY INFUSION OF LACTOSYLPHENYL TROLOX

Objective: The aim was to determine if lactosylphenyl Trolox could imp rove myocardial resistance to ischaemia and reperfusion. Lactosylpheny l Trolox is derived by coupling p-aminophenyl-beta-D-lactopyranoside t o Trolox. Trolox, a polar analogue of vitamin E, has been found to pro tect human cardiomyocytes against oxyradicals and to reduce myocardial damage by 66% in a canine ischaemia-reperfusion model. Methods: New Z ealand white rabbits (weighing approximately 3.5 kg) were subjected to 1 h ischaemia by ligation of the main branch of the anterior ventricu lar coronary artery. Approximately 1-2 min before release of ischaemia , a 30 ml bolus of saline (placebo control) or saline containing lacto sylphenyl Trolox was injected into the right external jugular vein, fo llowed by 3 h reperfusion. The area at risk was identified by staining with Evans Blue. Area of necrosis was indicated by tetrazolium red st aining, confirmed by histopathology and quantified by planimetry. Resu lts: The control group (n=6) had 46.6(SD 10.0)% necrosis of the area a t risk but the lactosylphenyl Trolox treated groups (n=6 per group) ha d reduced necrosis: 24.0(6.5)%, 17.4(8.2)%, and 6.9(3.6)% at doses of 2.5, 5.0, and 10 mumol.kg-1, respectively (each with p<0.05 v control value). These translated to 48.6(14.0)%, 62.7(17.6)%, and 85.3(7.8)% m yocardial salvage, respectively. In contrast, the salvages achieved wi th 2.5 and 10 mumol.kg-1 of Trolox were 31.0(11.0)% and 62.1(18.9)% re spectively (both p<0.05 v lactosylphenyl Trolox). Conclusions: Lactosy lphenyl Trolox reduces myocardial infarct size more effectively than T rolox in a rabbit model of ischaemia-reperfusion.