Japanese Circulation Journal · 1999 · 33 citations · 33 references
MedicineCardiologyPharmacologyCardiovascular PharmacotherapyClinical PharmacologyInterventional CardiologyCoronary Artery DiseaseIschemic Heart DiseaseOxidative StressReactive Metabolite FormationReactive MetabolitesReactive Oxygen SpeciesArachidonic Acid MetabolitesArachidonic Acid PeroxidationFree Radical GenerationOxidative BiomarkersOxidative Stress In Cardiovascular DiseaseOxidative Stress In Ischemia-reperfusion InjuryOxidative Stress InjuryProstaglandin Production
Reactive oxygen species are thought to mediate reperfusion injury after rapid revascularization for acute myocardial infarction (AMI) and 8-epi prostaglandin (PG) F2alpha, a free-radical catalyzed product of arachidonic acid, has been proposed as an indicator of oxidative stress in vivo during myocardial reperfusion. The time course of urinary 8-epi PGF2alpha excretion after primary coronary angioplasty (PTCA) for AMI was investigated, as well as the effect of prior administration of vitamin C. Urine samples, 1 before and 5 after primary PTCA (0-30, 30-60, 60-90, 90-120 and 120-150 min), were collected in 11 patients with AMI undergoing primary PTCA (Group 1), 10 patients with AMI treated with water-soluble vitamin C at an initial dose of 2.0 g followed by a constant infusion at 20mg/min prior to primary PTCA (Group 2), and 6 patients with stable effort angina undergoing elective PTCA (Group 3). 8-epi PGF2alpha was measured by enzyme immunoassay. There were no significant differences in urinary 8-epi PGF2alpha excretion at baseline among the 3 groups. In Group 1, urinary 8-epi PGF2alpha excretion (ng/mmol creatinine) significantly increased from 60+/-8 at baseline to 122+/-16 at 60-90 min (p<0.001), and declined to the baseline level at 120-150 min after primary PTCA. In Group 2, it also increased from 72+/-12 to 123+/-15 at 60-90 min (p<0.01), and the percent increase did not differ from that in Group 1. In Group 3, it remained unchanged during the study period. The free radical production is rapidly and transiently enhanced after primary PTCA for AMI, and vitamin C fails to suppress it.
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