Effect of intravenous nitroglycerin therapy on erythrocyte antioxidant enzymes.

Intravenous nitroglycerin (GTN) has been used as an anti-ischemic agent for the therapy of unstable and post-infarction angina. Nitric oxide (NO) and S-nitrosothiols constitute the biologically active species formed via nitroglycerin bioactivation. Increased levels of reactive oxygen species can diminish the therapeutic action of organic nitrates by scavenging donated NO and oxidizing tissue thiols important in nitrate biotransformation. Studies reported here show that the red cell activity of antioxidant enzymes, catalase and glutathione peroxidase, are significantly decreased after intravenous nitroglycerin treatment. Catalase activity (739.6 +/- 92.3 k/gHb) decreased to 440.1 +/- 111.9 and 459.8 +/- 130.7 k/gHb after 1 and 24 hr GTN infusion, respectively. Similarly, glutathione peroxidase activity (5.8 +/- 1.8 U/gHb) decreased to 3.2 +/- 1.7 and 3.8 +/- 1.1 U/g Hb after 1 and 24 hr GTN infusion, respectively. The reported decrease in antioxidant enzyme activities can lead to an oxidant milieu and contribute to the generation of nitrate tolerance.

[Peptic ulcer perforation: an analysis of risk factors]. / PEPTIK ULSER PERFORASYONU: AMELIYAT MORTALITESINE ETKI EDEN RISK FAKTORLERININ ANALIZI.

BACKGROUND: Despite decreasing incidence of peptic ulcer disease, peptic ulcer perforation remains a source of mortality. This retrospective study was performed to find riskfactors for mortality and to construct a score that predict outcome for patients with peptic ulcer perforation. METHODS: A review of94 patients operated (primer ciosure and omentoplasty) for perforated peptic ulcer in Iast ten years was undertaken to study. lndependent risk factors for mortality were found with Iinear regression analysis and risk score was constructed using standardized coefficients of risk factors. RESULTS: Acute renal failure (ARF) (p < 0,00 1 ), treatment delay more than 48 hours (> =48 hours) (p = 0,203 ) and age greater than 60 years (> 60 years) (p = 0, 199) were found signijicant factors independently injuencing mortality. The risk score was (Risk score = (ARF)XO,497 + (> =48 hours)XO,203 + (>60years)XO,199). The overall predictive accuracy of risk score was%95. CONCLUTION: Treatment delay and related acute renal failure and advanced age are determining factors for survival after ulcer perforation. Delay of treatment may be only changeable factor for mortality. lt is ciear that, the early diagnosis and treatment aredecreasing operative mortality of peptic ulcer perforation. Every effort to decrease the mortality should be this mannei: