ABSTRACT
INTRODUCTION: Hypertension is the most common medical problem encountered during pregnancy. Pregnancy Induced Hypertension (PIH) is also called a disease of maternal endothelium. Nitric-oxide being a potent vasodilator released by endothelial cells, its role has been implicated in PIH. AIM: To study the role of reactive nitrogen species in PIH. MATERIALS AND METHODS: One hundred and twenty samples were selected for the study. Of these, 60 patients had PIH (case) and the rest without PIH (control). Estimation of serum nitric- oxide, serum nitrothiol, serum total thiol was done. RESULTS: The study showed decreased NOx (Mono nitrogen oxide No and No2) levels in PIH as compared to control (p< 0.001). PIH patients had significantly higher levels of S-nitrothiols than control (p<0.01). Thiol levels were decreased in PIH as compared to control (p<0.001). CONCLUSION: Thus, it is concluded from this study that nitrosative stress represents a point of convergence for several contributing factors potentially leading to the clinical manifestations of pregnancy induced hypertension. The antioxidants are used up while scavenging the free radicals.
ABSTRACT
Sickle cell anaemia (SCA) is characterized with sever anaemia and vasoocclussive episodes. Nitric Oxide (NO) a potential vasodilator, synthesized from various cells including endothelial cell. However SCA is associated with endothelial dysfunction, a measure cognitive factor for pulmonary hypertension (PH) and vasoocclussive crisis. The present study was attempted to evaluate level of serum NO and plasma antioxidant vitamins A, E and C in homozygous (n = 30) and heterozygous (n = 30) sickle cell patients and compared with age and sex matched healthy controls (n = 30). We found, significantly (P < 0.0001) elevated level of serum NO and significantly (P < 0.0001) depleted antioxidant vitamins in homozygous and heterozygous sickle cell patients compared to healthy controls. Our study reveals that oxidative stress may be a responsible factor for the reduced bioavailability of NO which can impair the vasodilation in sickle cell patients.
