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Articles by Ayman Z. Elsamanoudy
Total Records ( 2 ) for Ayman Z. Elsamanoudy
  Amr M. Abbas , Ayman Z. Elsamanoudy and Adel Zalata
  Problem statement: We aim to evaluate the effects of acute and chronic inhibition of Neutral Endo Peptidase (NEP), by ONO-9902, on plasma and renal NEP gene expression, hemodynamic and renal parameters in rats with Chronic Heart Failure (CHF) following left Coronary Artery Ligation (CAL). Approach: Forty eight male Sprague-Dawley rats (220-240 g) were divided into sham and CAL groups. Myocardial infarction was induced by left CAL. All rats were further subdivided into untreated and orally treated with ONO-9902 (300 mg kg-1 day-1) from the 1st to 6th weeks after the operation. At the 1st and 6th weeks after the operation, gene expression of plasma and renal NEP, plasma ANP, cGMP and aldosterone concentrations, urine volume, Na and ANP excretion, creatinine clearance and renal cGMP generation were measured. Results: CAL leads to sodium and water retention, increased renal NEP gene expression, plasma ANP and aldosterone and decreased renal cGMP generation and plasma NEP gene expression. Acute treatment of CAL rats by ONO-9902, at the 1st week after the operation, inhibited plasma and renal NEP gene expression with increased plasma ANP, which caused diuresis, natriuresis and increased renal cGMP generation. Moreover, chronic treatment of those rats by ONO-9902 decreased plasma and renal NEP gene expression, plasma aldosterone, increased plasma ANP but non significantly and caused diuresis, natriuresis with increased renal cGMP generation. GFR was not significantly changed before or after treatment. Conclusion: Chronic treatment with NEP inhibitor decreases Na and water retention in rats with CHF by enhancing ANP action and suppressing aldosterone secretion. So, ONO-9902 may offer a new therapeutic approach in patients with CHF.
  Ayman Z. Elsamanoudy and Amr M. Abbas
  Problem statement: To assess the plasma concentrations and placental gene expression of soluble fms like tyrosine kinase (sFlt-1), Vascular Endothelial Growth Factor (VEGF), visfatin and Tumour Necrosis Factor α (TNFα) in a rat model of preeclampsia, induced by chronic Reduction of Uterine Perfusion Pressure (RUPP) and to investigate the involvement of Insulin Resistance (IR) in the pathophysiology of preeclampsia and the possible relation of visfatin and TNFα to IR in preclampsia. Approach: Twenty female Sprague-Dawley rats weighing 220-250 g were divided into either RUPP (n = 10) or Normal Pregnant (NP; n = 10) (control) groups. Plasma levels and placental gene expression of sFlt-1, VEGF, visfatin, TNFα, plasma endothelin (ET-1), glucose, serum insulin, creatinine, HOMA-IR and placental Malondialdehyde (MDA) and total antioxidants were measured. Also, Mean Arterial Pressure (MAP), fetal number and weight were determined. Results: In RUPP rats, MAP increased, plasma level and placental gene expression of sFlt-1, visfatin and TNFα increased while those of VEGF decreased. Moreover, plasma ET-1, glucose, insulin, HOMA-IR increased while GFR, fetal weight and number decreased. There is a significant positive correlation between TNFα, ET-1, sFlt-1 and MAP, between plasma visfatin or TNFα levels and both serum insulin and HOMA-IR, between visfatin and TNFα, between TNFα and ET-1 and between placental MDA and either sFlt-1 or ET-1. Furthermore, a negative correlation was reported between VEGF and MAP. Conclusion: RUPP increased sFlt-1, TNFα and decreased VEGF resulting in endothelial dysfunction which is manifested by increased MDA and ET-1. This results in altered renal function and hypertension. Moreover, IR may be involved in the pathophysiology of preeclampsia. Visfatin and TNFα, may have a role in IR during preclampsia.
 
 
 
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