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Role of Nitric Oxide, Endothelin-1, Interleukin-1, and Tumor Necrosis Factor-α in Hemodialysis-Induced Hypotension

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Serum level of nitrite plus nitrate (NO2 plus NO3), endothelin-1 (Et-1), interleukin-1 (IL-1), and tumor necrosis factor-α (TNF-α) have been estimated in 20 patients with end stage renal failure (ESRF) undergoing regular hemodialysis treatment in a trial to explain the hypotension occurring in some of these patients. According to the incidence of hypotension, patients were divided into GI (n = 10) hypotension prone patients and GII (n = 10) hypotension resistant patients (normotensive). Clinical examination with measurement of systolic and mean arterial blood pressure was performed in all cases before and after hemodialysis (HD) settings. After HD, GI showed significant increase in the serum levels of (NO2 plus NO3), IL-1, and TNF-α, whereas a significant decrease in serum Et-1 level was noticed. GII showed no significant change in serum level of the 4 parameters mentioned above. In hypotensive patients, there was a significant positive correlation between (NO2 plus NO3) and the duration of dialysis, and a significant negative correlation between (NO2 plus NO3) and post dialysis systolic blood pressure, also between IL-1 and Et-1. From the previous results, it could be concluded that the vascular endothelial factors studied (NO and Et-1) together with the inflammatory cytokines IL-1 and TNF-α contribute to the development of HD-induced hypotension in ESRF subjects which is evidenced by: (1) the coupling of decrease of blood pressure and increase in NO2 plus NO3 level after HD in group I; (2) Et-1, which is a powerful vasoconstrictor, showed a significant decrease postdialysis; and (3) levels of cytokines (IL-1 and TNF-α) (which are potent NO inducers) were found to be significantly increased postdialysis in group I.
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Document Type: Research Article

Affiliations: 1: Department of Chemical Pathology 2: Department of Internal Medicine, Medical Research Institute, Alexandria University, Alexandria, Egypt.

Publication date: 2004-01-01

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