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Increased concentration of serum TNF alpha and its correlations with arterial blood pressure and indices of renal damage in dogs infected with Babesia canis
Authors:Wojciech Zygner  Olga Gójska-Zygner  Piotr Bąska  Ewa Długosz
Affiliation:1. Division of Parasitology, Department of Preclinical Sciences, Faculty of Veterinary Medicine, Warsaw University of Life Sciences, Ciszewskiego 8, 02-786, Warsaw, Poland
2. Multiwet Small Animal Health Clinic, Gagarina 5, 00-753, Warsaw, Poland
3. Division of Pharmacology and Toxicology, Department of Preclinical Sciences, Faculty of Veterinary Medicine, Warsaw University of Life Sciences, Ciszewskiego 8, 02-786, Warsaw, Poland
Abstract:Canine babesiosis is a tick-borne disease caused by parasites of the genus Babesia. Tumour necrosis factor alpha (TNF-α) is a cytokine that plays a role in the pathogenesis of canine babesiosis. In this study, the authors determined the concentration of serum TNF-α in 11 dogs infected with Babesia canis and calculated Spearman’s rank correlations between the concentration of TNF-α and blood pressure, and between TNF-α and indices of renal damage such as: fractional excretion of sodium (FE(Na+)), urinary creatinine to serum creatinine ratio (UCr/SCr), renal failure index (RFI), urine specific gravity (USG) and urinary protein to urinary creatinine ratio (UPC). The results demonstrated statistically significant strong negative correlations between TNF-α and systolic arterial pressure (r?=??0.7246), diastolic arterial pressure (r?=??0.6642) and mean arterial pressure (r?=??0.7151). Serum TNF-α concentration was also statistically significantly correlated with FE(Na+) (r?=?0.7056), UCr/SCr (r?=??0.8199), USG (r?=??0.8075) and duration of the disease (r?=?0.6767). The results of this study show there is an increase of serum TNF-α concentration during canine babesiosis, and the increased TNF-α concentration has an influence on the development of hypotension and renal failure in canine babesiosis. This probably results from the fact that TNF-α is involved in the production of nitric oxide and induction of vasodilation and hypotension, which may cause renal ischaemia and hypoxia, and finally acute tubular necrosis and renal failure.
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