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Study on Hemorheological Properties of Erythrocytes in Asymptomatic Hyperuricemia Rat Model

Journal Name:

  • International Journal of Medical Research & Health Sciences

Publication Year:

  • 2017

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Author NameUniversity of Author
Abstract (2. Language): 
Background: Hyperuricemia causes gout syndrome, which can manifest as hemorheological damage. However, hemorheological properties have not been well characterized in asymptomatic conditions. Aims: The present study was aimed to investigate the hemorheological changes in rats with asymptomatic hyperuricemia. Methods and Materials: The rat model was established by intraperitoneal injection of 250 mg/(kg·d) oxonate acid for 8 weeks. In one group of rats, 70 mg/(kg·d) allopurinol was also administrated for the latter 4 weeks. Control rats were administered CMCNa solution and water. Results: Hyperuricemic rats had higher blood viscosity than control rats did. Moreover, their erythrocytes had reduced deformation index, orientation index, surface charges, and osmotic fragility. Treatment with allopurinol decreased the blood uric acid amounts and improved the hemorheological parameters. Conclusions: Our study suggests that there is deterioration in the hemorheology of hyperuricemic rats and that allopurinol can play a protective role on the deterioration. Therefore, hemorheology can be used as a diagnostic tool in asymptomatic hyperuricemia.
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REFERENCES

References: 

[1] So, Alexander, and Bernard Thorens. “Uric acid transport and disease.” The Journal of Clinical Investigation Vol.
120, No. 6, 2010, p. 1791.
[2] Nakagawa, Takahiko, et al. “The conundrum of hyperuricemia, metabolic syndrome, and renal disease.” Internal
and Emergency Medicine Vol. 3, No. 4, 2008, pp. 313-18.
[3] Zhao, Jiyuan, et al. “Purine metabolites in gout and asymptomatic hyperuricemia: analysis by HPLC–electrospray
tandem mass spectrometry.” Clinical Chemistry Vol. 51, No. 9, 2005, pp. 1742-44.
[4] De Luca, G., et al. “Uric acid does not affect the prevalence and extent of coronary artery disease. Results from a
prospective study.” Nutrition, Metabolism and Cardiovascular Diseases Vol. 22, No. 5, 2012, pp. 426-33.
[5] Krishnan, Eswar, et al. “Hyperuricemia and the risk for subclinical coronary atherosclerosis-data from a prospective
observational cohort study.” Arthritis Research & Therapy Vol. 13, No. 2, 2011, p. R66.
[6] Tang, Ri-Bo, et al. “Serum uric acid and risk of left atrial thrombus in patients with nonvalvular atrial fibrillation.”
Canadian Journal of Cardiology Vol. 30, No. 11, 2014, pp. 1415-21.
[7] Kuwabara, Masanari, et al. “Asymptomatic hyperuricemia without comorbidities predicts cardiometabolic diseases.”
Hypertension 2017, p. 116.
[8] Höieggen, Aud, et al. “Serum uric acid and hemorheology in borderline hypertensives and in subjects with established
hypertension and left ventricular hypertrophy.” Blood Pressure Vol. 12, No. 2, 2003, pp. 104-10.
[9] Ding, D.D., et al. “Changes of platelet α-particle membrane protein, platelet activating factor and platelet parameters
in patients with hyperuricemia.” Zhongguo shi yan xue ye xue za zhi/Zhongguo bing li sheng li xue hui
Journal of experimental hematology/Chinese Association of Pathophysiology Vol. 20, No. 2, 2012, pp. 394-97.
[10] Watanabe, Susumu, et al. “Uric acid, hominoid evolution, and the pathogenesis of salt-sensitivity.” Hypertension
Vol. 40, No. 3, 2002, pp. 355-60.
[11] Hong, Quan, et al. “Hyperuricemia induces endothelial dysfunction via mitochondrial Na+/Ca 2+ exchangermediated
mitochondrial calcium overload.” Cell Calcium Vol. 51, No. 5, 2012, pp. 402-10.
[12] Yamada, Harumi, et al. “Mechanism of the uricosuric action of the anti-inflammatory drug E3040 used to treat
inflammatory bowel disease I: study using a rat model of hyperuricemia.” Biopharmaceutics & Drug Disposition
Vol. 20, No. 2, 1999, pp. 77-83.
Kuihua Li, et al. Int J Med Res Health Sci 2017, 6(10): 1-7
7
[13] Conger, John D., and Sandor A. Falk. “Intrarenal dynamics in the pathogenesis and prevention of acute urate
nephropathy.” Journal of Clinical Investigation vol. 59, no. 5, 1977, p. 786.
[14] Chen, Chien-Chang, Yu-Jung Hsu, and Tsung-Ming Lee. “Impact of elevated uric acid on ventricular remodeling
in infarcted rats with experimental hyperuricemia.” American Journal of Physiology-Heart and Circulatory
Physiology Vol. 301, No. 3, 2011, pp. H1107-H1117.
[15] Song, Jian, et al. “The effects of non-ionic contrast medium on the hemorheology in vitro and in vivo.” Clinical
Hemorheology and Microcirculation Vol. 58, No. 3, 2014, pp. 385-93.
[16] Mazzali, Marilda, et al. “Elevated uric acid increases blood pressure in the rat by a novel crystal-independent
mechanism.” Hypertension Vol. 38, No. 5, 2001, pp. 1101-06.
[17] Sánchez-Lozada, Laura G., et al. “Role of oxidative stress in the renal abnormalities induced by experimental
hyperuricemia.” American Journal of Physiology-Renal Physiology Vol. 295, No. 4, 2008, pp. F1134-F1141.
[18] Schwartz, Idit F., et al. “Hyperuricemia attenuates aortic nitric oxide generation, through inhibition of arginine
transport, in rats.” Journal of Vascular Research Vol. 48, No. 3, 2011, pp. 252-60.
[19] Tamariz, Leonardo J., et al. “Blood viscosity and hematocrit as risk factors for type 2 diabetes mellitus: the
atherosclerosis risk in communities (ARIC) study.” American Journal of Epidemiology Vol. 168, No. 10, 2008,
pp. 1153-60.
[20] Wen, Zongyao, et al. “Biophysical meanings of orientation and deformation of RBCs in shear flow field of low
viscosity with new Ektacytometry.” Science in China Series C: Life Sciences Vol. 41, No. 2, 1998, pp. 195-202.

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