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1.
Chinese Journal of Tissue Engineering Research ; (53): 5042-5043, 2007.
Article in Chinese | WPRIM | ID: wpr-407917

ABSTRACT

AIM: To detect the change of urinary concentration of aquaporin-2 (AQP-2) by enzyme linked immunosorbent assay in rat models of different degrees of heart failure and make a comparison with sham-operation group.METHODS: This experiment was carried out between January 2000 and January 2002 in the animal laboratory of Nanfang Hospital of Southern Medical University. Forty-two male adult Sprague-Dawley rats were involved. Twenty-six rat models of chronic heart failure were prepared by ligation of left coronary artery. When left ventricle infarct area was≥20%, the rat models of congestive heart failure were successful (heart failure group, n =13); When left ventricle infarct area was<20%, the rat models of congestive heart failure were unsuccessful (compensation group, n =13). The other 16 rats were not ligated at coronary rtery (control group). Serum sodium concentration was determined with BeckmanC×3 equipment and urine osmole by cryoscopic method. Urine volume of 24 hours was monitored. Urinary concentration ofAQP-2 level of rats was determined by double antibodies sandwich enzyme linked immunosorbent assay (DABs-ELISA).RESULTS: Forty-two rats were involved in the result analysis. The 24-hour urine volume and serum sodium concentration in the heart failure group and compensation group were significantly lower than those in the control group (P<0.05-0.01), while urine osmole in two groups was significantly higher than that in the control group (P<0.05-0.01).②At postoperative 4 and 6 weeks, urinary concentration of AQP-2 level of rats in the control group was significantly lower than that in the other two groups (P<0.05-0.01), and urinary concentration of AQP-2 level of rats in the compensation group was significantly lower than that in the heart failure group (P<0.05, 0.01).In the compensation group and heart failure group, urinary concentration of AQP-2 level of rats was significantly higher at postoperative 6 weeks than at postoperative 4weeks (P<0.05).CONCLUSION:①AQP-2 is the key target protein of water retention and hyponatremia at heart failure.②Detection of urinary concentration of AQP-2 by ELISA can effectively reflect water retention and hyponatremia when heart failure occurs.

2.
Chinese Pharmacological Bulletin ; (12)1986.
Article in Chinese | WPRIM | ID: wpr-551694

ABSTRACT

AIM To observe Arg-Glu*ss activity of antiplatelet and anticoagulation in rats and to further explore its mechanism. METHODS Twenty four male sprague dewley rats were divided into three groups randomly (eight rats in each group).Each group was orally given Arg-Glu (61 4 mg?kg -1 ?d -1 ), ASA (36 mg?kg -1 ?d -1 ) and equal placebo solution respectively.Eight days later all rats were given anesthesia and blood was taken from abdominal aorta with a plastic catheter, then the indexes related to blood hemodynamics,coagulation and blood fibrinolysis were measured. Twenty four SD rats were treated in the same way mentioned above. Platelet aggregation was measured by turbidimetric method. Plasma level of cyclic GMP and prostacyclin was evaluated by radioimmunoassay and nitric oxide by spectrophotometric determination. Common carotid artery-external jugular vein bypass was established in another 24 rats, and the weight of wet thrombus was measured with high sensitive electrical scale. RESULTS In group of Arg-Glu, statistically significance decrease versus placebo group was observed on blood apparent viscosity, reduced viscosity, hematocrit and plasma viscosity, increase versus placebo was also observed on blood reciprocal calcium time, activated partial thromboplastin time and prothrombin time ( P 0 05). Platelet aggregation activation decreased compared with placebo 〔(0 75%?3.62%) vs (32 8%?6 62%) P 0 05)〕. CONCLUSION Arg-Glu with its properties of antiplatelet、anticoagulation and improvement of blood rheology status in rats could be regarded as one antiplatelet drug and one NO precursor .Its mechanism of action was thought to be by Arg-NO-cGMP metabolism pathway while other mechanism might be involved.

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