The Changes Of Cardiomyopathy Ultrastructure And Effect Of PPARgamma Agonist On It In Diabetic Rats

Diabetes mellitus is very population and represents a significant public health challenge, cardio-vascular complications are still the most frequent causes of death in these patients. Diabetes influences myocardial and coronary vessels function by coexisting macroangiopathy, microangiopathy, metabolic disturbances and autonomic nervous system neuropathy.Objectives:Thinking diabetic cardiomyopathy is a kind of independent heart disease at present. Cardiac function decline is often due to diabetes mellitus. But how diabetes mellitus to affect myocardium? How diabetic cardiomyopathy to display in the electron microscope? PPARgamma agonist-rosiglitazone (TZDs) is a kind of insulin-sensitizing agent. There is many research about this agent at present. In the research, finding this agent not only drop the glucose of diabetes but proect the cardiovascular system. The mechanism of proecting cardiovascular system, is not known at present. In china and outside, we do not find the literature about how cardiac structure alteration after taking the agent. Therefore, we try to study the outcome afterestablishing model of the diabeticcardiomyopathy and comparing the control with the rosiglitazone group. So we are sure it can provide the experimental theory to treat the diabetes and its complication by this research.Materials and Methods:1 Set up model of diabetic cardiomyopathy rats1. This study was conducted on 35 Sprague Dawley rats (provided by the experimental animals center of the zhejiang university ), 10 weeks old, body weight 313卤46 gram . Rats were maintained in alternating cycles of darkness (6.00 p. m. to 6.00 a. m. )and light (6.00 a. m. to 6.00 p. m. ) . Food and water were freely available;2. Streptozotocin, STZ, N-[Methylnitrosocarbamoyl]-D-glucosamine ,Sigma Chemical Co., Munchen, Protamine zinc insulin;3. SD rats were divided into two groups: Experimental group(male, n=10 female, n=15): treated with a single intraperitoneal injection 3 ml of STZ (55-60 mg/kg, di]uted in 0. 1M, pH 4. 5 sodium citrate buffer) ;after make succeeded of the diabetic mellitus rats, 5 male and 5 female was taken with rosiglitazone from the third day. Control (male, n=5; female, n=5)rtreated with a single intraperitoneal injection 3 ml of sodium citrate buffer, 0. 1M, pH 4. 5) ;4. Urine glucose were tested 2 days after the experiment daily. If urine glucose was less than ++(positive reaction), no treatment was given; if urine glucose was +++ "" ++++, 1 ~ 4 u of protamine zinc insulin was injected subcutaneously every day;5. 10 weeks after treatments described above , rats were killed under the condition of intraperitoneal injection of ketamine (35mg/kg), respectively. During the operation , blood samples were taken from venacava for the measurements of glucose (American Adantage) . The ratsheart samples were stored under 2.5% glutaraldehyde . 6. Statistical analysis: experimental values were expressed as means SD, The Student's test was used for calculating probabilities, andthose less than 5% (p<0. 05) were considered significant, those less than 1% (p<0.01) were considered very significant. 2 Preparation the sample of the transmission electron microscope1. fixed, flushed, stained and desiccated the constitution;2. embed;3. sectioned (semithin section and repair the block and ultrathin section);4. draged the block: using the 200 hole cuprum net (ultrasonic wave cleaned the cuprum net);5. Stained the ultrathin section;6. Used the Dutuch Philip TECNA10 transmission electron microscope to observe the sample;Results: The experimental group rats all presented polydipsia,polyuria, polyphagia and urine sugar raised, above + + from the second day of the injected STZ. But the urine sugar of the 5 femal rats in the experimental group was ++"+++at the 3 weeks and the urine sugar was - " or + at thesubsequence 7 weeks. We called the 5 femal rats the diabeticrats. Rat body weight: Compared the control, the body weight of the experimental gro...