1.Evaluation of Hypertensive Myocardial Fibrosis By Quantitative Myocardial Acoustic Densitometry
Naili DU ; Fang JIA ; Ruizhi DU ; Enkui HAO
Chinese Journal of Hypertension 2006;0(12):-
Objective To evaluate the clinical value of quantitative myocardial acoustic densitometry in myocardial fibrosis in relative to the alteration in serum procollagen type Ⅲ amino-terminal propeptide(PⅢNP) concentration in hypertensive patients. Methods Seventy-five consecutive hypertensive patients were recruited with 75 normal persons served as healthy controls. The indexes of acoustic densitometry were evaluated by echocardiography and the concentrations of the serum PⅢNP peptide by radioimmunoassay. Results Calibrated acoustic intensity in septal(CAI1) and posterior wall(CAI2) in hypertension group(0.88?0.06, 0.73?0.06) were greater than that in healthy control group (0.66?0.19, 0.54?0.06) (P
2.Angiotensin Ⅱ and its Antagonists on Cultured Cardiac M yocytes Hypertrophy
Naili DU ; Wenhang QI ; Dingliang ZHU ; Pingjin GAO ; Xisheng QIU
Chinese Journal of Hypertension 2001;9(2):130-133
Aim To investigate the effects of angiotensin Ⅱ(AngⅡ),AT1 receptor antagonist losartan and AT2 receptor antagonist PD123177 on protein synthesis rate and AT1 receptor mRNA expression in cultured neonatal rat cardi ac myocytes. Methods The protein synthesis rate in cultured cardiac myocytes w as determined by the3H-leucine incorporation,AT1 receptor mRNA expressi on of cardiac myocytes was assessed by reverse transcription-polymerase chain reaction(RT-PCR). Results AngⅡ increased the 3H-leucine incorporation in cultured cardiac myocytes in a dose dependent manner,losartan but not PD12317 7 could significantly inhibit AngⅡ induced protein synthesis,;AT1 receptor mRNA expression was upregulated after AngⅡ,and inhibited by losartan,but not PD123177. Conclusion AngⅡ can induce cardiac myocytes hypertrophy via upregulating AT1 receptor,and AT1 receptor antagonist can decrease AT1 rec eptor expression,reduce cardiac myocytes hypertrophy.
3.Biventricular pressure-volume change in acute pulmonary embolism model
Enkui HAO ; Zhiming GE ; Guohai SU ; Shiming ZHU ; Naili DU ; Lingzhi YU ; Wei ZHANG ; Yun ZHANG
Chinese Journal of Pathophysiology 1989;0(06):-
AIM: To establish the experimental acute pulmonary embolism(APE) model and observe the left and right ventricular pressure-volume relationship in different overload situations. METHODS: The present study consisted of seven anesthetized mongrel dogs that were divided into the control group, moderate APE group and severe APE group according to the various phase and different pressure load during the experiment. APE model was induced by suture piece injection through right cardiac catheterization. The hemodynamic indexes were measured by the simultaneous cardiac catheterization and echocardiography.RESULTS: (1) In the group with moderate APE, the pressure-volume relationship of right ventricle tended to right-upward shift, the area of chart increased, the shape of chart transformed form triangle to rectangle. The mild parallel leftward shift, the area of chart decreased mildly and no change of chart shape was observed in the pressure-volume relationship of left ventricle. (2) In the group with severe APE, the chart of right ventricular pressure-volume relationship tended to right-upward shift continuously, the area of chart decreased. The chart of the left ventricle tended to left-downward shift and no change of chart shape was observed in the pressure-volume relationship of left ventricle, the area of chart decreased. The erose shape of charts was also found.CONCLUSION: The chart of ventricular pressure-volume relationships is a practical and reliable method to evaluate left and right ventricular hemodynamic in APE.