Intracoronary effects of calcitonin gene related peptide (CGRP) on coro-nary hemodynamics were observed in the normal and following different extent of coro-nary stenosis using graded coropary- stenosis modl in dogs. The results showed that CGRPincreased the coronary artery blood flow (CBF) and distant coronary blood prepsure (DCP),but decreased mean artery pressure (MAP), coronary vessels total resistance (R_T),large co-ronary vessels, resistance (R_L) and small coronary vessels resistance (R_s). Thirty minutesafter. coronary middle. stenosis, CGRP was given intracoronary, MAP had no significantchange, but CBF insreased and R_T R_L, R_s decreased, and which maintained for 30 min. 30min after coronary severe stenosis, CGRP increased CBF and MAP, but decreased DCP,R_T, R_L, R_S continuously. These results suggested that CGRP could ameliorate myocardialischemia through enlargement of coronary vessels and by increasing CBF.

To determine the regulatory effect of ? opioid receptor stimulation on ? adrenoceptor signaling and its underlying mechanism, single ventricular myocytes were isolated from the heart of rat subjected to chronic hypoxia for 4 weeks. The electrically induced [Ca 2+ ] i transient were measured using a spectrofluorometric method. RT PCR was used to determine the mRNA of ? opioid receptor, and Western blot was used to determine the Gi and Gs protein. ? adrenoceptor stimulation with isoproterenol increased the amplitude of the electrically induced [Ca 2+ ] i transient in myocytes of normoxic rats. U50488H, a selective ? opioid receptor agonist, significantly inhibited the effect of isoproterenol. In the heart of chronically hypoxic rats, the inhibition of U50488H was blunted. RT PCR revealed no significant change in mRNA of ? opioid receptor. Western blot showed no change in Gi protein. While biologically active Gs small protein decreased significantly. The results indicate that the negative modulation of ? opioid receptor on ? adrenoceptor is attenuated in the heart of chronically hypoxic rat. The decrease in Gs protein may be partially responsible for the attenuation.

Objective To explore the imaging features and clinical significance of solitary costal hot spots on bone scintigraphy (BS). Methods Eighty-four patients with single costal hot spots were enrolled in the study. The sites of lesions were classified into four types: junction betweenaor rib. The shapes of hot spots were classified into three forms: Punctiform, clumping and strip. The above data were respectively analyzed. Results Single hot spots were mainly showed in the punctiform and strip shapes, and the distribution of punctiform spots were mainly in the sites of junction between costal cartilage and rib and frontal ribs, also mainly due to costal fractures (42/61, 68.85%). The majority of spots in strip shape were costal metastases(18/19, 94.74%). Hot spots in posterior ribs were also mainly costal metastases (24/29,82.76%). Conclusion Useful imaging features can be obtained from BS with al diagnosis of benign and malignant lesions.

AIM: The present study was to investigate the time course of ?-adrenoceptor desensitization and changes in the calcium transient in rat ventricular myocytes following chronic hypoxia. METHODS: With the spectrofluorometric method, the intracellular calcium( i) transient and its response to ?-adrenoceptor stimulation were determined in the single right ventricular myocytes, loaded with Fura-2.RESULTS: After 2-3 weeks of chronic hypoxia, the amplitudes of electrically induced i transient and caffeine-induced i transient started to decrease and the duration of i transient prolonged. The enhanced electrically induced i transient evoked by isoprotrenol was also decreased. After 3 or 4 weeks of chronic hypoxia, these changes aggravated gradually. After 8 weeks of chronic hypoxia, the changes of all these parameters were convalescent, meanwhile there was no significant difference compared with that of 4 weeks group. CONCLUSIONS: After 2-4 weeks of chronic hypoxia, the ?-adrenoceptor desensitization occurs, the underlying mechanism is related to the decreased function of L-type of calcium channel, ryanodine receptor-operated calcium channel and calcium ATPase, which is responsible for the decreased cardiac functionl. At 8 weeks of hypoxia, the heart is in adaptation and compensatory process.

Aim To investigate the effects of U50488H,a selective ?-opioid receptor agonist,on the blood pressure in the rats and explore their mechanisms.Methods Heart rate(HR),arterial blood pressure(ABP),left ventricular pressure(LVP),contractive function(+ dp/dt_(max)) and diastolic function(-dp/dt_(max)) were examined in rats.Physiological experimental technique was used to collect urine and to determine the volume of urine output;isolated artery perfusion technique was used to investigate the direct action of U50488H on abdominal aorta of rats.Results HR,ABP,LVP and ?dp/dt_(max) in rats were decreased with the administration of U50488H;the urine volume increased significantly with the administration of U50488H.U50488H induced a dose-dependent vasodilation in the aortic artery.These effects of U50488H were totally abolished by nor-BNI,a selective ?-opioid receptor antagonist.Conclusion Stimulation of ?-opioid receptor with U50488H depresses the blood pressure mainly by reducing the strength of cardiac muscle,enhancing the urine volume and relaxing the vessel.

AIM: To observe the changes of NO, ET-1, SOD and MDA levels in plasma of rats exposed to infrasound. METHODS: Using infrasound (frequency: 8 Hz; sound pressure level:130 dB), the rats were exposed for 1 d, 7 d, 14 d, 21 d and 28 d, 2 h daily, then the levels of NO, ET-1, SOD and MDA were measured after exposure. RESULTS: The changes of NO levels in plasma significantly declined at 7 d and 14 d (P0.05). The changes of ET-1 levels in all groups in plasma were significantly increased (P

Objective:Our aim was to study the levels of atrial natriuretic peptide (ANP) and pulmonary perfusion imaging in determining of pulmonary artery hypertension (PAH). Methods: We measured ANP levels by using radioimmunoassay after making various types of PAH in rabbits. Catheterization and pulmonary perfusion tomographic imaging were used in the control group. Results: When the pulmonary artery pressure increased slightly, the ANP levels were lower in PAH group than that of control group, but the difference was not significant (t=1, P>0.05). At the same time, pressure measured by catheterization did not change as the control group, but the ratio of back/abdomen radiopharmaceuticals distribution which was measured with pulmonary perfusion tomographic imaging was significantly higher in PAH group than that of the control (t=2.5, P<0.05). The difference between the ANP levels when the pulmonary artery pressure increased medially and seriously was significant (t＝4.0 and 6.5, P＜0.05). The other two methods got the same result (P＜0.05). Results of three examining methods were positively related. Conclusion:The ANP levels can determine the degree of PAH, and it was simple. But it was not as sensitive as that of pulmonary perfusion tomographic imaging.

Objective To investigate the role of miR-203 in radiation-induced thymic lymphoma (RITL).Methods A 60Co irradiator was used for total-body irradiation.MicroRNAs(miRNAs) level was assayed by qRT-PCR.Cell proliferation was assayed by MTT assay.Cell apoptosis was examined by fluorescence activated cell sorter (FACS).Dual luciferase reporter assay system was used to detect the 3'UTR reporter.Results MiR-203 was down-regulated in RITL tissues.Overexpression of miR-203 strongly inhibited the proliferation of both NIH3T3 cells and EL4 cells and vice versa.MiR-203 inhibited cells proliferation and induced apoptosis via TANK-binding kinase (TBK1),SLUG (SNAI2) and Cyclin D1 (CCND1).Conclusions Radiation down-regulated the level of miR-203 in thymic,which promoted radiation-induced thymic lymphoma by targeting TBK1,SNAI2 and CCND1.

AIM:To investigate effect of hypoxia on the expression of proliferating cell nuclear antigen(PCNA) a nd phenotype of cardiac fibroblasts(CFs). METHODS: The purif ied cardiac fibro blasts were cultured and divided randomly into there groups :control group, mode rate hypoxia(MH) group and severe hypoxia(SH) group. After 72 h,MTT method was u s ed to investigate the proliferation of CFs, and the ultrastructure of fibroblast s were observed with transmission electron microscopy The expression of PCNA a n d ?-actin in cardiac fibroblasts were measured by the means of immunohistochemi s try and laser scanning confocal microscopy, respectively. RESULTS: MTT A 490 nm value of MH group was significantly higher than that of control group by (18 4?25 0)% ( P

Objective To investigate the effects of quiet respiratory intrathoracic pressure changes on ventricular dimensions and left ventricular systolic function,and to further verify our newly proposed hypothesis of the mechanism of respiratory effects on hemodynamics.Methods Twenty healthy volunteers aged 18 to 40 years average(24?7) years were included.The respiratory curve and electrocardiogram were simultaneously recorded.The interventricular septum movement,ventricular dimensions and ventricular systolic excursions were recorded by two-dimensional and M-mode echocardiography during quiet respiration.The respiratory variations of the above parameters were derived,and the parameters for assessing ventricular systolic function were calculated.Results With quiet respiration,the interventricular septum moved towards the left ventricle on inspiration,and then towards the right ventricle on expiration.The right ventricular diastolic dimension increased significantly on inspiration compared with those on expiration.The opposite changes occurred with left ventricular diastolic dimensions.The left ventricular posterior wall systolic excursion and the left ventricular stroke volume significantly increased during expiration compared with those during inspiration.No significant differences were found in left ventricular ejection fraction and fractional shortening between inspiration and expiration.Conclusions The respiratory intrathoracic pressure change is one of the factors influencing the reciprocal changes of the left and right ventricular parameters related to ventricular dimensions and systolic function.