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1.
AIM:To explore the effects of different β-adrenergic receptors (β-AR) on the left and right ventricular systolic and diastolic functions in rats under acute hypoxic stress. METHODS:The healthy male SD rats were randomly divided into 4 groups (n=7):control group, non-selected β-AR blocker propranolol group, selected β1-AR blocker atenolol group and selected β2-AR blocker ICI 118,551 group, and then the rats were exposed to normoxia (20.9% O2, 79.1% N2) and hypoxia (15.0% O2, 85.0% N2) condition respectively at the altitude of 2 260 m (Xining, China). The heart rate (HR), the left ventricular systolic pressure (LVSP), the right ventricular systolic pressure (RVSP), and the maximum raise/decline rate of left and right ventricular pressure (±dp/dtmax) were monitored, and the arterial blood gas in normoxia and hypoxia condition were compared to explore the effect of β-AR on the left and right ventricular systolic and diastolic functions in acute hypoxic stress rats. RESULTS:Under normoxia condition, the LVSP, ±dp/dtmax of left ventricular were decreased in propranolol group, atenolol group and ICI 118,551 group, the RVSP and ±dp/dtmax of right ventricle were decreased in propranolol group and atenolol group (P<0.05). Under hypoxia condition, the PaO2, LVSP, ±dp/dtmax of left ventricle were decreased in all groups compared with the normoxia group, and the ±dp/dtmax of right ventricle was increased in all groups (P<0.05), also the degree of index change in control group was more obvious than that in propranolol group and atenolol group. CONCLUSION:The activation of β1-AR is an important compensatory regulation for heart function during hypoxic stress. However, the compensatory enhancement of right heart function under acute hypoxia condition which through tonogenic dilation is more significant for maintaining the normal circulating blood flow.  相似文献   

2.
AIM: To observe the myocardial protective effects of trimetazidine on myocardial infarction (MI) in Sprague-Dawley (SD) rats. METHODS: Ninety SD rats were randomly assigned to 3 groups (n=30 each): myocardial infarction group (MI group), MI+trimetazidine group (MT group) and sham group (S group). By permanently ligating the left anterior descending artery, the MI model was set up in the rats in MI group and MT group. Before and after setting up the MI model, normal saline was given to the rats in MI and S group by gavage. On the other hand, trimetazidine (3 mg/kg,twice per day) was given to the rats in MT group by gavage. At 8 h, 24 h and 48 h after applying trimetazidine, the serum level of cardiac troponin I (cTnI) was measured. At the 1st week, 2nd week and 4th week after treated with trimetazidine, the size of myocardial infarction, the maximum rising rate of the left ventricular systolic pressure (+dp/dtmax) and the maximum descending rate of the left ventricular diastolic pressure (-dp/dtmax) were measured. Also at the 1st week after applying trimetazidine, the cardiomyocyte apoptotic index was detected. RESULTS: Compared with MI group 2 weeks after applying trimetazidine, +dp/dtmax significantly increased in MT group , and -dp/dtmax also significantly increased in MT group . Four weeks after applying trimetazidine, +dp/dtmax significantly increased in MT group , and -dp/dtmax also significantly increased in MT group . At 8 h and 48 h after applying trimetazidine, no statistically significant difference (P＞0.05) of serum cTnI between MI group and MT group was observed. However, at 24 h after applying trimetazidine, the serum level of cTnI decreased in MT group as compared with MI group . Aditionally, trimetazidine significantly decreased the infarction size of myocardium in MT group (0.248±0.052) as compared with MI group (0.362±0.082, P<0.01). CONCLUSION: Trimetazidine has short-term cardioprotective effects on the rats with acute MI by improving myocardial systolic and diastolic functions, reducing infarct size and inhibiting apoptosis.  相似文献   

3.
AIM:To explore the effect of Xinshuaikang on myocardial autophagy in the rats with chronic heart failure and its relationship with the MAPK/ERK1/2 signaling pathway. METHODS:The rats were divided into sham group, model group (rat model of chronic heart failure was established by ligation of anterior descending branch of left coronary artery), low-, middle-, and high-dose Xinshuaikang treatment (TL, TM and TH) groups and captopril group (treated with captopril as positive control), with 12 in each group. Doppler echocardiography was used to evaluate the cardiac function. The morphological changes of the myocardium were observed by HE staining. TUNEL staining was used to detect cardiomyocyte apoptosis. The expression of microtubule-associated protein 1 light chain 3-Ⅱ (LC3-Ⅱ) in the myocardium was detected by immunofluorescence labeling. The protein levels of p-ERK, p-p38 MAPK, LC3-Ⅱ, beclin-1 and p62 in the myocardium were determined by Western blot. RESULTS:Compared with sham group, left ventricular end-diastolic dia-meter (LVEDD) and left ventricular end-systolic diameter (LVESD) in model group were increased, while left ventricular posterior wall thickness at end-diastole (LVPWTd), left ventricular posterior wall thickness at end-systole (LVPWTs), left ventricular ejection fraction (LVEF), cardiac output (CO), left ventricular diastolic pressure (LVDP), left ventricular systolic pressure (LVSP) and maximum rate of rise/decrease of left ventricular pressure (+dp/dtmax/-dp/dtmax) were decreased (P<0.05). The myocardial cells were deformed and necrotic, and the myocardial fibers were broken, with inflammatory cell infiltration. The apoptotic rate, the positive rate of LC3-Ⅱ, and the protein levels of p-ERK, p-p38 MAPK, LC3-Ⅱ/LC3-I and beclin-1 were increased, and the protein expression of p62 was decreased (P<0.05). Compared with model group, the levels of LVEDD and LVESD were decreased, LVPWTd, LVPWTs, LVEF, CO, LVSP, LVDP, +dp/dtmax and -dp/dtmax were increased in Xinshuaikang groups and captopril group (P<0.05). The morphological changes of myocardial cells were gradually returned to normal, and inflammatory cell infiltration, the apoptotic rate and the positive rate of LC3-Ⅱ were decreased. The protein levels of p-ERK, p-p38 MAPK, LC3-Ⅱ/LC3-I and beclin-1 were decreased, and the protein expression of p62 was increased (P<0.05). CONCLUSION:Xinshuaikang inhibits myocardial auto-phagy to play a role of cardiac protection in the rats with chronic heart failure, and its mechanism may be related to inhibition of MAPK/ERK1/2 signaling pathway.  相似文献   

4.
AIM:To investigate the influences of bradykinin(BK)on left ventricular hypertrophy and cardiac function in angiotensin-converting enzyme inhibitor(ACEI) therapy in rats after myocardial infarction.METHODS:The effects of enalapril (500 μg·kg-1·d-1), enalapril (500 μg·kg-1·d-1)with BKB2 receptor antagonist (Hoe-140 500 μg·kg-1·d-1), losartan(3 mg·kg-1·d-1) on left ventricular end-diastolic pressure (LVEDP), maximum positive left ventricular pressure change (+dp/dtmax) and LVW/BW as well as V(m)n of noinfarcted area were examined after 4 weeks treatment in rats after myocardial infarction.RESULTS:The values of LVEDP, LVW/BW and V(m)n of three treatment groups were higher than that of untreated MI group (P＜0.05),but the +dp/dtmax of three treatment groups were not significantly different compared with the untreated MI group. In addition, no significant difference in MAP was observed among the three treatment groups, but the LVW/BW and V(m)n of enalapril+Hoe-140-treated group were higher than that of enalapril-treated group (P＜0.05) .CONCLUSION:Enalapril can prevent left ventricular hypertrophy and improve cardiac function independent of blood pressure after myocardial infarction, which is partly due to the inhibition of BK degradation.  相似文献   

5.
AIM: To investigate the effects of long-term TCV116 on left ventricular remodeling and heart function after myocardial infarction. METHODS: Myocardial infarction (MI) was caused by ligation of the left anterior descending coronary artery in rats. One week after the surgical performance, the surviving rats were randomly assigned to the following treatment protocols: (1) MI rats with no therapy; (2) MI rats treated with TCV116 2 mg/kg per day; (3) Sham-operated control; (4) Sham-operated rats, treated with TCV116 2 mg/kg per day. At 22 weeks, cardiac hemodynamic parameters such as MAP, LVSP, dp/dtmax and LVEDP, and histomorphometric parameters such as LVW/BW and LVCA/BW were measured, mRNA of cardiac genes such as βMHC, BNP, TGF-β1, collagen I and III were quantified, and survival rates were calculated. RESULTS: Compared with sham-operated rats, MI rats without therapy showed significant increases in histomorphometric parameters as well as in mRAN expressions of cardiac genes (P<0.01); While their hemodynamic parameters were significantly impaired (P<0.01), and survival duration shortened (P<0.05). Compared with MI rats without therapy, MI rats treated with TCV116 showed significant attenuation of mRAN expression of cardiac genes (P<0.01); While their hemodynamic parameters were significantly improved (P<0.05 or P＜0.01), and survival duration extended (P<0.05). CONCLUSION: Treatment with long-term angiotensin II type 1 receptor antagonist may improve left ventricular remodeling and cardiac function after MI in rats.  相似文献   

6.
AIM: To study the effect of livin gene-modified bone marrow mesenchymal stem cells(BM-MSCs) transplantation on the cardiac function following acute myocardial infarction in a rat model and the expression of livin, caspase-3, caspase-7 and caspase-9 in the livin gene-modified BM-MSCs. METHODS: The MSCs were obtained by the whole bone marrow culture method, and the apoptosis of the MSCs after infection with adenovirus vector carrying enhanced green fluorescent protein(EGFP) gene and livin recombinant vector(rAd-livin) were detected by flow cytometry. The expression of livin, caspase-3, caspase-7 and caspase-9 was detected by Western blot. After permanent left anterior descending artery occlusion, the rats were randomized to receive intramyocardial injection of DMEM without cells(vehicle group), or containing MSCs(MSCs group), MSCs(EGFP)(rAd-control/MSCs group) or MSCs(livin)(rAd-livin/MSCs group). Left ventricular systolic pressure(LVSP), left ventricular end-diastolic pressure(LVEDP), the maximum increased rate of left ventricular pressure(-dp/dtmax) and the maximum decline rate of left ventricular pressure(+dp/dtmax) were recorded for evaluating the cardiac functions. RESULTS: The apoptosis of rAd-livin/MSCs was significantly decreased as compared with MSCs and rAd-control/MSCs(P<0.05). Meanwhile, the expression of caspase-3, caspase-7 and caspase-9 was significantly downregulated as compared with the other 2 groups(P<0.05). The cardiac function in rAd-livin/MSCs group was significantly improved as compared with DMEM group, and those in the other 2 groups got the similar results, but the function in rAd-livin/MSCs group was better improved. Meanwhile, the number of surviving cells in rAd-livin/MSCs group was significantly improved as compared with the other 2 groups. CONCLUSION: The apoptosis of MSCs is decreased after rAd-livin transfection, and the expression of caspase-3, caspase-7 and caspase-9 is also significantly downregulated while the expression of livin is significantly upregulated. Transplantation of livin-modified BM-MSCs by lentiviral vector results in better prognosis for treating myocardial infarction by enhancing cell survival.  相似文献   

7.
AIM:To elucidate the relationship between the intracellular calcium concentration changes and left ventricular hypertrophy and function in the spontaneously hypertensive rats (SHR).METHODS:Intracellular free calcium concentrations were measured by Fura 2 methodology and left ventricular function quantitated by cardiac catheterization in 20 SHR aged 10, 22, and 34 weeks and 20 age-matched Wistar-kyoto (WKY) rats.RESULTS:(1) The systolic blood pressure(SBP), intracellular calcium concentrations and left ventricular mass / body weight index (LVM/BW) were significantly higher in all three age groups of SHR than the corresponding groups of WKY; (2) Compared with age-matched WKY groups, the peak left ventricular pressure descending rate(-dp／dtmax) decreased while left ventricular relaxation time constant (τ)increased significantly in SHR aged 22 and 34 weeks. The peak left ventricular pressure ascending rate(dp／dtmax) and the left ventricular contractility index were significantly increased only in the 34 weeks SHR; (3) Intracellular calcium concentrations showed a positive correlation with LVM/BW,SBP,-dp／dtmax and τ(r=0.47-0.83,P<0.01)and a negative correlation with dp／dtmax and the left ventricular contractility index (r=-0.46,P<0.05 and r=-0.81, P<0.01).CONCLUSION:Intracellular calcium overload is one of the potential mechanisms in the induction of left ventricular hypertrophy as well as of systolic and diastolic dysfunction.  相似文献   

8.
AIM: To investigate the effects of cardiac contractility modulation (CCM) applied to different locations of the heart on cardiac functions and cardiac dys-synchrony in the rabbits with chronic heart failure, and to explore the best pattern of CCM.METHODS: Forty rabbits were divided into 4 groups according to the location of receiving CCM: heart failure (HF) group, left ventricular anterior wall (LVAW-CCM) group, left ventricular posterior lateral wall (LVPLW-CCM) group and right ventricular apex (RVA-CCM) group. The model of chronic heart failure was made by ligating ascending aortic root of the rabbits. After 12 weeks, the electrical stimulations during the absolute refractory period were delivered in different locations of the heart, lasting 6 h everyday for 7 days. The changes of cardiac functions and cardiac dys-synchrony were observed by cardiac ultrasonic cardiogram before and after CCM stimulation. The plasma level of brain natriuretic peptide (BNP) was detected by ABC-ELISA method. Pulsed-wave Doppler was used to acquire aortic pre-ejection interval (APEI) and pulmonary pre-ejection internal (PPEI), and inter-ventricular mechanical delay (IVMD) was calculated to evaluate the cardiac dys-synchrony.RESULTS: Compared with HF group, left ventricular end-systolic dimension (LVESD) and left ventricular end-diastolic dimension (LVEDD) in LVAW-CCM group, LVPLW-CCM group and RVA-CCM group were significantly decreased (P<0.05), while left ventricular ejection fraction (LVEF) and left ventricular fractional shortening (LVFS) were significantly increased (P<0.05), especially in LVAW-CCM group. Interventricular septal thickness (IVS) and left ventricular posterior wall thickness (LVPW) were similar among groups. No significant difference of plasma BNP level before CCM delivery among the 4 groups was observed. However, the plasma BNP level in control group was the highest, followed by LVPLW-CCM group and RVA-CCM group, and LVAW-CCM group was the lowest after CCM delivery. No change of IVMD was observed among groups before and after CCM delivery.CONCLUSION: The effect of CCM applied to different locations of the heart on cardiac functions is different.The optimal site of CCM delivery is left ventricular anterior wall. No influence of interventricular dys-synchrony was observed during application of CCM.  相似文献   

9.
ZHOU Li  LIAN Hui  WANG Zhi-yong 《园艺学报》2018,34(9):1565-1570
AIM:To explore the effects of carnosine (CAR) on cardiac dysfunction in type 1 diabetic mellitus rats and the underlying mechanism. METHODS:The SD rats were randomly divided into 4 groups:control (C) group, control+carnosine (C+CAR) group, diabetes mellitus (DM) group and diabetes mellitus+carnosine (DM+CAR) group (n=10). The rats were sacrificed after 12 weeks. The cardiac function was assessed by ventricular cannulation. The activity of superoxide dismutase (SOD) and the content of malondialdehyde (MDA) were assessed by ELISA. The mRNA levels of tumor necrosis factor α(TNF-α), interleukin-1β(IL-1β) and IL-6 were measured by real-time PCR. The distribution of connexin 43 (Cx43) was examined by immunofluorescence. The protein levels of Cx43 and protein kinase C (PKC) were determined by Western blot. RESULTS:Compared with the C group, the left ventricular end diastolic pressure (LVEDP) was increased whereas the left ventricular pressure maximum rise/fall velocity (±dp/dtmax) was decreased in the DM group (P<0.01). The activity of SOD decreased while the MDA increased in the left ventricular tissues (P<0.01). The mRNA levels of TNF-α, IL-1β and IL-6 were increased (P<0.01). The Cx43 distribution was irregular. The protein levels of phosphorylated Cx43 and PKCε were elevated (P<0.01). Compared with the DM group, the cardiac function of LVEDP and ±dp/dtmax in DM+CAR group was ameliorated (P<0.01), with increased SOD activity and decreased MDA content (P<0.05). The mRNA levels of TNF-α, IL-1β and IL-6 were reduced (P<0.01). The Cx43 distribution was improved and the protein levels of phosphorylated Cx43 and PKCε were decreased (P<0.01). CONCLUSION:CAR treatment can improve the cardiac function by its anti-oxidative and anti-inflammation effects and suppression of Cx43 abnormalities through PKCε in DM rats.  相似文献   

10.
LUO Wen  LI Yue-shan 《园艺学报》2011,27(8):1502-1507
AIM: To investigate the protective effects and mechanisms of combinational use of trimetazidine(TMZ) and parecoxib sodium on acute myocardial infarction (AMI) in rats. METHODS: Sixty-six Sprague-Dawley rats were randomly divided into 5 groups: sham group; AMI group; AMI+TMZ group; AMI+parecoxib group; AMI+TMZ+parecoxib group. All rats were sacrificed and cardiac functions (HR, LVSP, LVEDP, +dp/dtmax,-dp/dtmax) were measured with a Pclab-3804 biological signal processing system on the 8th day. The infarct size in each group was checked up by TTC staining method. RT-PCR was employed to detect the bax mRNA and bcl-2 mRNA. The protein levels of COX-2, Bax, Bcl-2 and cleaved caspase-3 in myocardium were determined by Western blotting. The activity of caspase-3 in each group was measured by colorimetric assay kit, and the apoptotic rates were detected with DNA ladder kit.RESULTS: Compared with sham group, increased expression of COX-2 protein (P<0.01) was observed in AMI group. The expression of COX-2 protein in parecoxib group was lower than that in AMI group (P<0.01). Compared with AMI group, the combinational use of trimetazidin and parecoxib improved contractile functions (LVSP and +dp/dtmax), reduced the infarct size and lowered the apoptotic rates remarkably. Specifically, the combinational use of trimetazidin and parecoxib showed better effects than use of trimetazidin or parecoxib alone. Reduced expression of Bax/Bcl-2 mRNA and protein, the reduced caspase-3 activity and cleaved caspase-3 expression were also found in combinational group as compared with other groups (P<0.05).CONCLUSION: The combinational use of trimetazidin and parecoxib effectively improves cardiac functions and reduces infarct size. The mechanism of the protective effect is probably associated with inhibiting apoptosis of cardiac myocytes.  相似文献   

11.
AIM: To evaluate the effects of atorvastatin on nitric oxide(NO), endothelin-1(ET-1)and myocardial no-reflow in a rabbit model of acute myocardial infarction and reperfusion(AMI/R). METHODS: Twenty-four rabbits were randomized into 3 groups: 8 in AMI/R group, 8 in atorvastatin-treated group(5 mg·kg-1·d-1)and 8 in sham-operated group. Animals in the former two groups were subjected to 60 min of coronary occlusion followed by 120 min of reperfusion. Data on haemodynamics were collected. NO in blood sample, and in normal, and in infarcted reflow and no-reflow myocardium were evaluated respectively by nitrate reductase method. The levels of ET-1 in blood sample, and in normal, infarcted reflow and no-reflow myocardium were determined by radioimmunoassay. RESULTS: (1)Compared to the baselines, the heart rate(HR), systolic blood pressure(SBP), diastolic blood pressure(DBP), left ventricular systolic pressure(LVSP), maximal rate of increase and decline in left ventricular pressure(±dp/dtmax)and cardiac output(CO)in AMI/R and atorvastatin-treated groups were significantly declined, whereas left ventricular end-diastolic pressure(LVEDP)was increased after 60 min of coronary occlusion and 120 min of reperfusion(P<0.05 or P<0.01). However, in atorvastatin-treated group, LVSP, LVEDP, ±dp/dtmax and CO at the time point of 120 min of reperfusion recovered more significantly than those at the time point of 60 min of coronary occlusion(P<0.01), which was more significant than those in AMI/R group(P<0.05 or P<0.01). Compared to AMI/R group, the SBP and DBP were significantly heigher in atorvastatin-treated group(P<0.01).(2)In atorvastatin-treated group, the levels of ET-1 in blood sample were significantly lower than those in AMI/R group(P<0.01), and the levels of NO were significantly higher(P<0.01). Moreover, the levels of NO or ET-1 in infarcted reflow myocardium were significantly lower than that in AMI/R group(P<0.05 or P<0.01).(3)Atorvastatin could ameliorate myocardial function. CONCLUSION: Atorvastatin is effective in increasing NO and reducing ET-1 in blood plasma and local myocardium, and in protection of endothelial cells. Atorvastatin also has a beneficial effect on improving left ventricular function during acute myocardial infarction and reperfusion in rabbits.  相似文献   

12.
AIM: To investigate cardiomyocyte apoptosis and the expression of caspase-3, Bcl-2 and Bax after acute myocardial infarction (AMI) in rats.METHODS: AMI model was established with the ligation of left coronary artery in 78 randomly selected female SD rats.Twenty-four hours after operation, 43 survivors were randomly divided into 48-hour and 4-week two groups according to the time points: MI 48 h (n=11) and MI4 weeks (n=13) groups, sham-operated rats (S, n=27) were also randomly selected and reassigned to S48 h (n=10) and S4 weeks (n=10) groups.Cardiomyocyte apoptosis was detected with in situ terminal deoxynucleotidyl transferase (TdT)-dUTP nick-end labeling (TUNEL staining) and DNA gel electrophoresis.Caspase-3, Bcl-2 expression and Bax expression were detected with immunohistochemistry and Western blotting analysis.RESULTS: Compared with sham-operated group, after AMI, systolic, diastolic, and mean arterial blood pressures (SBP, DBP, MAP), left ventricular systolic pressure (LVSP) and the maximum change rate of left ventricular pressure rise and fall (±dp/dt) were significantly decreased (P<0.05, P＜0.01), while left ventricular end diastolic pressure (LVEDP) was significantly increased (P<0.05) in MI 48 h group.All the above indices in MI 4 weeks group had the same change as that in MI48h group, with the LVEDP significantly higher (P<0.01), except for a non-significantly change in SBP, DBP and MAP (all P>0.05).In both MI 48 h and MI 4 weeks groups, myocyte apoptotic index was significantly increased in the infracted/scar, border and non-infarcted areas (P<0.05,P＜0.01) with caspase-3 and Bax expressions increased significantly (P<0.05, P＜0.01) in myocytes of the above three areas and Bcl-2 expression increased only in myocytes of the infracted area in MI 48 h group.Western blotting indicated that Bcl-2/Bax ratio was also decreased in MI 48 h subgroup.CONCLUSIONS: After AMI in rats, cardiomyocyte apoptosis happened in the infarction/scar, border and non-infarcted areas, with caspase-3 and Bax expression in myocytes increased, and with Bcl-2 expression increased in myocytes of infracted area and Bcl-2/Bax ratio decreased only early after AMI.  相似文献   

13.
AIM: To investigate the evaluation method of left ventricular diastolic function and myocardial hypertrophy induced by pressure overload in rats.METHODS: Male Sprague-Dawley rats were subject to left ventricular pressure overload by transverse aortic constriction (TAC).Cardiac structure and diastolic function were evaluated by echocardiography, hemodynamic analysis and examination of hydroxyproline concentration in the myocardial tissues.RESULTS: Compared with the sham-operated controls, left ventricular wall dimension in diastole significantly increased in the rats 3 weeks after TAC .Left ventricular early diastolic posterior wall motion velocity (E') significantly decreased in the rats 3 weeks after TAC , and was much lower than that in the rats 6 weeks after TAC.Left ventricular mass to tibia length in TAC rats was much higher than that in sham-operated controls .The ratio of maximum rate of degression of left ventricular pressure (dp/dtmin) to left ventricular systolic pressure (dp/dtmin/LVSP) started to decrease in TAC rats in the 3rd week (48.9±5.9 vs 63.5±9.9) and significantly decreased in TAC rats in the 6th week as compared with sham-operated controls (35.4±4.0 vs 54.4±2.9, P<0.01).Sirius red-stained collagen in cardiac interstitium, especially around the blood vessels, was increased in TAC rats.Six weeks after TAC, a significant increase in the content of myocardial hydroxyproline was observed.CONCLUSION: The early diastolic posterior wall motion velocity (E') detected by tissue Doppler imaging is a sensitive indicator of diastolic dysfunction at the early stage of myocardial remodeling induced by pressure overload in rats.  相似文献   

14.
AIM:To observe the expression of corticotropin releasing hormone (CRH) within the paraventricular nucleus of hypothalamus (PVN) and to explore the relationship between the activated CRH-containing neurons and sympathetic activity in rats with heart failure (HF).METHODS:Healthy male Sprague-Dawley (SD) rats were subjected to coronary artery ligation to induce HF,and chronic intracerebroventricular (ICV) infusion was performed by osmotic pump for 4 weeks.The rats in sham group and HF group were given vehicle (VEH;artificial cerebrospinal fluid 0.25 μL/h).The rats in HF plus treatment group were treated with CRH competitive inhibitor αh-CRH (15 mg/h).Meanwhile,the Lewis rats and Fischer 344 rats for control study also underwent coronary ligation to induce HF or sham surgery.After 4 weeks,left ventricular end-diastolic pressure (LVEDP) and maximum positive/negative change in pressure over time (±dp/dtmax) were determined.The right ventricular-to-body weight (RV/BW) and lung-to-body weight (lung/BW) ratios were calculated.The renal sympathetic nerve activity (RSNA) was recorded and the plasma norepinephrine (NE) level was measured.The expression of CRH in the PVN combined with the plasma adrenocorticotrophic hormone (ACTH) levels were measured.RESULTS:Compared with the sham-SD rats,the HF-SD rats had a greater number of CRH positive neurons in the PVN (accordingly the plasma ACTH levels were increased),accompanied by decreased±dp/dtmax and increased RSNA,plasma NE,LVEDP,lung/BW and RV/BW.However,ICV treatment with αh-CRH attenuated these changes in the HF-SD rats (P<0.05).Compared with the sham-Fisher 344 rats,the HF-Fisher 344 rats also had a greater number of CRH positive neurons in the PVN (accordingly the plasma ACTH levels were increased).In addition,they had significantly increased RSNA and plasma NE level,higher LVEDP,RV/BW and lung/BW,and lower±dp/dtmax(P<0.05).Compared with the SHAM-Lewis rats,the HF-Lewis rats had not significantly changed in the above parameters.CONCLUSION:In CHF,the CRH-containing neurons in PVN are activated,thus aggravating cardiac function by increasing sympathoexcitation.  相似文献   

15.
AIM: To investigate the cardiac AMP-activated protein kinase (AMPK) activity and the effects of AMPK activator on cardiac structure and function in the mice with different β-adrenoceptor (β-AR) stimulation patterns. METHODS: Male BALB/c mice were subcutaneously injected with AMPK activator (AICAR, 250 mg· kg-1·d-1) or saline, and infused with β-AR agonist isoproterenol (ISO, 5 mg·kg-1·d-1) for 14 d. The cardiac functions were evaluated by echocardiography or hemodynamic method, and the hearts were harvested after infusion cessation immediately or 3 d later. Phosphorylated AMPK (p-AMPK) was measured by Western blot. RESULTS: Sustained ISO infusion increased p-AMPK level. AICAR did not further increase p-AMPK but attenuated ISO-induced increase in heart weight. Sustained ISO infusion increased cardiac systolic function as indicated by left ventricular fractional shortening (FS) and maximum rate of pressure rise (+dp/dtmax). The cardiac systolic function was not further increased by AICAR. The cardiac diastolic function as indicated by left ventricular end-diastolic pressure (LVEDP) was not different in each group. In contrast, cardiac p-AMPK level was similar between the control mice and the mice with sustained ISO infusion and ceased infusion for 3 d. In this model, AICAR improved the cardiac systolic and diastolic functions, which were impaired by ISO. Moreover, the increased pattern of p-AMPK level was similar with that of heart rate upon ISO stimulation. CONCLUSION: Sustained ISO infusion increases p-AMPK. After ISO infusion cessation for 3 d, p-AMPK is decreased to the basal level. β-AR-induced inotropic effects should be avoided to investigate the cardioprotective role of AMPK activation in the β-AR stimulation models.  相似文献   

16.
AIM: To investigate the role of mitochondrial calcium uniporter (MCU) in the cardioprotection by hypoxic preconditioning (HPC) and its relationship to mitochondrial permeability transition pore (MPTP). METHODS: Intraventricular balloon technique was employed to measure the left ventricular developed pressure (LVDP), the maximum rise/fall rate of left ventricular pressure (±dp/dtmax), and the left ventricular end-diastolic pressure (LVEDP) in Langendorff isolated rat heart. The hypoxia was achieved by ligation of left anterior coronary artery for 30 min followed by release of ligation for 120 min as reoxygenation. Hypoxic preconditioning was set as two episodes of 5 min global hypoxia and 5 min reoxygenation. RESULTS: Both HPC and treatment with ruthenium red (5 μmol/L) during the first 10 min reoxygenation improved recovery of LVDP, ±dp/dtmax and decreased LVEDP, which was associated with reduced infarct size and lactate dyhydrogenase release. These protective effects were attenuated by treatment with spermine (20 μmol/L) during the first 10 min reoxygenation. Administration of cyclosporin A (0.2 μmol/L) during the last 5 min of hypoxia period and first 15 min of reoxygenation period reduced the injury effect by spermine. CONCLUSION: These results indicate that inhibition of MCU is involved in the cardioprotection of HPC via inhibiting MPTP.  相似文献   

17.
AIM:To observe the effects of glycine on hypoxia-reoxygenation (H/R)-induced myocardial dysfunction, and to further clarify the protection of glycine (GLY) against myocardial ischemia/reperfusion injury and its mechanism. METHODS:A cardiac H/R model was established using a Langendorff isolated heart preparation. The left ventricular systolic pressure (LVSP), left ventricular end diastolic pressure (LVEDP), left ventricular developed pressure (LVDP), the maximum rising and dropping rates of left ventricular pressure (dp/dtmax and dp/dtmin) were observed. The coronary effluents at different time points were collected respectively to detect the concentration of superoxide dismutase (SOD) and malondialdehyde (MDA). RESULTS: The indexes of cardiac functions in H/R group were lower than those in other groups. After H/R, the indexes in GLY plus H/R group were higher than those in H/R group. Glycine inverted the effects of the decrease in SOD and the increase in MDA concentrations induced by H/R. CONCLUSION:Glycine ameliorates the cardiac functions under the condition of hypoxia-reoxygenation injury in isolated rat hearts. The mechanisms may be related to suppressing lipid peroxidation.  相似文献   

18.
AIM and METHODS:To investigate the cardioprotective effect of adenosine infusion before ischemic preconditioning on immature myocardial reperfusion injury in rabbit heart. Isolated perfused working heart model were performed, all hearts were subjected to 2-hour global hypothermic ischemia and received intermittent cold cardioplegia perfusion.RESULTS:During reperfusion, the recovery of left ventricular systolic pressure, left ventricular end-diastolic pressure, +dp/dtmax, and -dp/dtmax of hearts received adenosine infusion before ischemic preconditioning were significantly improved, myocardial adenosine triphosphate and adenosine diphosphate content and superoxide dismutase activity were higher, the leakage of myocardial creatine kinase and the malondialdehyde content were lower, and myocardial water content was obviously less.CONCLUSION:These results suggest adenosine infusion before ischemic preconditioning enhances cardioprotection of ischemic preconditioning against immature myocardial reperfusion injury in the rabbit heart.  相似文献   

19.
AIM: To determine the effects of valsartan on calcium channel and sodium-calcium exchanger current in isolated ventricular myocytes of congestive heart failure (CHF) rats. METHODS: Eight weeks after coronary ligation, the rats with heart failure were confirmed by measuring the hemodynamic parameters and divided randomly into the group treating with valsartan (CHF-T, 20 mg/kg) and placebo (CHF-C). Sham-operated group rats served as negative controls (PS). Twelve weeks later, 6 rats were selected randomly for the study of ion channel. Single ventricular myocytes of rats were isolated by enzymatic dissociation. The whole-cell patch-clamp recording technique was used to record calcium channel current and sodium-calcium exchanger current. RESULTS: (1) In the hemodynamic variables, HR and blood pressure were not significantly different in three groups. Compared CHF-C with PS group, LVEDP and Cm increased, LVSP and ±dp/dtmax decreased (P<005). Compared CHF-T group with CHF-C group, LVEDP and Cm decreased, LVSP and ±dp/dtmax increased (P<005). (2) Calcium channel current in CHF-C decreased significantly (P<005). Calcium channel current in CHF-T group was larger significantly than that in CHF-C group (P<005). (3) The activation, inactivation and recovery curves were not altered in 3 groups (P>005). (4) Na+-Ca2+ exchanger current in CHF-C group increased significantly. Na+-Ca2+ exchanger current in CHF-T group was smaller significantly than that in CHF-C group. However, CHF-T group and PS group were not significantly different. CONCLUSION: Administration of valsartan is effective in preventing from cardiac function deterioration, increases calcium channel current and decreases Na+-Ca2+ exchanger current in ventricular myocytes of heat failure rats.  相似文献   

20.
AIM:To investigate the alterations of phospholamban (PLB) expression and cardiac sarcoplasmic reticulum (SR) Ca2+-ATPase activity,and the change of cardiac function in rats with diabetes mellitus (DM).METHODS: The diabetes mellitus in male Wistar rats was induced by intraperitoneal injection of streptozotocin.The levels of PLB mRNA and PLB protein,the activity of SR Ca2+-ATPase and the left ventricular hemodynamics parameters were measured 4　weeks,6 weeks and 8 weeks after DM was induced in rats,while the normal rats served as control group.RESULTS: There was no significant difference in PLB mRNA level and protein level between 4-week-DM rats and normal control rats.6-week-DM rats and 8-week-DM rats had markedly increased PLB mRNA and protein level compared with normal control rats.SR Ca2+-ATPase activity was not significantly changed in 4-week-DM rats compared with normal control rats,and was markedly depressed in 6-week-DM rats and 8-week-DM rats.LVSP,LVEDP and ±dp/dtmax were not significantly changed in 4-week-DM rats compared with normal control rats.In 6-week-DM rats and 8-week-DM rats,LVSP and ±dp/dtmax were decreased,LVEDP was increased compared with normal control rats.CONCLUSION: The elevated levels of PLB mRNA and PLB protein contribute to SR Ca2+-ATPase activity reduction,which leads to cardiac dysfunction in DM rats.  相似文献   

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