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1.
AIM: To investigate the effect of volatile anesthetics on function,metabolism,ATPase activity and free radicals in isolated ischemia /reperfusion (I/R) rat hearts.METHODS: 136 SD rats were anesthetized with pentobarbital and randomly divided into six groups and 17 sub-groups (n=8),according to the given drug.In a normal thermal isolated Langendorff rat heart model,four volatile anesthetics in 1.5 MAC concentration were given before global ischemia 25 min and during reperfusion 30 min.Coronary flow (CF),LVEDP,left ventricular developed pressure (LVDP),±dp/dt were monitored at 15 min of equilibrium,15 min of drug treatment,the end of reperfusion.Myocardial adenosine triphosphate (ATP),malodialdehyde (MDA),activity of Ca2＋-ATPase and Na＋-K＋-ATPase,and superoxide dismutase (SOD) were determined at 15 min of equilibrium,15 min of drug treatment or absence,10 min global ischemia and the end of reperfusion.RESULTS: CF and LVEDP were increased significantly after exposured to volatile anesthetics 15 min,and LVDP,+dp/dtmax were significantly decreased.However,LVDP and +dp/dtmax were increased at the end of reperfusion in the treated groups.HR in halothane and isoflurane groups was decreased before ischemia and after reperfusion.The myocardial ATP content was significantly increased before and after ischemia in the treated groups.At the end of reperfusion,the activity of SOD was significantly higher and myocardial MDA content was significantly lower in the treated groups than those in control group.The activity of Ca2＋-ATPase,compared with the control group,was markedly decreased before ischemia in halothane,enflurane and isoflurane group.Nonetheless,the activity of Ca2＋-ATPase was clearly increased in the treated groups during ischemia and at the end of reperfusion.The activity of Na＋-K＋-ATPase was only enhanced in halothane group at the end of reperfusion among groups.CONCLUSION: The volatile anesthetics depress myocardial systolic function.There are markedly protective effects against myocardial I/R injury.Meanwhile,the volatile anesthetics improve the recovery of function and metabolism,and increase CF and the activity of Ca2＋-ATPase and Na＋-K＋-ATPase in rats.  相似文献   

2.
AIM: To study the effects and mechanism of peroxisome proliferator-activated receptors (PPARs) ligands,fenofibrate and pioglitazone,on ventricular remodeling in pressure overload rats.METHODS: A pressure overload model was established by the constriction of abdominal aorta in Wistar rats.The hemodynamics and ventricular remodeling parameters,plasma and myocardial renin activity,angiotensin Ⅱ and aldosteron,the mRNA expression of angiotensin Ⅱ type 1 receptor (AT1) were investigated in the constriction of abdominal aorta group (CAA group,n=7) at 12-week after operation and treated experimental groups in which rats were treated with fenofibrate (F group,n=8),pioglitazone (P group,n=7),concomitant fenofibrate and pioglitazone (F+P group,n=6) for 12 weeks since 2 days after operation.The sham-operated rats served as controls (n=8).RESULTS: The ratio of left ventricular weight to body weight,mean arterial pressure,left ventricular systolic pressure,left ventricular end diastolic pressure,left ventricular systolic pressure and heart rate were significantly lower,the maximum left ventricular pressure rising and declining rates(±dp/dtmax) were significantly higher in all treated experimental groups than those in CAA group.Fenofibrate or pioglitazone had no effect on plasma and myocardial levels of renin,angiotensin Ⅱand aldosteron.The mRNA expression of AT1 was downregulated in treated groups except F group.CONCLUSION: PPAR ligands have no effect on plasma and myocardial levels of renin,angiotensin Ⅱand aldosteron,but fenofibrate and pioglitazone inhibit ventricular remodeling,decrease preload and afterload,increase ±dp/dtmax in pressure overload rats.The expression of mRNA of AT1 is downregulated in myocardium of pressure overload rats by the PPARγ signaling pathway.  相似文献   

3.
AIM: To observe the effect of exogenous spermine (low concentration) on myocardial ischemia/reperfusion injury in rats.METHODS: 40 Wistar rats were randomly divided into 4 groups: sham- operation group (Sham), ischemic reperfusion group (I/R), spermine group (Sp) and natural saline group (NS). The model of ischemic/reperfusion injury was established by ligating rat coronary artery. In Sp group, spermine (0.5 mmol/L, 2 mL/kg) was injected slowly into rat vein. During the process, we recorded the electrocardiogram and the LV functional parameters, assayed the levels of SOD, LDH, NO and MDA in serum, and examined the ultrastructure of the myocardium. RESULTS: In I/R group, the incidence of arrhythmia was 90%, myocardial ultrastructure was injured seriously, values of LVSP and ±dp/dtmax decreased, levels of LDH, NO and MDA increased while SOD activity decreased (P<0.05 or P<0.01, compared with Sham group). Compared with I/R and NS group, all those indexes in Sp group changed significantly (P<0.05 or P<0.01). CONCLUSION: Exogenous spermine alleviates myocardial ischemia/ reperfusion injury in rats. The mechanism may be related to its antioxidant effect and relieving the injury caused by oxygen free radical.  相似文献   

4.
AIM: To investigate the expression of calcium sensing receptor(CaSR) during myocardial injury induced by ischemia/reperfusion and disclose the relationship between CaSR and myocardial ischemia/reperfusion. METHODS: The experimental model was established by the 30 min ligating and 1 h, 2 h, 4 h, 6 h reperfusing the left descending coronary artery (LAD) in rats. Wistar rats were randomly divided into 5 groups: sham group, ischemia/reperfusion 1 h, 2 h, 4 h, 6 h groups (I/R 1 h, 2 h, 4 h, 6 h group). CaSR mRNA expression was detected by RT-PCR. Left ventricular function was recorded. The levels of plasma lactate dehydrogenase (LDH), alondialdehyde (MDA) and superoxide dismutase (SOD) were measured. The change of ultrastructure in the ischemia/reperfusion myocardium of rats was observed by electron microscopy. RESULTS: LVSP,±dp/dtmax and SOD activity decreased gradually with the reperfusion time prolonged. LDH and MDA peaked at 2 h. The ultramicro-structural injury at the 1 h and 2 h was more serious than that at 4 h and 6 h. The expression of CaSR increased significantly after reperfusion of 1 h and 2 h, and decreased after 4 h and 6 h. CONCLUSION: The increased expression of CaSR mRNA and serious injure of myocardium were observed. CaSR may be associated with the myocardial ischemia/reperfusion injury.  相似文献   

5.
AIM: To investigate the protective effects and mechanisms of modified acidic fibroblast growth factor (maFGF) in anoxic reperfusion of rat hearts. METHODS: Using Langendorff apparatus, we established the model of anoxia/reperfusion of isolated hearts to compare the protective effects of maFGF and acidic fibroblast growth factor (aFGF). The changes of left ventricle development pressure (LVDP) and maximal rates of rise of ventricular pressure(dp/dtmax), maximal rates of decline of ventricular pressure (dp/dtmin) were determined, changes of LDH and MDA levels，SOD activity in efflux from coronary artery were also detected at different time point. RESULTS: Pretreatment with maFGF and aFGF produced a similar protective effect on myocardium during anoxia /reperfusion, including promoting obviously heart functional recovery after myocardial anoxia/reperfusion and reversing changes of LDH, MDA contents and SOD activity induced by anoxic/reperfusion. CONCLUSION: maFGF has a protective effect on anoxia/reperfusion heart, and the mechanism of this effect may be related to suppression of lipid peroxidation.  相似文献   

6.
AIM: To investigate the effects of angiotensin converting enzyme inhibitor (ACEI), benazepril (B), on cardiac function , free oxygen radicals, sarcoplasmic reticulum(SR) Ca2+-ATPase following ischemia-reperfusion in sportaneously hypertensive rats (SHRs). METHODS: Thirty 10-week-old female SHRs were randomly assigned into two groups: group SHR was control; The animal in group SHR+B was given with 10 mg/kg of benazepril per day. Another 15 Wistar rats with the same age and sex were normal control (group Wistar). After 12 weeks of pretreatment, all rats in each group were subjected to 30 min of left anterior descending coronary artery occlusion and 30 min of reperfusion. Hemodynamic parameters, left heart-to-body weight ratio (LVW/BW), myocardial malondialdehyde (MDA) concentration, superoxide dismutase (SOD) activity, and SR Ca2+-ATPase activity were measured. RESULTS: Compared to group Wistar, the rats in group SHR had higher blood pressure, LVW/BW and myocardial MDA concentration, more serious left cardiac function injury and lower myocardial SOD activity and SR Ca2+-ATPase activity; group SHR+B had lower myocardial MDA concentration, higher myocardial SOD activity, but no difference in blood pressure, LVW/BW, the degree of left cardiac function injury and myocardial SR Ca2+-ATPase activity. CONCLUSION: Benazepril can attenuate ischemia-reperfusion-induced cardiac function injury by regression of left ventricular hypertrophy (LVH), improving SR Ca2+-ATPase activity and decreasing oxygen free radicals injury in SHRs.  相似文献   

7.
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   

8.
AIM: To investigate the effect of hydrogen sulfide (H2S) donor (NAHS) on oxidative stress of adriamycin-induced dilated cardiomyopathy rats. METHODS: Weight-matched adult male Wistar rats were randomly divided into 5 groups as follows: (1) ADR group (n=12), in which 2.5 mg/kg of adriamycin was injected intraperitoneally once a week for 10 weeks (total dose of 25 mg/kg). (2) ADR+small-dose NaHS group (n=12), in which the dosage and the use of adriamycin were as mentioned above, while NaHS solution was injected to rats at a dosage of 2.8 μmol·kg-1·d-1 at the same time. (3) ADR + large-dose NaHS group (n=12), in which the dosage and the use of adriamycin were as mentioned above, while NaHS solution was injected to rats at a dosage of 14 μmol·kg-1·d-1 at the same time. (4) Control group (n=9), in which an equivalent volume of physiological saline was administered weekly for a total of 10 weeks. (5) NaHS group (n=9), in which 14 μmol/kg of NaHS solution was injected to rats intraperitonealy once a week for 10 weeks. Hemodynamic and echocardiographic measurements were obtained 10 weeks after the treatment. Meanwhile, H2S and malondialdehyde (MDA) concentrations, the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in serum and myocardial tissues were evaluated, respectively. RESULTS: The cardiac functions in the group of ADR rats depressed obviously. H2S concentrations, SOD and GSH-Px activities in serum and myocardial tissues of ADR group rats were all significantly decreased as compared with those in the control group (P<0.01). The MDA concentrations in serum and myocardial tissues in ADR group rats were both increased significantly (P<0.01). Exogenous administration of H2S donor NaHS markedly attenuated ADR-induced cardiac dysfunction, and MDA concentration in myocardial tissues was significantly reduced (P<0.01). Serum SOD activity was obviously increased in ADR+large-dose NaHS group compared with control group (P<0.01), and GSH-Px activity in myocardial tissues was markedly increased in ADR+large-dose NaHS group compared with control group (P<0.05). CONCLUSION: H2S might play an important role in the development of adriamycin-induced dilated cardiomyopathy. Administration of exogenous H2S effectively improves myocardial contractile activity, reduces the accumulation of lipid peroxides and increases the capability of antioxidants to inhibit oxidative stress and prevents myocardial damage.  相似文献   

9.
AIM:To determine the relationship between microhistology and cardiac contractility in myocarditis animal model. METHODS: Setting up myocarditis animal model by injecting Coxsackivevirus B3 (CVB3) into mice, then observed myocardial morphological changes and measured left ventricular function of mice at the time of first three days and two weeks after injecting CVB3. RESULTS:Subcellular structure (mitochondria) changed at the first three days after injecting CVB3. The left ventricular pressure (LVP) and the rate of intraventricular pressure development (dp/dt) which is the index of reflecting cardiac contractility depressed in this stage (14.2±0.8) kPa and (273.1±10.0)kPa/s, respectively. There were (17.1±0.7)kPa and (359.8±9.3)kPa/s in normal mice, respectively (P＜0.01). Myocardial lesions were more severe during immune response stage-two weeks after injecting CVB3, including myocardial inflammation and necrosis. LVP was (11.8±0.2)kPa and dp/dt was (209.5±6.1)kPa/s in immune response stage. There was significant difference between mice with myocarditis at early stage and at immune response stage (P＜0.01).CONCLUSIONS:The factor of causing the depression of cardiac contractility in early stage (virus-induced damage) is mainly change of subcellular structure. Mitochondria cannot provide energy as normal. There were more severe myocardial lesions in later stage (cell-mediated autoimmune response)than in early stage. The depression of cardiac contractility is a consequence of multifactor.  相似文献   

10.
AIM: To study the protection of Glycyl-L-Glutamine(Gly-Gln) against myocardial ischemia/reperfusion(I/R) injury in the isolated rat heart.METHODS: A model of myocardial ischemia-reperfusion injury was established with a Langendorff apparatus. Thirty male SD rats were randomly divided into four groups: control group, Gly-Gln group, I/R group and I/R+Gly-Gln group. Both I/R and I/R+Gly-Gln group were pre-perfused for 30 min, followed by 20 min ischemia and 40 min reperfusion. During reperfusion I/R+Gly-Gln group was perfused with Gly-Gln perfusate. Control group was kept perfused for 90 min. Gly-Gln group Gly-Gln perfusate was also kept perfused for 90 min. The left ventricular end-diastolic pressure(LVEDP), left ventricular developed pressure (LVDP), ±dp/dtmax, heart rate (HR), monophasic action potentials(MAP) was measured during perfusion. The coronary effluent fluid was collected at different certain times. The activities of lactic dehydrogenase (LDH) and creatine kinase(CK) were determined.RESULTS: The isolated rat heart function decreased severely after 20 min ischemia and 40 min reperfusion(I/R): the LVEDP increased and the LVDP, ±dp/dtmax decreased. But the LVEDP decreased and the LVDP, ±dp/dtmax increased in I/R+Gly-Gln group compared with I/R group. Moreover, the activities of LDH and CK in the coronary effluent fluid decreased remarkably in I/R+Gly-Gln group compared with I/R group.CONCLUSION: Gly-Gln can play a protective role against myocardial I/R injury in isolated rat hearts via maintaining the left ventricular function and decreasing the release of LDH and CK.  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 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   

13.
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   

14.
AIM：To investigate the effect of ginkgo-dipyridamole injection (GD) on ischemia/reperfusion (I/R) injury in rat hearts in vitro and its possible mechanism. METHODS：Forty male Sprague-Dawley rats were randomly divided into 5 groups (n=8): normal control (NC) group, I/R group, ischemic preconditioning (IPC)+I/R group, GD+I/R group and GD+LaCl3+I/R group. Cardiac function indexes, including heart rate (HR), left ventricular systolic pressure (LVSP) and the maximal rise/fall rate of left ventricular pressure (±dp/dtmax), were detected at 5 time points, including stabilizing point, 30 min after ischemia, and 5, 30 and 60 min after reperfusion. The activity of lactate dehydrogenase (LDH) and creatine kinase (CK) in coronary effluent at the five time points was assayed. The concentration of Ca2+ and the content of α-ketoglutarate dehydrogenase (α-OGDH) in myocardial mitochondria were determined at the end of the whole experiment. RESULTS：Compared with I/R group, the cardiac function indexes in IPC+I/R and GD+I/R groups were improved at the reperfusion period (P<0.05), the activity of LDH and CK in coronary effluent and the concentration of Ca2+ in mitochondria were significant reduced (P<0.01), and the content of α-OGDH was increased (P<0.05). However, the protective effect of GD was inhibited by LaCl3 (P<0.05). CONCLUSION：GD protects rat hearts against I/R injury by inhibiting calcium overload and improving mitochondrial enzyme activity to stabilize mitochondrial energy metabolism.  相似文献   

15.
AIM:To investigate whether glycine receptor is involved in the protection of glycine against anoxia/reoxygenation injury in cardiomyocytes by detecting oxygen free radical metabolism, apoptosis and intracellular calcium overload. METHODS:The neonatal rat cardiomyocytes were cultured and exposed to anoxia and reoxygenation (A/R) in the presence of glycine receptor antagonist, glycine or in free chloride buffer. The superoxide dismutase (SOD) activity, the contents of malondialdehyde (MDA) and nitric oxide (NO), the intracellular free calcium concentration and the apoptotic rate in the cardiomyocytes were determined. RESULTS:SOD activity and NO content in cardiomyocytes were lower, but MDA content, intracellular free calcium concentration and apoptotic rate in cardiomyocytes were higher in A/R group than those in control. Pretreatment with glycine inhibited the above changes caused by A/R, which was reversed by strychnine treatment and in the free chloride medium. CONCLUSIONS:Glycine inhibits free radical production, attenuates calcium overload, decreases apoptotic rate and increases SOD activity and NO release in cardiomyocytes exposed to A/R. These findings suggest that glycine exerts a protective effect against A/R injury via glycine receptor and glycine protects the neonatal rat cardiomycytes from A/R-induced injury in a chloride-dependent manner.  相似文献   

16.
Wang Li-Ping 《园艺学报》2014,30(10):1760-1764
AIM:To explore the effect of erythropoietin （EPO） on the expression of myocardial NADPH oxidase （Nox） in the pressure overload rats. METHODS:Male SD rats (n=36) were used to establish a pressure overload myocardial hypertrophy model by abdominal aorta ligation. The animals were divided into model group, control group (sham, without narrowing abdominal aorta, the rest of the operation was the same as the model) and recombinant human erythropoietin (rhEPO) treatment group (intraperitoneal injection of rhEPO postoperatively, 4 000 U/kg, twice a week). After 8 weeks, the cardiac ultrasound imaging and hemodynamic evaluation were conducted to determine the cardiac functions. Masson staining was used to observe the degree of myocardial fibrosis. The expression of Nox2 and Nox4 at mRNA and protein levels was detected by real-time quantitative PCR and Western blotting. The protein levels of myocardial inflammatory factors CD45, F4/80 and TGF-β were determined by Western blotting. RESULTS:Compared with model group, the left ventricular ejection fraction (LVEF), left ventricular fractional shortening (LVFS), left ventricular end-systolic pressure (LVESP) and left ventricular pressure maximum rising and falling rates (±dp/dtmax) increased significantly in EPO treatment group (P<0.01). At the same time, left ventricular end-systolic diameter (LVESD), left ventricular end-diastolic diameter (LVEDD) and left ventricular end-diastolic pressure (LVEDP) were decreased in EPO treatment group (P<0.01). EPO reduced the degree of myocardial fibrosis caused by pressure overload (P<0.01) and decreased the expression of Nox2 and Nox4 at mRNA and protein levels in the myocardium (P<0.05 or P<0.01), and reduced the protein expression of myocardial inflammatory factors CD45, F4/80 and TGF-β. CONCLUSION: EPO inhibits rat myocar-dial fibrosis induced by pressure overload, improves heart functions by decreasing NADPH oxidase activity and inhibiting myocardial oxidative stress levels and myocardial inflammatory reaction.  相似文献   

17.
AIM: To investigate the characteristics of adaptation of the heart to high altitude in Tibetan antelope.METHODS: Both Tibetan antelope and Tibetan sheep were captured at altitude of 4 300 m and then transported to Gurmud (2,800 m), where the study was conducted immediately after arrival. The heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DBP) and the maximum rate of change in left ventricular pressure (±dp/dt) were measured directly by cardiac catheterization. After the baselines of the parameters were obtained, the animals were inhaled hypoxic gas of 14.6% O2 or 12.5% O2, which was simulated to the altitudes of 5,300 m and 6,300 m, and then those measurements were repeated within 15 min. The ratios of heart weight to body weight (HW/BW) and right to left ventricular plus septum weights were determined.The Ultra-structural changes of the cardiac muscle were also observed under electron microscope.RESULTS: The HW/BW of Tibetan antelope was significantly greater than that of Tibetan sheep (P<0.01), and no difference of RV/(LV+IVS) was observed between both animals. At baselines, HR and SBP of Tibetan antelope were significantly lower than those of Tibetan sheep . The value of +dp/dt in Tibetan antelope was similar to that of Tibetan sheep . However, after inhaled 14.6% or 12.5% hypoxic-gas for simulating the altitudes of 5,300 m and 6,300 m, the +dp/dt of Tibetan antelope was significantly increased to 145.1% and 148.1% respectively, while the Tibetan sheep was decreased to 68.4% and 70.5% of those in normoxia condition, respectively. Ultra-structural changes of the cardiac muscle indicated that there were more abundant mitochondria in the myocardium of the Tibetan antelope than those in the Tibetan sheep.CONCLUSION: The heart functions of Tibetan antelope are well adapted to hypoxic environment in the high altitude by increasing myocardial weight and mitochondria. On the other hand, the cardiac contractility of Tibetan antelope is normal in the rest, but obviously increases under stress conditions.  相似文献   

18.
AIM: To investigate the changes of Gq-phosphoinositide pathway in left ventricular tissue of rats with chronic heart failure in order to assess the role of this signal pathway in the formation of heart failure. METHODS: Male Sprague-Dawle rats were divided into three groups: control, chronic heart failure and benazepril therapy group. Chronic heart failure was induced with adriamycin. Rats in benazepril group received benazepril 10 mg·kg-1·d-1 and adriamycin at the same time. Hemodynamic measurement was carried out after 4 weeks. The expression of Gα q/11 protein in left ventricle was detected by Western blotting analysis and activity of phospholipase C was measured by the method of hydrolysis of nuclear substrate. RESULTS: Compared with control group, the ±dp/dtmax in chronic heart failure group significantly decreased, and protein Gα q/11 expression, basic and stimulated phospholipase C activity significantly increased (P<0.01). The ±dp/dtmax in benazepril group was significantly lower than that in control but obviously higher than that in chronic heart failure group (P<0.05). Gα q/11 expression, basic and stimulated phospholipase C activity in benazepril group were significantly higher than those in control but obviously lower than those in heart failure group (P<0.01). CONCLUSION: Gq-phosphoinositide signaling pathway may play a role in the formation of chronic heart failure. Benazepril partialy attenuates the activation of phosphoinositide signaling pathway.  相似文献   

19.
AIM: To observe the effect of glycine liposomes on the mitochondrial membrane potential and the apoptosis rate in cardiomyocytes induced by hypoxia/reoxygenation injury. METHODS: A cardiomyocyte injury model was established by using hypoxia/reoxygenation. DiOC6(3) as fluorescence molecular probe was used to detect the mitochondrial membrane potential in each group. The method of Annexin V associated with PI was used to detect the apoptosis ratio in each group. RESULTS: (1) The result of flow cytometry showed that the mitochondrial membrane potential of cardiomyocytes in H/R group was obviously lower than that in control group (P<0.01). The decrease in mitochondrial membrane potential in Gly-liposome group was the lowest, the percentage of cells about the part of hypofluorescence was (9.61±0.76)%, which was lower than that in glycine group (P<0.01). (2) The apoptosis rate of cardiomyocytes in H/R group was higher than that in control group (20.78±1.58)%,P<0.01. After the treatment of Gly-liposome, the apoptosis rate of cardiomyocytes was lower than that in glycine group (P<0.01). No difference in the apoptosis ratios between blank-liposome group and H/R group was observed(P>0.05).CONCLUSION: Glycine liposomes protect cultured cardiomyocytes against hypoxia/reoxygenation injury. Glycine liposomes produce the better protective effects than glycine.  相似文献   

20.
AIM: To investigate the effects of external counterpulsation (ECP) on the hemodynamics indexes and endothelin-1 (ET-1) in myocardial ischemia canines. METHODS: Nineteen health dogs were randomly divided into controls, ischemia and ECP groups. The blood pressure, left ventricular systolic and diastolic pressure, +dp/dtmax and -dp/dtmax, brachiocephalic trunk blood flow were recorded. Plasma and myocardium ET-1levels were determined by radioimmunoassay. RESULTS: 60 minutes after left anterior descending of coronary artery ligation, compared with controls, the blood pressure decreased greatly, left ventricular systolic and diastolic function declined, brachiocephalic trunk blood flow reduced, but plasma ET-1 levels were increased significantly in ischemia and ECP groups (P<0.05). After 2 h ECP treatment, compared with ischemia, blood pressure increased, left ventricular systolic and diastolic function improved, brachiocephalic trunk blood flow raised, but the plasma and myocardium ET-1 levels were decreased in ECP group (P<0.05). CONCLUSION: The results suggest that ECP improves the hemodynamics indexes in myocardial ischemia canine, and ET-1 may play an important role.  相似文献   

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