首页 | 本学科首页   官方微博 | 高级检索  
相似文献
 共查询到20条相似文献，搜索用时 31 毫秒
1.
AIM: To study the effects of 1. 5 MAC halothane and sevoflurane on ischemic myocardium. METHODS: The isolated rat heart were perfused with halothane and sevoflurane and HR, LVEDP, LVDP, +dp/dt, -dp/dt, coronary flow (CF), the myocardial ATP content and Ca2+-ATPase activity were determined before and 10 min and 25 min after ischemia. In the meantime, LVP was recorded during 25 min ischemia. RESULTS: 1. 5MAC sevoflurane significantly increased CF in normal isolated rat hearts. Both halothane and sevoflurane depressed myocardial contractile function, increased normal myocardial energy storage. After 10 min ischemia, the decrease of myocardial ATP content were slowed down by halothane and sevoflurane, especially halothane. During 25 min of ischemia, the onset time of contracture was significantly delayed, and the contracture intensity was alleviated by halothane, but not sevoflurane. CONCLUSION: Halothane has better protective effect on ischemic myocardium than sevoflurane through preventing the decrease of myocardial ATP content and Ca2+-ATPase activity during ischemia.  相似文献   

2.
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   

3.
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   

4.
AIM: To investigate the effect of dexamethasone (DEX) preconditioning on reperfusion arrhythmia. METHODS: 46 Sprague-Dawley rats were divided randomly into DEX and control (CON) group, the rats were pretreated with DEX or sodium chloride before their hearts were separated for Langendorff perfusion and for ischemia/reperfusion. The reperfusion arrhythmias were observed dynamically after 60 min reperfusion following 30 min ischemia. The expression of HSP72 in myocardium was examined by Western blotting and immunohistochemistry at reperfusion 60 min. The levels of malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) and the activities of Na+-K+-ATP ase, Ca2+-Mg2+-ATPase on myocardial plasma membrane were detected. RESULTS: Compared with control group, the accumulated points and persistence time of ventricular arrhythmia were reduced significantly in DEX group (P<0.05), the expression of HSP72 was significant upregulated (P<0.05), the level of MDA was reduced significantly, the activities of SOD, CAT, GSH-Px and Na+-K+-ATPase were significantly higher (P<0.05). CONCLUSION: Dexamethasone pretreatment markedly reduces the reperfusion ventricular arrhythmias in rats, which may be attributed to upregulation of HSP72, SOD, CAT, GSH-Px , Na+-K+-ATPase and inhibition of lipid peroxidation.  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 analyze and compare the changes of pressure phase plane (PPP) derived τ and K on isolated rat heart during ischemia/reperfusion, and to explore the value of PPP derived τ and K for evaluation of left ventricular diastolic dysfunction. METHODS: LVEDP, -(dp/dt)max, τ and K were measured and calculated during ischemia/reperfusion in Sprague-Dawley rat hearts. Meanwhile, the level of lactate dehydrogenase (LDH) in the coronary effluent was measured, and the ultrastructure changes in myocardium were observed under electron microscope. RESULTS: Compared with control group, τ increased and K reduced significantly in each ischemic group in a time dependent manner (P<0.05). With prolonged ischemia, τ was even higher and K was even lower (P<0.05). Compared with control group, except ischemia 15 min, LDH in other groups increased significantly at 10 min and 20 min after reperfusion (P<0.05). Compared with ischemia 30 min, LDH of ischemia 45 min and ischemia 60 min were even higher at 10 min and 20 min after reperfusion (P<0.05). With prolonged ischemia, the abnormal changes of the myocardial ultrastructure were observed. CONCLUSION: PPP derived τ and K may be promising indexes for quantitative assessment of left ventricular diastolic function on isolated rat heart during ischemia/reperfusion, and indication of the severity of ischemia/reperfusion injury.  相似文献   

7.
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   

8.
AIM：To observe the sensitivity of myocardium to ischemia/reperfusion (I/R) injury in the rats with chest radiotherapy. METHODS：The radiation-induced heart disease model was established by local 20 Gy of X-ray irradiation in the chest. Male Wistar rats (n=42) were randomly divided into 6 groups:sham trauma group, trauma group, sham trauma+sham operation group, sham trauma +I/R group, trauma+sham operation group and trauma+I/R group. The rats were subjected to 30 min of ischemia and 1 h of reperfusion 2 week after trauma. The left ventricular developed pressure (LVDP) and ±dp/dtmax were recorded by BL-410 biological signal recording and analysis system. The serum cardiac troponin I (cTnI) and creatine kinase isoenzyme (CK-MB) were measured by ELISA. The myocardial infarct size was determined by nitroblue tetrazolium(NBT) staining method and BI2000 image analysis software. RESULTS：Compared with sham trauma+I/R group, significant decreases in LVDP and ±dp/dtmax were observed in trauma+I/R group (P<0.01) with significant increases in the infarct size and the concentrations of cTnI and CK-MB (P<0.01). CONCLUSION:Chest X-ray irradiation increases the sensitivity of myocardium to I/R injury in rats.  相似文献   

9.
AIM: To study the potential effects of lipoteichoic acid (LTA)-induced delayed preconditioning (PC) on cardioplegic arrest/reperfusion injury in donor rat heart. METHODS: The rats were pretreated with LTA (1 mg/kg, ip) 24 h before the experiment, and the isolated hearts were subjected to arrested by cardioplegic solution and stored in Eurocollin's solution for 4 h by the Langendorff method, and to evaluate the changes of cardiac function at the reperfusion for 30 min and 60 min, to measure the amounts of MB isoenzyme of creatine kinase (CK-MB), lactate dehydrogenase (LDH) and total nitric oxide (NO) oxidation products in the coronary effluent, and to detect myocardial apoptosis on tissue samples of left ventricle at the end of reperfusion by TUNEL staining. RESULTS: Pretreated with LTA significantly improved the recovery of cardiac function with a significant increase in coronary flow (CF), left ventricular developed pressure (LVDP), maximal rate of left ventricular developed pressure (+dp/dtmax), and minimal rate of left ventricular decline pressure (-dp/dtmax) at 30 min and 60 min of reperfusion (all P<0.01), reduced CK-MB (P<0.01) and LDH (P<0.01) release and raised the concentrations of NO2-/NO3- in coronary effluent. In addition, LTA pretreatment obviously decreased myocardial apoptosis in left ventricle at the end of reperfusion (P<0.01). The protective effects were abrogated by pretreatment of the rats with L-nitroarginine methyl eater (L-NAME, 10 mg/kg, ip). CONCLUSION: LTA pretreatment significantly improves cardiac function after cardioplegic arrest/reperfusion injury in donor heart of rats, and endogenous NO plays an essential role as an effector of delayed PC induced by LTA.  相似文献   

10.
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   

11.
AIM:To study the protective effect of hyperpolarized cardioplegic arrest on reperfused rat heart performance and to investigate the role of mitochondrial ATP-sensitive K+ channels (mitoKATP) opening in the protection of hyperpolarized cardioplegia against ischemia/reperfusion damage. METHODS:Forty Sprague-Dawley rats were randomized into five groups (n=8 in each group): control group (Con); depolarized arrest group (D); hyperpolarized arrest group (H); depolarized cardioplegia with 5-hydroxydecanoate (5-HD) group (5HD+D); hyperpolarized cardioplegia with 5-HD group (5HD+H). The rat hearts were quickly removed to Langendorff apparatus. The heart perfusion was performed for 20 min with 37 ℃ Krebs-Henseleit buffer balanced with gas mixture (O2∶〖KG-*2〗CO2=95%∶〖KG-*2〗5%) at 5.8 kPa perfusion pressure, then cardial arrest was induced by different cardioplegic solution. Hearts were subjected to ischemia at 37 ℃ for 40 min followed by 30 min reperfusion. (1) The hemodynamics was detected at recovery after 30 min reperfusion. (2) Before ischemia and at the end-reperfusion, tissue was harvested for mitochondrial isolation and ultrastructure was observed by transmission electron microscopy (TEM). (3) Production of reactive oxygen species (ROS) was also determined at different time points. RESULTS:(1) Compared with end-equilibration, 30 min reperfusion caused significant differences in left ventricular developed pressure (LADP), left ventricular end-diastolic pressure (LVEDP), double product (DP), heart rate (HR), coronary flow (CF) (P<0.01). TEM showed that the ultrastructures of myocardial and mitochondrial were damaged remarkably. (2) When H group was compared with D, 5HD+H and Con group, significant differences were found in LVDP, LVEDP, DP, HR and CF (P<0.01). TEM showed that the myocardial and mitochondrial ultrastructures were improved remarkably. (3) The rate of ROS generating was lower in group H than that in other four groups at end-reperfusion (P<0.01). CONCLUSION:(1) Of the four cardioplegias, hyperpolarized cardioplegia is superior to improve myocardial performance, attenuates myocardial and mitochondrial injury, and reduces rate of ROS generating. (2) Mitochondrial preservation is one of mechanisms of myocardial protection in hyperpolarized cardioplegia, opening of mitoKATP enhances cardioprotection through decreasing ROS generating, providing better energe supply for reperfused myocardium.  相似文献   

12.
AIM: To investigate the protective effect of fluvastatin and its influence on ICAM-1 mRNA expression in ischemia/reperfusion myocardium of normocholesterolemic rabbits. METHODS: 24 rabbits were divided into three groups randomly and myocardial ischemia/reperfusion model in the rabbit was made. Rabbits were subjected to 45 min of regional myocardial ischemia and 2 h of reperfusion. 10 mg·kg－1·d－1 fluvastatin were administered for one week. Dynamic index of blood flow was recorded and analyzed. Serum activity of CK, CKMB, LDH and LDH-1 were measured. The expression of ICAM-1 mRNA in ischemic myocardium was detected with semi-quantitative RT-PCR. RESULTS: In comparison with control group, pretreatment with fluvastatin decreased LVEDP at the whole observed duration, and spontaneously increased ±dp/dtmax. Serum activities of CK, CKMB and LDH-1 in control group were significantly higher than those in sham group, but heavily reduced in fluvastatin group. Increased expression of ICAM-1 mRNA due to ischemia reperfusion was reduced significantly in fluvastatin group compare to control group. CONCLUSION: Pretreatment of fluvastatin may reduce inflammation reaction in reperfused myocardium, and this may contribute to its protective effect against experimental myocardial ischemia reperfusion injury.  相似文献   

13.
AIM: To compare the effects of hypotensive and aggressive resuscitation strategies on blood loss, fluid requirements, hematocrit (Hct), tissue Na＋-K＋-ATPase and Ca2＋-Mg2+-ATPase activities in a clinically relevant model of uncontrolled hemorrhagic shock in pregnancy rabbits. METHODS: Thirty anesthetized New Zealand white rabbits at mid and late gestation underwent uncontrolled hemorrhagic shock by transecting a small artery of mesometrium, followed by bleeding via carotid artery to mean arterial pressure (MAP) of 40-45 mmHg. Animals were randomly divided into five groups (n=6 each): sham shock (SS); shock without resuscitation (SH); aggressive resuscitation in pre-hospital phase with 4 mL/kg normal saline, followed by Ringer’s solution to MAP of 80 mmHg (NS), hypotensive resuscitation with 4 mL/kg of normal saline (NH) or hypertonic hydroxyl ethyl starch (7.5% NaCl + hydroxy ethyl starch, HHES, HHH) followed by Ringer’s solution to MAP of 60 mmHg. Finally, all the resuscitated animals received hemorrhage controlled and fully resuscitated to MAP of 80 mmHg. At the end of the experiment, survivors were sacrificed, skeletal muscle, cardiac muscle, liver, kidney, lung and ileum were harvested for determination of Na＋-K＋-ATPase and Ca2＋-Mg2+-ATPase activities. RESULTS: Total blood loss and infused volume were compared between NH［(4.3±0.2)mL/kg, (47.2±4.1)mL/kg］ and HHH［(4.1±0.3)mL/kg,(44.9±4.3)mL/kg］ groups, both were significantly less than NS［(5.5±0.2)mL/kg, (65.5±3.8）mL/kg］　group. Hct in NH (21.0%±2.1%) and HHH (21.5%±1.8%) were significantly higher than NS (14.2%±1.5%) and SH (12.5%±1.4%).Tissue Na＋-K＋-ATPase and Ca2＋-Mg2+-ATPase activities were stimulated in all shock groups. Na＋-K＋-ATPase in skeletal muscle, cardiac muscle, liver, kidney was significantly lower in the NH (5.42±1.41, 4.54±2.01, 4.13±0.62, 3.42±0.84) and HHH (3.97±0.91, 2.94±0.66, 3.22±1.42, 3.03±0.53) than that in NS (7.34±1.41, 6.23±1.53, 6.11±0.97, 5.82±0.69) and SH (9.11±0.52, 8.40±1.08, 7.04±1.13, 6.55±1.45). CONCLUSION: Hypotensive resuscitation with normal saline or HHES reduces blood loss, decreses total infused volume, leads to higher hematocrit and finally alleviates metabolism derangement after uncontrolled hemorrhagic shock.  相似文献   

14.
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   

15.
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   

16.
AIM: To investigate the effect of Dendranthema morifolium (Ramat) Tzvel (DM) on isolated rat heart and ventricular myocytes during ischemia/anoxia and reperfusion/reoxygenation.METHODS: The Langendorff perfused rat hearts were used to measure intraventricular pressure and coronary flow. The cell contraction and intracellular calcium transient in enzymatically isolated ventricular myocytes were determined. RESULTS: (1) DM (0.5 g/L) significantly attenuated the inhibitory effects induced by ischemia/reperfusion on left ventricular developed pressure (LVDP), ±dp/dtmax, coronary flow and LVDP×HR, meanwhile increased the content of SOD and decreased the content of MDA in the myocardium; (2) DM (0.5 g/L) attenuated the inhibitory effects of anoxia and reoxygenation on i transient and cell contraction in isolated ventricular myocytes. CONCLUSION: DM attenuated the effects on contractility and intracellular calcium induced by ischemia/anoxia and reperfusion/reoxygenation in the isolated rat heart and the ventricular myocytes. The mechanism might be related to increase in SOD activity and maintaining [Ca]i homeostasis.  相似文献   

17.
LI Li  HUANG Qi-fu 《园艺学报》2003,19(11):1472-1475
AIM: To observe the effect of Shenmai injection on the acute myocardial ischemia/ reperfusion injury in rats. METHODS: The left-anterior coronary artery was ligated for 10 minutes and then loosed for 15 minutes to establish the animal model of acute myocardial ischemia/reperfusion injury. During the process, electrocardiogram was traced continuously to observe the arrhythmia caused by reperfusion. The levels of SOD, MDA, Na+, K+-ATPase and Ca2+ -ATPase in ventricular myocardium were measured. The mitochondria was observed through electron microscope. RESULTS: Shenmai injection decreased the incidence of arrhythmia caused by reperfusion and shortened its duration. Shenmai injection improved the activity of SOD, Na+, K+-ATPase and Ca2+ -ATPase, decreased the content of MDA in myocardium and relieved the injury of mitochondria. CONCLUSION: Shenmai injection had a protective effect on acute myocardial ischemia/reperfusion injury in rats. The mechanism may be related to relieving the injury caused by oxygen free radical and calcium overload.  相似文献   

18.
AIM: The changes of myocardial nuclear membrane Ca2+ -ATPase function was investigated in ischemia/reperfusion injury. METHODS: The model of myocardial ischemia/reperfusion injury was established in rats. Myocardial nuclei were purified with sucrose density centrifugation, the activity of Ca2+ -ATPase was measured and calcium uptake was assayed with [45 Ca2+ ] . RESULTS: Plasma levels of malondialdehyde (MDA) and free fatty acid (FFA) in myocardial ischemia/reperfusion injury increased significantly( P<0.01 vs control). Ca2+ -ATPase activity and [45 Ca2+ ] uptake was lower than normal at below 10 μmol/L, while higher at 50 μmol/L. CONCLUSION:These data indicate dysfunction of nuclear menbrane calcium pump and [45 Ca2+ ] uptake function in myocardial ischemia/reperfusion injury.  相似文献   

19.
AIM: In order to study the relationship between the ERK and p38 MAPK activation and the protection of 11, 12-epoxyeicosatrienoic acid (11, 12-EET) and ischemia preconditioning (IP), the effects of 11, 12-EET and ischemic preconditioning on phosphorylated ERK and p38 MAPK during ischemia and reperfusion in rat myocardium were examined. METHODS: The rat heart was subjected to ischemia for 5 min by ligating the left anterior descending coronary artery followed by reperfusion for 5 min (two times) to undergo ischemia preconditioning. The rats were divided into 5 groups: (1) control; (2) sham group; (3) ischemia/reperfusion (I/R) group, in which the rat heart suffered from 60 min ischemia followed by 30 min reperfusion; (4) IP plus I/R group; (5) EET plus I/R group, in which 6.28×10-8 mol/L 11, 12-EET was injected intravenously 20 min before I/R. The heart function was examined, and phosphorylated ERK and p38 MAPK were detected by Western blot. RESULTS: At 30 min reperfusion, +dp/dtmax, -dp/dtmax and LVDP decreased significantly in I/R group compared with sham group, IP plus I/R group and EET plus I/R group; Phosphorylated ERK1/2 level was higher in I/R group than sham group, but was lower in I/R group than IP plus I/R group and EET plus I/R group; Phosphorylated p38 MAPK level was lower in control, sham, IP plus I/R and EET plus I/R group than I/R group. CONCLUSION: 11,12-EET protects rat heart against ischemia/reperfusion injury, the mechanism may be related to activation of ERK1/2 and inhibition of p38 MAPK.  相似文献   

20.
AIM: To assess the role of the cAMP signaling in cardioprotection by brief intermittent ischemia at the time of onset of reperfusion (i.e. postconditioning). METHODS: The model of rat myocardial ischemia/reperfusion (I/R) was used. The left ventricular functions were assessed by measuring the left ventricular developed pressure (LVDP) and the coronary flow (CF). The injury of myocardium was further confirmed by detecting the releases of lactate dehydrogenase(LDH) and creatine kinase(CK) in coronary effluent. The mRNA expression of caspase-3, bcl-2 and bax in myocardium was determined by real-time PCR. RESULTS: I/R treatment led to the decrease in LVDP and CF, and the increase in the releases of CK and LDH in coronary artery effluent. The mRNA expression of caspase-3 and bax/bcl-2 ratio was up-regulated simultaneously. Postconditioning treatment relieved the injury induced by I/R, which was enhanced by the specific phosphodiesterase 4(PDE4) inhibitor rolipram. On the other hand, the specific adenylyl cyclase inhibitor SQ22536 attenuated those protective effects of postconditioning. CONCLUSION: The cAMP signaling participates in the protective effect of postconditioning on heart from I/R injury, and the effect may be associated with the regulation of apoptosis.  相似文献   

设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号