ABSTRACT
To investigate the relationship between family history of cancer, coping style and psychological distress. Total 80 patients with family history of cancer and 72 normal controls were analyzed using self-reporting inventory [SCL-90], coping style scale and impact of event scale-revised [IES-R]. Results: 1. Between the two groups of patients, there were significant differences in anxiety, depression, cancer-specific distress and coping style. 2. Psychological distress [anxiety, depression and cancer-specific distress] had positive correlation with negative coping style and family history. 3. Negative coping style played an intermediary role in the family history and psychological distress. The negative coping style will predispose to a more stronger psychological distress among the individuals with family history of cancer
ABSTRACT
AIM: To investigate the role of nitric oxide synthase (NOS), soluble guanylyl cyclase (sGC) and protein kinase C (PKC) signaling in tumor necrosis factor-? (TNF-?)-induced cardioprotection against hypoxia/reoxygenation (H/R) injury. METHODS: Neonatal rat ventricular myocytes were pretreated with TNF-? or sodium nitroprusside (SNP) or L-arginine (L-Arg), respectively, for 12 h and then subjected to continuous hypoxia for 12 h, followed by reoxygenation for 6 h. The manganese superoxide dismutase (Mn-SOD) activity of the cells was measured after H/R. Myocyte injury was determined by the release of lactic dehydrogenase (LDH). RESULTS: TNF-? (10~5 (U/L)) significantly increased the Mn-SOD activity and decreased release of LDH from ventricular myocytes. The cardioprotection against H/R injury was induced by the pretreatment with SNP (5 ?mol/L) or L-Arg (5 mmol/L), which was blocked by ODQ (10 ?mol/L), the specific sGC inhibitor, and Chel (5 ?mol/L), the specific PKC inhibitor. Pretreatment with L-NAME (100 ?mol/L), ODQ, Chel, antoxidant 2-MPG (400 ?mol/L) or tyrosine kinase inhibitor genistein (50 ?mol/L) attenuated the increased Mn-SOD activity and reduced LDH level induced by TNF-?. CONCLUSION: The results suggest that NO may play a role in TNF-?-induced cardioprotection, which is mediated by sGC and PKC. [
ABSTRACT
AIM: We examined the effect of interleukin- 2 (IL-2) on calcium handlin g of rat cardiomyocytes. METHODS: The effects of steady state an d transient chan ges in stimulus frequency on the intracellular calcium transient were investigat ed in the isolated ventricular myocytes with spectrofluorometry technique. RESULTS: Under the steady state (0.2 Hz), IL-2 at 2?10 5 U/L decr eased the peak [Ca 2+ ] i and amplitude of the [Ca 2+ ] i transient, increas ed the diastolic calcium level, and prolonged the decay of the calcium transient . At 1.25 mmol/L of extracellular [Ca 2+ ], when increasing the stimulus frequency from 0.2 to 1.0 Hz, diastolic calcium level and peak [Ca 2+ ] i as well as the amplitude of the transient were inc reased. The positive frequency relationship was blunted in the IL-2-treated myoc ytes and this was not normalized by increasing extracellular [Ca 2+ ] t o 2.5 mmol/L . The caffeine induced Ca 2+ release was increased with increase in stimu lus freq uency. IL-2 inhibited the frequency relationship of caffeine induced Ca 2+ releas e. The restitution was not different between control and IL-2 groups at the 1.25 mmol/L of extracellular [Ca 2+ ], which was slowed in IL-2-treated myo cytes when t he extracellular [Ca 2+ ] was increased to 2.5 mmol/L. CONCLUSIO NS: It is concluded that the blunted frequency response of IL-2-treated myocytes was resulted from the decrease in SR Ca 2+ release, which was related to depression of SR funct ion. Despite the evidence of depressed SR Ca 2+ uptake, the restitution o f ca lcium transient at 1.25 mmol/L of extracellular [Ca 2+ ] remains uncha nged, which maybe due to the increase in the Na +/Ca 2+ exchanger activi ty.
ABSTRACT
AIM: To investigate the effect of interleukin-2 (IL-2) on the intracellular calcium in electrically stimulated adult rat ventricular myocytes during anoxia and reoxygenation. METHODS: The isolated cardiac ventricular myocytes were exposed to 5 min anoxia followed by 10 min reoxygenation. Chemical anoxia was introduced by Krebs-Henseleit (K-H) solution containing 10 -3 mol/L sodium dithionite. The spectrofluorometric method was used to verify intracellular calcium transient with fura-2/AM as calcium fluorescence probe. RESULTS: It was shown that during anoxia, the amplitude of Ca 2+ transient was decreased, diastolic [Ca 2+ ] i, time to peak and time to relaxation of Ca 2+ transient were increased. All the parameters were got back but did not returned to the pre-anoxia level during reoxygenation. IL-2 at 2?10 5 U/L administrated during anoxia aggravated the effect of rexoxygenation on [Ca 2+ ] i transient. Pretreatment with a specific ? opioid antagonist, nor-BNI (10 -8 mol/L), abolished the effect induced by IL-2 during anoxia on the [Ca 2+ ] i transients, whereas specific ? opioid antagonist, naltrindole (10 -6 mol/L), did not cancel the effect. CONCLUSION: It is concluded that administration of IL-2 during anoxia aggravated the effect of reoxygenation on the [Ca 2+ ] i transients of isolated ventricular myocytes, which was mediated by cardiac ? opioid receptor pathway.
ABSTRACT
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/dt max, 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 [Ca 2+]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 2+]i homeostasis.
ABSTRACT
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/dt_ max ), 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 ?mol/L) during the first 10 min reoxygenation improved recovery of LVDP, ?dp/dt_ max and decreased LVEDP, which was associated with reduced infarct size and lactate dyhydrogenase release. These protective effects were attenuated by treatment with spermine (20 ?mol/L) during the first 10 min reoxygenation. Administration of cyclosporin A (0.2 ?mol/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.
ABSTRACT
AIM: To investigate whether tumor necrosis factor ? (TNF?) pretreatment can inhibit mitochondrial permeability transition pore opening in isolated rat hearts subjected to hypoxia and reoxygenation. METHODS: Isolated perfused rat hearts were subjected to 30 min regional hypoxia (occlusion of left anterior descending artery) and 120 min reoxygenation. The infarct size, lactate dehydrogenase (LDH) release during reoxygenation and ventricular hemodynamic parameters were measured. RESULTS: Pretreatment with TNF? at concentration of 1?104 U/L for 7 min followed by 10 min washout reduced the infarct size and LDH release, and improved the left ventricular performance (left ventricular developed pressure and rate-pressure product) and left ventricular end-diastolic pressure during hypoxia and reoxygenation. Administration of atractyloside (Atr, an opener of mitochondrial permeability transition pore, 20 ?mol/L) for 20 min (last 5 min of hypoxia and first 15 min of reoxygenation) and paxilline (Pax, a calcium activated potassium channel antagonist, 1 ?mol/L) for 5 min before hypoxia attenuated the reduction of infarct size and LDH release and improved the left ventricular performance induced by TNF?. CONCLUSION: The findings indicate that in the isolated rat heart model, TNF? protects myocardium against hypoxia and reoxygenation injury via inhibiting mitochondrial permeability transition pore opening as well as activating calcium, activated potassium channel.
ABSTRACT
AIM: To study the effect of salvia miltiorrhiza (SM) on cell contraction and intracellular calcium of enzymatically isolated rat ventricular myocytes during normoxia and anoxia/reoxygenation. METHODS: Contraction and intracellular calcium were determined with video tracking system and spectrofluorometric method, and the chemical anoxic method was employed. RESULTS: The ?d L /d t max , dL of cell contraction and the amplitude of [Ca 2+ ] i in the cardiomyocytes following SM treatment were decreased in a dose-dependent manner. During anoxia, the ?d L /d t max , dL and amplitude of [Ca 2+ ] i were decreased, while the diastolic Ca 2+ level was elevated compared with control group. All the contractile parameters and the diastolic Ca 2+ level were back toward pretreatment values during reoxygenation, but could not return to control level. After the treatment with SM (3 g/L), ?d L /d t max and dL of cell contraction and the amplitude of [Ca 2+ ] i were higher and the diastolic Ca 2+ level was lower than those in anoxia/reoxygenation group. CONCLUSION: SM antagonized effects of anoxia and reoxygenation on cell contraction and intracellular calcium in isolated ventricular myocytes.
ABSTRACT
AIM: To investigate the effect and possible mechanisms of interleukin-2 (IL-2) on the cell contractility in cardiomyocytes during hypoxia and reoxygenation.METHODS: Glucose-free Krebs-Henseleit (K-H) solution, gassed with 95% N 2 and 5% CO 2 for hypoxia, were used. The cell contractility were determined after 20 min of hypoxia and 30 min of reoxygenation by the video tracking system. The parameters of cell contractility included peak velocity of cell shortening (+d L /d t max), peak velocity of cell relengthening (-d L /d t max), contraction amplitude (dL) and end-diastolic cell length.RESULTS: It was shown that during hypoxia, the cell contraction was depressed. All the parameters were unable to return to the pre-hypoxia level during reoxygenation. Pretreatment with IL-2 at 2?10 3 U/L attenuated the inhibitory effect of hypoxia/reoxygenation on contractility in single ventricular myocytes. The effect of IL-2 was reduced in the presence of 10 -8 mol/L nor-binaltorphimine (nor-BNI), a selective ?-opioid receptor antagonist. On blockade of protein kinase C with 3?10 -6 mol/L chelerythrine, the effect of IL-2 was significantly attenuated. The effect of IL-2 was also blocked by 10 -4 mol/L 5-hydroxydecanoate (5-HD), a mitochondrial ATP-sensitive potassium (K ATP ) channel blocker. CONCLUSIONS: The results of the present study provide evidence that pretreatment with IL-2 at 2?10 3 U/L attenuates the effect of hypoxia/reoxygenation on cell contraction in the isolated ventricular myocytes. The ?-opioid receptor mediates the effect of IL-2, in which activation of PKC and opening of mitochondrial ATP-sensitive potassium (mito K ATP ) channel are involved.
ABSTRACT
AIM: To explore the effects and mechanism of interleukin-2 (IL-2) on the positive effect of isoproterenol (ISO) in the isolated rat cardiomyocytes. METHODS: Enzymatically isolated cardiomyocytes were used. Peak twitch amplitude and maximal velocity of shortening/relaxation (?dL/dt_~max ) in the isolated cardiomyocytes were recorded with a microscope coupled to a charge-coupled device camera and [Ca~2+ ]i transients were determined with a fluorometric ratio method by using Fura-2/AM as Ca~2+ indicators. RESULTS: ① ISO increased the peak twitch amplitude and ?dL/dt_~max of the isolated cardiomyocytes. Perfusion for 15 min with IL-2 at 2?103 U/L, which had no effect at all, attenuated the enhancing effect of ISO on the peak twitch amplitude and ?dL/dt_~max . ② ISO increased the [Ca~2+ ]i transients of the single ventricular myocytes in a dose dependent manner and the corresponding EC_~50 values of ISO was (0.12?0.01) ?mol/L. Perfusion for 15 min with IL-2 at 2?103 U/L, which had no effect on the ~[Ca~2+ ]i transient at all, attenuated the enhancing effect of ISO and the corresponding EC_~50 was (0.44?0.06) ?mol/L. ③ The electrically induced [Ca~2+ ]i transient was significantly increased by pretreatment with 20 mg/L cholera toxin for ~12 h. The elevation of the [Ca~2+ ]i transient induced by cholera toxin was significantly attenuated by 2?103 U/L IL-2. ④ Forskolin (1 ?mol/L), the activator of adenyl cyclase, significantly increased the electrically induced [Ca~2+ ]i transient, which was attenuated by IL-2 at 2?103 U/L. CONCLUSION: IL-2 inhibits the positive effect of isoproterenol in the isolated single ventricular myocytes, in which Gs protein and adenyl cyclase are involved. [