scholarly journals Pleiotropic Effects of Simvastatin Are Associated With Mitigation of Apoptotic Component of Cell Death Upon Lethal Myocardial Reperfusion-Induced Injury

2012 ◽  
pp. S33-S41 ◽  
Author(s):  
T. RAJTÍK ◽  
S. ČARNICKÁ ◽  
A. SZOBI ◽  
L. MESÁROŠOVÁ ◽  
M. MÁŤUŠ ◽  
...  
Keyword(s):  
Cell Death ◽  
Ischemia Reperfusion ◽  
Active Form ◽  
Plasma Lipid ◽  
Left Ventricular ◽  
Control Group ◽  
Rat Hearts ◽  
Pleiotropic Action ◽  
Developed Pressure ◽  
Transcription 3

Although statins exert non-lipid cardioprotective effects, their influence on cell death is not fully elucidated. For this purpose, we investigated whether simvastatin treatment (S, 10 mg/kg, 5 days) is capable of mitigating ischemia/reperfusion-induced (IR) apoptosis in the isolated rat hearts, which was examined using immunoblotting analysis. In addition, the content of signal transducer and activator of transcription 3 (STAT3) and its active form, phosphorylated STAT3 (pSTAT3-Thr705), was analyzed. Simvastatin induced neither variations in the plasma lipid levels nor alterations in the baseline content of analysed proteins with the exception of upregulation of cytochrome C. Furthermore, simvastatin significantly increased the baseline levels of pSTAT3 in contrast to the control group. In the IR hearts, simvastatin reduced the expression of Bax and non-cleaved caspase-3. In these hearts, phosphorylation of STAT3 did not differ in comparison to the non-treated IR group, however total STAT3 content was slightly increased. The improved recovery of left ventricular developed pressure co-existed with the increased Bcl-2/Bax ratio. In conclusion, pleiotropic action of statins may ameliorate viability of cardiomyocytes by favouring the expression of anti-apoptotic Bcl-2 and downregulating the pro-apoptotic markers; however STAT3 does not seem to be a dominant regulator of this anti-apoptotic action of simvastatin.

Effect of diazoxide on flavoprotein oxidation and reactive oxygen species generation during ischemia-reperfusion: a study on Langendorff-perfused rat hearts using optic fibers

2008 ◽  
Vol 294 (5) ◽  
pp. H2088-H2097 ◽  
Author(s):  
Philippe Pasdois ◽  
Bertrand Beauvoit ◽  
Liliane Tariosse ◽  
Béatrice Vinassa ◽  
Simone Bonoron-Adèle ◽  
...  
Keyword(s):  
Ischemia Reperfusion ◽  
Reactive Oxygen Species Generation ◽  
Left Ventricular ◽  
Rate Pressure Product ◽  
Control Group ◽  
Rat Hearts ◽  
Perfused Rat Hearts ◽  
Optic Fibers ◽  
The One ◽  
Isolated Perfused Rat Hearts

This study analyzed the oxidant generation during ischemia-reperfusion protocols of Langendorff-perfused rat hearts, preconditioned with a mitochondrial ATP-sensitive potassium channel (mitoKATP) opener (i.e., diazoxide). The autofluorescence of mitochondrial flavoproteins, and that of the total NAD(P)H pool on the one hand and the fluorescence of dyes sensitive to H2O2 or O2•− [i.e., the dihydrodichlorofluoroscein (H2DCF) and dihydroethidine (DHE), respectively] on the other, were noninvasively measured at the surface of the left ventricular wall by means of optic fibers. Isolated perfused rat hearts were subjected to an ischemia-reperfusion protocol. Opening mitoKATP with diazoxide (100 μM) 1) improved the recovery of the rate-pressure product after reperfusion (72 ± 2 vs. 16.8 ± 2.5% of baseline value in control group, P < 0.01), and 2) attenuated the oxidant generation during both ischemic (−46 ± 5% H2DCF oxidation and −40 ± 3% DHE oxidation vs. control group, P < 0.01) and reperfusion (−26 ± 2% H2DCF oxidation and −23 ± 2% DHE oxidation vs. control group, P < 0.01) periods. All of these effects were abolished by coperfusion of 5-hydroxydecanoic acid (500 μM), a mitoKATP blocker. During the preconditioning phase, diazoxide induced a transient, reversible, and 5-hydroxydecanoic acid-sensitive flavoprotein and H2DCF (but not DHE) oxidation. In conclusion, the diazoxide-mediated cardioprotection is supported by a moderate H2O2 production during the preconditioning phase and a strong decrease in oxidant generation during the subsequent ischemic and reperfusion phases.

scholarly journals Hemidesmus indicusandHibiscus rosa-sinensisAffect Ischemia Reperfusion Injury in Isolated Rat Hearts

2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Vinoth Kumar Megraj Khandelwal ◽  
R. Balaraman ◽  
Dezider Pancza ◽  
Táňa Ravingerová
Keyword(s):  
Infarct Size ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Left Ventricular ◽  
Moderate Increase ◽  
Dependent Manner ◽  
Hemidesmus Indicus ◽  
Rat Hearts ◽  
Perfused Rat Hearts ◽  
Developed Pressure

Hemidesmus indicus(L.) R. Br. (HI) andHibiscus rosa-sinensisL. (HRS) are widely used traditional medicine. We investigated cardioprotective effects of these plants applied for 15 min at concentrations of 90, 180, and 360 μg/mL in Langendorff-perfused rat hearts prior to 25-min global ischemia/120-min reperfusion (I/R). Functional recovery (left ventricular developed pressure—LVDP, and rate of development of pressure), reperfusion arrhythmias, and infarct size (TTC staining) served as the endpoints. A transient increase in LVDP (32%–75%) occurred at all concentrations of HI, while coronary flow (CF) was significantly increased after HI 180 and 360. Only a moderate increase in LVDP (21% and 55%) and a tendency to increase CF was observed at HRS 180 and 360. HI and HRS at 180 and 360 significantly improved postischemic recovery of LVDP. Both the drugs dose-dependently reduced the numbers of ectopic beats and duration of ventricular tachycardia. The size of infarction was significantly decreased by HI 360, while HRS significantly reduced the infarct size at all concentrations in a dose-dependent manner. Thus, it can be concluded that HI might cause vasodilation, positive inotropic effect, and cardioprotection, while HRS might cause these effects at higher concentrations. However, further study is needed to elucidate the exact mechanism of their actions.

Isoflurane and Halothane Increase Adenosine Triphosphate Preservation, but Do Not Provide Additive Recovery of Function after Ischemia, in Preconditioned Rat Hearts

1997 ◽  
Vol 86 (1) ◽  
pp. 109-117 ◽  
Author(s):  
Ashraf Boutros ◽  
Jun Wang ◽  
Christine Capuano
Keyword(s):  
Adenosine Triphosphate ◽  
Coronary Flow ◽  
Recovery Of Function ◽  
Left Ventricular ◽  
Untreated Group ◽  
Control Group ◽  
Time Control ◽  
Rat Hearts ◽  
Developed Pressure ◽  
Isolated Rat

Background Brief ischemic periods render the myocardium resistant to infarction from subsequent ischemic insults by a process called ischemic preconditioning. Volatile anesthetics have also been shown to be cardioprotective if administered before ischemia. The effect of preconditioning alone and combined with halothane or isoflurane on hemodynamic recovery and preservation of adenosine triphosphate content in isolated rat hearts was evaluated. Methods Seven groups of isolated rat hearts (n = 6 each) were perfused in a retrograde manner at constant temperature and pressure. A latex balloon was placed in the left ventricle to obtain isovolumetric contraction. Heart rhythm, coronary flow, left ventricular pressure and its derivative dP/dt (positive and negative), and developed pressure were monitored. The hearts were paced at 300 beats per minute. Each heart was randomly allocated to (1) a time-control group that received no ischemia, (2) an untreated group that received 25 min of normothermic ischemia only. (3 and 4) an isoflurane group and a halothane group that received 40 min of anesthetic (2.2% and 1.5%, respectively) before ischemia; (5) a preconditioning group that received two 5-min periods of ischemia separated by 10 min of reperfusion before ischemia; or (6 and 7) a isoflurane+preconditioning group and a halothane+preconditioning group that received anesthetic for 10 min at concentrations of 2.2% or 1.5%, respectively, before two 5-min periods of ischemia separated by 10 min of reperfusion. All treated groups received 25 min of normothermic ischemia followed by 30 min of reperfusion. Results The time-control group remained hemodynamically stable for the entire experiment, and the adenosine triphosphate content was 18.3 +/- 1.7 (SEM) microM/g at the end of 115 min. The untreated group had depressed recovery after 25 min of normothermic ischemia, and the developed pressure was significantly depressed and recovered only 30 +/- 9% (P &lt; 0.001) of its preischemic value. There was also a significant increase in the incidence of ventricular fibrillation (P &lt; 0.001). Adenosine triphosphate content was significantly lower in this group than in all other groups. Five minutes of ischemia in the preconditioning group had little effect on hemodynamics and decreased developed pressure only 6.4%. Halothane depressed developed pressure by 16 +/- 5% (P &lt; 0.001), and isoflurane increased coronary flow by 145 +/- 9% (P &lt; 0.001) but had no significant hemodynamic effect. The treated groups had significantly better recovery of postischemic function than did the untreated group. In the preconditioning group, developed pressure recovered to 85% of control and dP/dt+ to 87% of control. The addition of halothane or isoflurane to preconditioning did not provide additional functional recovery but did increase the level of adenosine triphosphate preservation (13.1 +/- 1.1 and 12.4 +/- 1.1 microM/g, respectively). Conclusions The results indicate that preconditioning, halothane, and isoflurane provide significant protection against ischemia. The combination of preconditioning and halothane or isoflurane did not improve hemodynamic recovery but did increase preservation of adenosine triphosphate.

Abstract 38: A Decoy Peptide Selectively Inhibiting Dephosphorylation of Phospholamban

2012 ◽  
Vol 111 (suppl_1) ◽  
Author(s):  
Woo Jin Park ◽  
Jae Gyun Oh ◽  
Dongtak Jeong ◽  
Roger J Hajjar
Keyword(s):  
Ischemia Reperfusion ◽  
Left Ventricular ◽  
Cardiac Sarcoplasmic Reticulum ◽  
Rat Cardiomyocytes ◽  
Adult Rat ◽  
Rat Hearts ◽  
Cell Permeable Peptide ◽  
Phosphorylated Peptide ◽  
Developed Pressure

Cardiac sarcoplasmic reticulum Ca2+ ATPase (SERCA2a) plays a crucial role in Ca2+ handling in cardiomyocytes. Phospholamban (PLB) is an endogenous inhibitor of SERCA2a and its inhibitory activity is enhanced by dephosphorylation by protein phosphatase 1 (PP1). Therefore, blocking PP1-mediated dephosphorylation of PLB would be an efficient strategy for restoration of the reduced SERCA2a activity in failing hearts. We sought to develop a decoy peptide that mimics the phosphorylated PLB and thus competitively inhibits the PP1-mediated dephosphorylation of PLB. The phosphorylation sites, Ser16 and Thr17, are located within the flexible extra-membrane loop (amino acids 14-22) of PLB. We therefore synthesized a 9-mer pseudo-phosphorylated peptide derived from this region with a replacement of Ser16 with Glu (ψ-PLB-SE). Two other 9-mer peptides with wild type PLB sequence (ψ-PLB) or with a replacement of Ser16 with Ala (ψ-PLB-SA) were also synthesized. These peptides were coupled to a cell-permeable peptide TAT to facilitate cellular uptake. Treatment of adult rat cardiomyocytes with TAT-ψ-PLB-SE, but not with TAT-ψ-PLB or TAT-ψ-PLB-SA, significantly elevated the phosphorylation level of PLB, concomitant with an increase in contractile parameters in vitro. Perfusion of isolated rat hearts with TAT-ψ-PLB-SE significantly restored the left ventricular developed pressure that was suppressed by ischemia-reperfusion (Fig. 1). These data indicate that ψ-PLB-SE prevented dephosphorylation of PLB by acting as a decoy for PP1 and it would provide effective modality to regulate SERCA2a activity in failing hearts.

Effects of the AT1 Receptor Blocker Candesartan on Myocardial Ischemia/Reperfusion in Isolated Rat Hearts

2014 ◽  
Vol 17 (5) ◽  
pp. 263 ◽  
Author(s):  
C. Murat Songur ◽  
Merve Ozenen Songur ◽  
Sinan Sabit Kocabeyoglu ◽  
Bilgen Basgut
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Left Ventricular ◽  
Relaxation Rates ◽  
Cardioplegic Solution ◽  
Rat Hearts ◽  
Developed Pressure ◽  
Contraction And Relaxation ◽  
Isolated Rat

<p><b>Background:</b> We sought to investigate the effects of the angiotension II receptor blocker candesartan on ischemia-reperfusion injury using a cardioplegia arrested isolated rat heart model.</p><p><b>Methods:</b> Ischemia-reperfusion injury was induced in isolated rat hearts with 40 minutes of global ischemia followed by a 30-minute reperfusion protocol. Throughout the experiment, constant pressure perfusion was achieved using a Langendorff apparatus. Cardioplegic solution alone, and in combination with candesartan, was administered before ischemia and 20 minutes after ischemia. Post-ischemic recovery of contractile function, left ventricular developed pressure, left ventricular end-diastolic pressure and contraction and relaxation rates were evaluated.</p><p><b>Results:</b> In the control group, left ventricular developed pressure, rate pressure product, contraction and relaxation rates and coronary flow significantly decreased but coronary resistance increased following reperfusion. With the administration of candesartan alone, parameters did not differ compared to controls. Contractile parameters improved in the group that received candesartan in combination with the cardioplegia compared to the group that received cardioplegia alone; however, the difference between these two groups was insignificant.</p><p><b>Conclusion:</b> In this study, the addition of candesartan to a cardioplegic arrest protocol routinely performed during cardiac surgery did not provide a significant advantage in protection against ischemia-reperfusion injury compared with the administration of cardioplegic solution alone.</p>

Adenosine A3-receptor stimulation attenuates postischemic dysfunction through KATP channels

1999 ◽  
Vol 277 (1) ◽  
pp. H228-H235 ◽  
Author(s):  
Vinod H. Thourani ◽  
Masanori Nakamura ◽  
Russell S. Ronson ◽  
James E. Jordan ◽  
Zhi-Qing Zhao ◽  
...  
Keyword(s):  
Katp Channels ◽  
Left Ventricular ◽  
Rate Of Change ◽  
Control Group ◽  
Receptor Stimulation ◽  
Rat Hearts ◽  
Positive Rate ◽  
Perfused Rat Hearts ◽  
Adenosine Agonists ◽  
Developed Pressure

We tested the hypothesis that selective adenosine A3-receptor stimulation reduces postischemic contractile dysfunction through activation of ATP-sensitive potassium (KATP) channels. Isolated, buffer-perfused rat hearts ( n = 8/group) were not drug pretreated (control) or were pretreated with adenosine (20 μM), 2-chloro- N 6-(3-iodobenzyl)-adenosine-5′- N-methyluronamide (Cl-IB-MECA; A3 agonist, 100 nM), Cl-IB-MECA + 8-(3-noradamantyl)-1,3-dipropylxanthine (KW-3902; A1 antagonist, 5 μM), Cl-IB-MECA + glibenclamide (Glib; KATP-channel blocker, 0.3 μM), or Glib alone for 12 min before 30 min of global normothermic ischemia followed by 2 h of reperfusion. After 2 h of reperfusion, left ventricular developed pressure (LVDP, %baseline) in control hearts was depressed to 34 ± 2%. In hearts pretreated with Cl-IB-MECA, there was a statistically significant increase in LVDP (50 ± 6%), which was reversed with coadministration of Glib (37 ± 1%). Control hearts also showed similar decreases in left ventricular peak positive rate of change in pressure (dP/d t). Therefore, the A3 agonist significantly attenuated postischemic cardiodynamic injury compared with the control, which was reversed by Glib. Cumulative creatine kinase (CK in U/min) activity was most pronounced in the control group (10.4 ± 0.6) and was significantly decreased by Cl-IB-MECA (7.5 ± 0.4), which was reversed by coadministration of Glib (9.4 ± 0.2). Coronary flow was increased during adenosine infusion (160% of baseline) but not during Cl-IB-MECA infusion. Effects of Cl-IB-MECA were not reversed by the specific A1 antagonist KW-3902. We conclude that cardioprotection afforded by A3-receptor stimulation may be mediated in part by KATP channels. Cl-IB-MECA may be an effective pretreatment agent that attenuates postischemic cardiodynamic dysfunction and CK release without the vasodilator liability of other adenosine agonists.

Erythropoietin protects against doxorubicin-induced heart failure

2011 ◽  
Vol 301 (6) ◽  
pp. H2413-H2421 ◽  
Author(s):  
Hania Ibrahim Ammar ◽  
Soliman Saba ◽  
Rasha Ibrahim Ammar ◽  
Laila Ahmed Elsayed ◽  
Wael Botros Abu-Alyamin Ghaly ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Ischemia Reperfusion ◽  
Treated Group ◽  
Left Ventricular ◽  
Rate Pressure Product ◽  
Control Group ◽  
Maximal Increase ◽  
Male Wistar Rats ◽  
Developed Pressure

The hormone erythropoietin (EPO) has been demonstrated to have cardioprotective properties. The present study investigates the role of EPO to prevent heart failure following cancer treatment with doxorubicin [adriamycin (AD)]. Male Wistar rats (150 ± 10 g) were treated with saline (vehicle control group); with EPO, subcutaneously at 1,000 IU/kg body wt, three times per week for 4 wk (EPO group); with adriamycin, intraperitoneally at 2.5 mg/kg body wt, three times per week for 2 wk (AD group); and with adriamycin and EPO (EPO-AD group). Echocardiographic measurements showed that EPO-AD treatment prevented the AD-induced decline in cardiac function. Each of the hearts was then exposed to ischemia and reperfusion during Langendorff perfusion. The percentage of recovery after ischemia-reperfusion was significantly greater in EPO-AD than the AD-treated group for left ventricular developed pressure, maximal increase in pressure, and rate pressure product. The level of oxidative stress was significantly higher in AD (5 μM for 24 h)-exposed isolated cardiomyocytes; EPO (5 U/ml for 48 h) treatment prevented this. EPO treatment also decreased AD-induced cardiomyocyte apoptosis, which was associated with the decrease in the Bax-to-Bcl2 ratio and caspase-3 activation. Immunostaining of myocardial tissue for CD31 showed a significant decrease in the number of capillaries in AD-treated animals. EPO-AD treatment restored the number of capillaries. In conclusion, EPO treatment effectively prevented AD-induced heart failure. The protective effect of EPO was associated with a decreased level of oxidative stress and apoptosis in cardiomyocytes as well as improved myocardial angiogenesis.

Cardioprotective mechanisms of Prunus cerasus (sour cherry) seed extract against ischemia-reperfusion-induced damage in isolated rat hearts

2006 ◽  
Vol 291 (3) ◽  
pp. H1329-H1336 ◽  
Author(s):  
Istvan Bak ◽  
Istvan Lekli ◽  
Bela Juhasz ◽  
Norbert Nagy ◽  
Edit Varga ◽  
...  
Keyword(s):  
Cardiac Function ◽  
Ischemia Reperfusion ◽  
Sour Cherry ◽  
Left Ventricular ◽  
Prunus Cerasus ◽  
Seed Kernel ◽  
Action Mechanisms ◽  
Rat Hearts ◽  
Developed Pressure ◽  
Postischemic Recovery

The effects of kernel extract obtained from sour cherry ( Prunus cerasus) seed on the postischemic cardiac recovery were studied in isolated working rat hearts. Rats were treated with various daily doses of the extract for 14 days, and hearts were then isolated and subjected to 30 min of global ischemia followed by 120 min of reperfusion. The incidence of ventricular fibrillation (VF) and tachycardia (VT) fell from their control values of 92% and 100% to 50% (not significant) and 58% (not significant), 17% ( P < 0.05), and 25% ( P < 0.05) with the doses of 10 mg/kg and 30 mg/kg of the extract, respectively. Lower concentrations of the extract (1 and 5 mg/kg) failed to significantly reduce the incidence of VF and VT during reperfusion. Sour cherry seed kernel extract (10 and 30 mg/kg) significantly improved the postischemic recovery of cardiac function (coronary flow, aortic flow, and left ventricular developed pressure) during reperfusion. We have also demonstrated that the extract-induced protection in cardiac function significantly reflected in a reduction of infarct size. Immunohistochemistry indicates that a reduction in caspase-3 activity and apoptotic cells by the extract, beside other potential action mechanisms of proanthocyanidin, trans-resveratrol, and flavonoid components of the extract, could be responsible for the cardioprotection in ischemic-reperfused myocardium.

Effects of endotoxin on neutrophil-mediated I/R injury in isolated perfused rat hearts

2001 ◽  
Vol 280 (2) ◽  
pp. H802-H811 ◽  
Author(s):  
Brian P. Lipton ◽  
Abraham P. Bautista ◽  
Joseph B. Delcarpio ◽  
Kathleen H. McDonough
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Isolated Heart ◽  
Ischemia Reperfusion ◽  
Left Ventricular ◽  
Isolated Rat Heart ◽  
Polymorphonuclear Neutrophils ◽  
Rat Hearts ◽  
Perfused Rat Hearts ◽  
Developed Pressure

With the use of a syngeneic model, we demonstrate that rat polymorphonuclear neutrophils (PMNs) exacerbate ischemia-reperfusion injury in the isolated rat heart. However, PMNs (19 × 106cells) from lipopolysaccharide (LPS)-treated rats (LPS-PMNs; 100 mg/kg administered 7 h before exsanguination) induce less reperfusion injury in the isolated heart. Average recovery of left ventricular developed pressure after 20 min of ischemia and 60 min of reperfusion was 51 ± 4% in hearts receiving PMNs from saline-treated control rats (saline-PMNs) versus 78 ± 2% in hearts receiving LPS-PMNs. Ischemic hearts reperfused with LPS-PMNs recovered to the same extent as did hearts reperfused with Krebs buffer only. LPS-PMNs and saline-PMNs showed no difference in basal or phorbol ester-induced superoxide production. Whereas twice the number of LPS-PMNs was positive for nitroblue tetrazolium, the percent positive for L-selectin, a receptor integral in PMN-adhesion to endothelium, was 50% less in LPS-PMNs than in controls. After reperfusion, three-fourths of the saline-PMNs remained within the hearts, whereas only one-fourth of LPS-PMNs were trapped. These data suggest that PMNs from LPS-treated rats do not exacerbate ischemia-reperfusion injury as do control PMNs, possibly, due to impaired PMN adhesion to endothelium as a result of decreased L-selectin receptors.

The role of K+ATP channels in the control of pre- and post-ischemic left ventricular developed pressure in septic rat hearts

2001 ◽  
Vol 79 (3) ◽  
pp. 213-219 ◽  
Author(s):  
Jitka A Ismail ◽  
Kathleen H McDonough
Keyword(s):  
Coronary Flow ◽  
Myocardial Protection ◽  
Myocardial Function ◽  
Ischemia Reperfusion ◽  
Left Ventricular ◽  
Lv Function ◽  
Rat Hearts ◽  
Developed Pressure ◽  
Septic Group

Myocardial function is impaired 24 h after the induction of sepsis, however, recovery of left ventricular (LV) function after 35 min of global ischemia is complete. The mechanisms by which this protection occurs are unknown. Ischemic preconditioning, another form of myocardial protection from ischemia/reperfusion (I/R) injury, has been shown to be modulated by ATP-sensitive potassium (K+ATP) channels. To investigate the role of K+ATP channels in the regulation of coronary flow (CF) and protection from I/R injury in septic rat hearts, we assessed the effects of the K+ATP channel antagonist glibenclamide (GLIB) and the agonist cromakalim (CROM) on pre- and post-ischemic CF and left ventricular developed pressure (LVDP). Although GLIB decreased pre-ischemic CF in both control and septic rat hearts, LVDP was unaffected. After I/R, CF was decreased in GLIB-treated control and septic rat hearts and LVDP was more severely depressed in control rat hearts than in septic rat hearts. CROM increased pre-ischemic CF in the septic group although LVDP was unaltered in both groups. After I/R, control rat heart CF was depressed but LVDP completely recovered. Post-ischemic CF in septic rat hearts was elevated compared with vehicle-treated septic rat hearts, but the recovery of LVDP was not improved. These results suggest that K+ATP channels modulate CF in septic rat hearts, but do not mediate cardioprotection as observed in control rat hearts.Key words: K+ATP channel, preconditioning, ischemia, reperfusion, sepsis.

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