Does Noradrenaline Influence the Extracellular Accumulation of Potassium, Sodium, Calcium, and Hydrogen Ions ([K+]e, [Na+]e, [Ca2+]e, [H+]e) during Global Ischemia in Isolated Rat Hearts?

1991 ◽  
pp. 283-292 ◽  
Author(s):  
Hj. Hirche ◽  
H. Knopf ◽  
H. Homburg ◽  
R. Walser
Keyword(s):  
Global Ischemia ◽  
Hydrogen Ions ◽  
Potassium Sodium ◽  
Sodium Calcium ◽  
Rat Hearts ◽  
Isolated Rat

scholarly journals The Effects of Potassium Cyanide on the Functional Recovery of Isolated Rat Hearts after Ischemia and Reperfusion: The Role of Oxidative Stress

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Anica M. Petkovic ◽  
Vladimir Lj. Jakovljevic ◽  
Jovana V. Bradic ◽  
Jovana N. Jeremic ◽  
Nevena S. Jeremic ◽  
...  
Keyword(s):  
Cytochrome C ◽  
Functional Recovery ◽  
Heart Function ◽  
Potassium Cyanide ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Global Ischemia ◽  
Albino Rats ◽  
Rat Hearts ◽  
Isolated Rat

This investigation is aimed at examining the effects of pharmacological PostC with potassium cyanide (KCN) on functional recovery, gene expression, cytochrome c expression, and redox status of isolated rat hearts. Rats were divided into the control and KCN groups. The hearts of male Wistar albino rats were retrogradely perfused according to the Langendorff technique at a constant perfusion pressure of 70 cmH2O. After stabilisation, control hearts were subjected to global ischemia (5 minutes), followed by reperfusion (5 minutes), while experimental hearts underwent global ischemia (5 minutes) followed by 5 minutes of reperfusion with 10 μmol/L KCN. The following parameters of heart function were measured: maximum and minimum rates of pressure development, systolic and diastolic left ventricular pressure, heart rate, and coronary flow. Levels of superoxide anion radical, hydrogen peroxide, nitrites, and index of lipid peroxidation (measured as thiobarbituric acid-reactive substances) were measured in coronary venous effluent, and activity of catalase was determined in heart tissue. Expression of Bax, Bcl-2, SOD-1, SOD-2, and cytochrome c was studied as well. It was shown that expression of Bax, Bcl-2, and SOD-2 genes did not significantly differ between groups, while expression of SOD-1 gene and cytochrome c was lower in the KCN group. Our results demonstrated that KCN improved the recovery of myocardial contractility and systolic and diastolic function, enhanced catalase activity, and diminished generation of prooxidants. However, all possible mechanisms and potential adverse effects of KCN should be further examined in the future.

scholarly journals Preconditioning in rat hearts is independent of mitochondrial F1F0ATPase inhibition

1998 ◽  
Vol 274 (1) ◽  
pp. H90-H97 ◽  
Author(s):  
David W. Green ◽  
Holt N. Murray ◽  
Paul G. Sleph ◽  
Feng-Lai Wang ◽  
Anne J. Baird ◽  
...  
Keyword(s):  
Atp Hydrolysis ◽  
Contractile Function ◽  
Atp Synthesis ◽  
Isolated Rat Heart ◽  
Global Ischemia ◽  
Mitochondrial Atpase ◽  
Atpase Inhibitor ◽  
Lactate Dehydrogenase Release ◽  
Rat Hearts ◽  
Isolated Rat

Mitochondrial F1F0adenosinetriphosphatase (ATPase) is responsible for the majority of ATP synthesis during normoxic conditions, but under ischemic conditions it accounts for significant ATP hydrolysis. A previous study showed that preconditioning in isolated rat hearts is mediated by inhibition of this ATPase during ischemia. We tested this hypothesis in our isolated rat heart model of preconditioning. Preconditioning was accomplished by three 5-min periods of global ischemia separated by 5 min of reperfusion. This was followed by 20 min of global ischemia and 30 min of reperfusion. Preconditioning significantly enhanced reperfusion contractile function and reduced lactate dehydrogenase release but paradoxically reduced the time to onset of contracture during global ischemia. Myocardial ATP was depleted at a faster rate during the prolonged ischemia in preconditioned than in sham-treated hearts, which is consistent with the reduced time to contracture. ATP during reperfusion was repleted more rapidly in preconditioned hearts, which is consistent with their enhanced contractile function. Preconditioning significantly reduced lactate accumulation during the prolonged ischemia. We were not able to demonstrate that mitochondrial F1F0ATPase (measured in submitochondrial particles) was inhibited by preconditioning before or during the prolonged ischemia. The mitochondrial ATPase inhibitor oligomycin significantly conserved ATP during ischemia and increased the time to the onset of contracture, which is consistent with inhibition of the mitochondrial ATPase. Our results show that preconditioning in rat hearts can be independent of mitochondrial ATPase inhibition as well as ATP conservation.

scholarly journals The effects of N -acetylcysteine on cisplatin-induced cardiotoxicity on isolated rat hearts after short-term global ischemia

2015 ◽  
Vol 2 ◽  
pp. 996-1006 ◽  
Author(s):  
Gvozden Rosic ◽  
Ivan Srejovic ◽  
Vladimir Zivkovic ◽  
Dragica Selakovic ◽  
Jovana Joksimovic ◽  
...  
Keyword(s):  
Global Ischemia ◽  
Short Term ◽  
Rat Hearts ◽  
Isolated Rat

Pyruvate increases threshold for preconditioning in globally ischemic rat hearts

1994 ◽  
Vol 267 (4) ◽  
pp. H1403-H1409 ◽  
Author(s):  
C. A. Sargent ◽  
S. Dzwonczyk ◽  
P. Sleph ◽  
M. Wilde ◽  
G. J. Grover
Keyword(s):  
Lactate Dehydrogenase ◽  
Ischemic Preconditioning ◽  
Enhanced Recovery ◽  
Recovery Of Function ◽  
High Energy ◽  
Global Ischemia ◽  
High Energy Phosphates ◽  
Lactate Dehydrogenase Release ◽  
Rat Hearts ◽  
Isolated Rat

Isolated rat hearts can be protected by preconditioning, although this has not been found when they are perfused with pyruvate. We addressed the question of whether pyruvate could increase the threshold for preconditioning in isolated rat hearts and whether this could be overcome with increased durations of ischemia. A protocol of four periods of 5 min of ischemic preconditioning (4 x 5 min) protected hearts (improved recovery of function, reduced lactate dehydrogenase release) not perfused with pyruvate from a subsequent 30-min period of global ischemia, but did not protect pyruvate-perfused hearts. Pilot studies indicated that hearts perfused in the presence of pyruvate must be ischemic for approximately 40% longer to produce equivalent ischemic damage in nonpyruvate-treated hearts. Thus the preconditioning period of 5 min was increased by approximately 40% to 7 min to produce equivalent degrees of preconditioning. Hearts preconditioned with the 4 x 7 min protocol with pyruvate were significantly protected against a subsequent severe global ischemia (enhanced recovery of function, reduced lactate dehydrogenase release). High-energy phosphates were measured at the end of the preconditioning protocol (before final global ischemia) to determine whether there was a correlation between cardioprotection and high-energy phosphate levels. There was no correlation between ATP, ADP, or AMP levels and the efficacy of preconditioning. However, an increase in creatine phosphate was associated with cardioprotection, although the importance of this in mediating preconditioning is doubtful. Thus the ability to precondition rat hearts is somewhat dependent on their energy source, but this appears to be due to changes in the severity of the ischemic preconditioning event.

Relative contributions of Na+/H+ exchange and Na+/HCO3− cotransport to ischemic Nai+ overload in isolated rat hearts

2005 ◽  
Vol 288 (1) ◽  
pp. H287-H292 ◽  
Author(s):  
Michiel Ten Hove ◽  
Marcel G. J. Nederhoff ◽  
Cees J. A. Van Echteld
Keyword(s):  
Nmr Spectroscopy ◽  
Intracellular Ph ◽  
Coronary Flow ◽  
Global Ischemia ◽  
The Other ◽  
Hepes Buffer ◽  
Rat Hearts ◽  
Isolated Rat

The Na+/H+ exchanger (NHE) and/or the Na+/HCO3− cotransporter (NBC) were blocked during ischemia in isolated rat hearts. Intracellular Na+ concentration ([Na+]i), intracellular pH (pHi), and energy-related phosphates were measured by using simultaneous 23Na and 31P NMR spectroscopy. Hearts were subjected to 30 min of global ischemia and 30 min of reperfusion. Cariporide (3 μM) or HCO3−-free HEPES buffer was used, respectively, to block NHE, NBC, or both. End-ischemic [Na+]i was 320 ± 18% of baseline in HCO3−-perfused, untreated hearts, 184 ± 6% of baseline when NHE was blocked, 253 ± 19% of baseline when NBC was blocked, and 154 ± 6% of baseline when both NHE and NBC were blocked. End-ischemic pHi was 6.09 ± 0.06 in HCO3−-perfused, untreated hearts, 5.85 ± 0.02 when NHE was blocked, 5.81 ± 0.05 when NBC was blocked, and 5.70 ± 0.01 when both NHE and NBC were blocked. NHE blockade was cardioprotective, but NBC blockade and combined blockade were not, the latter likely due to a reduction in coronary flow, because omission of HCO3− under conditions of NHE blockade severely impaired coronary flow. Combined blockade of NHE and NBC conserved intracellular H+ load during reperfusion and led to massive Na+ influx when blockades were lifted. Without blockade, both NHE and NBC mediate acid-equivalent efflux in exchange for Na+ influx during ischemia, NHE much more than NBC. Blockade of either one does not affect the other.

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