Differential effects of superoxide dismutase on high energy phosphates, creatine kinase release, and arrhythmias during post-ischaemic reperfusion in isolated rat hearts

1988 ◽  
Vol 83 (2) ◽  
pp. 149-157 ◽  
Author(s):  
H. J. Heuer ◽  
E. Müller ◽  
W. Bernauer
Keyword(s):  
Superoxide Dismutase ◽  
Creatine Kinase ◽  
High Energy ◽  
High Energy Phosphates ◽  
Differential Effects ◽  
Rat Hearts ◽  
Isolated Rat

scholarly journals Effects of oxidant exposure on substrate utilization and high-energy phosphates in isolated rat hearts.

1994 ◽  
Vol 75 (1) ◽  
pp. 97-104 ◽  
Author(s):  
K P Burton ◽  
J G Jones ◽  
T H Le ◽  
A D Sherry ◽  
C R Malloy
Keyword(s):  
High Energy ◽  
Substrate Utilization ◽  
High Energy Phosphates ◽  
Rat Hearts ◽  
Isolated Rat

Adrenergic influences on cardiac function during ventricular fibrillation in isolated rat hearts

1991 ◽  
Vol 261 (5) ◽  
pp. H1452-H1456
Author(s):  
I. Derad ◽  
I. Funk ◽  
P. Pauschinger ◽  
J. Born
Keyword(s):  
Blood Flow ◽  
Oxygen Consumption ◽  
Ventricular Fibrillation ◽  
Cardiac Function ◽  
Coronary Blood Flow ◽  
High Energy ◽  
High Energy Phosphates ◽  
Tissue Concentrations ◽  
Rat Hearts ◽  
Isolated Rat

Effects of norepinephrine (NE, 10(-6) M), epinephrine (E, 10(-6) M), and vehicle on coronary blood flow (CF), oxygen consumption, and lactate release were compared in 32 isolated rat hearts during 5 min of ventricular fibrillation (VF). After VF, tissue concentrations of ATP, AMP, creatinine phosphate (CP), and lactate were measured. Perfusion of treatments started 30 s after onset of VF and was maintained throughout VF. CF during VF was greater (P less than 0.005) during perfusion of E (mean +/- SE, 5.73 +/- 0.15 ml/min) than NE (5.06 +/- 0.32 ml/min) or vehicle (5.11 +/- 0.18 ml/min). Oxygen consumption during VF was higher during perfusion of E (29.5 +/- 0.9 microliters.min(-1).g wet heart wt(-1)) than vehicle (27.3 +/- 0.7 microliters.min(-1).g(-1); P less than 0.05); average oxygen consumption during NE (27.6 +/- 1.4 microliters.min(-1).g(-1)) and vehicle were comparable. After NE, but not E, tissue AMP concentrations were significantly increased, and CP concentrations were reduced compared with vehicle (P less than 0.05). Enhanced consumption of high-energy phosphates during NE suggests that there is also an enhanced demand for oxygen. However, unlike during E, during NE this demand is not met by an augmented CF. Thus, compared with E, NE treatment during VF may increase the risk of hypoxic damage.

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.

Complete inhibition of creatine kinase in isolated perfused rat hearts

1987 ◽  
Vol 252 (1) ◽  
pp. E124-E129 ◽  
Author(s):  
E. T. Fossel ◽  
H. Hoefeler
Keyword(s):  
Creatine Kinase ◽  
Systolic Pressure ◽  
Creatine Phosphate ◽  
High Energy ◽  
Complete Inhibition ◽  
High Energy Phosphates ◽  
Rat Hearts ◽  
Perfused Rat Hearts ◽  
Low Levels ◽  
Developed Pressure

Transient exposure of an isolated isovolumic perfused rat heart to low concentrations (0.5 mM) of perfusate-born iodoacetamide resulted in complete inhibition of creatine kinase and partial inhibition of glyceraldehyde-3-phosphate dehydrogenase in the heart. At low levels of developed pressure, hearts maintained mechanical function, ATP, and creatine phosphate levels at control values. However, iodoacetamide-inhibited hearts were unable to maintain control values of end diastolic pressure or peak systolic pressure as work load increased. Global ischemia resulted in loss of all ATP without loss of creatine phosphate, indicating lack of active creatine kinase. These results indicate that isovolumic perfused rat hearts are able to maintain normal function and normal levels of high-energy phosphates without active creatine kinase at low levels of developed pressure.

Independent dual perfusion of left and right coronary arteries in isolated rat hearts

1991 ◽  
Vol 261 (6) ◽  
pp. H2082-H2090 ◽  
Author(s):  
M. Avkiran ◽  
M. J. Curtis
Keyword(s):  
High Energy ◽  
Low Flow ◽  
Blue Dye ◽  
Ischemia And Reperfusion ◽  
Langendorff Preparation ◽  
Rat Hearts ◽  
Left And Right ◽  
Conventional Models ◽  
Aortic Cannula ◽  
Isolated Rat

A novel dual lumen aortic cannula was designed and constructed to permit independent perfusion of left and right coronary beds in isolated rat hearts without necessitating the cannulation of individual arteries. Stability of the dual-perfusion preparation was shown to be similar to that of the conventional Langendorff preparation, in terms of coronary flow, heart rate, and high-energy phosphate content. The independence of left and right perfusion beds was confirmed by unilateral infusion of disulfine blue dye and spectrophotometric detection of the dye in ventricular homogenates. Transient cessation of flow to the left coronary bed resulted in severe ventricular arrhythmias upon reperfusion, as in conventional models of regional ischemia and reperfusion. The dual-perfusion model is technically undemanding, reproducible, inexpensive, and can be used in several species. It enables studies with 1) regional low flow ischemia, 2) regional zero-flow ischemia without coronary ligation (with attendant damage to vasculature), 3) selective application of drugs or interventions to the ischemic-reperfused zone, and 4) selective application of components of ischemia and reperfusion to a site anatomically relevant to ischemic heart disease.

An increase in intracellular [Na+] during Ca2+ depletion is not related to Ca2+ paradox damage in rat hearts

1998 ◽  
Vol 274 (3) ◽  
pp. H846-H852 ◽  
Author(s):  
Maurits A. Jansen ◽  
Cees J. A. Van Echteld ◽  
Tom J. C. Ruigrok
Keyword(s):  
Nuclear Magnetic Resonance ◽  
Creatine Kinase ◽  
Magnetic Resonance ◽  
Rate Pressure Product ◽  
Free Solution ◽  
Rat Hearts ◽  
Significant Change ◽  
Group Recovery ◽  
Isolated Rat ◽  
Nuclear Magnetic

Ca2+paradox damage has been suggested to be determined by Na+ entry during Ca2+ depletion and exchange of Na+ for Ca2+ during Ca2+ repletion. With the use of23Na nuclear magnetic resonance, we previously observed a Ca2+ paradox without a prior Na+ increase. We have now demonstrated a Na+ increase during Ca2+ and Mg2+ depletion without the occurrence of the Ca2+ paradox during Ca2+ repletion. Isolated rat hearts were perfused for 20 min with a Ca2+-free or a Ca2+- and Mg2+-free (Ca2+/Mg2+-free) solution under hypothermic conditions (20 and 25°C). Intracellular Na+ concentration ([Na+]i) increased from 11.9 ± 1.2 to 26.9 ± 5.8 mM ( P < 0.001) during Ca2+/Mg2+-free perfusion at 20°C, whereas no significant change in [Na+]ioccurred during 20 min of Ca2+-free perfusion at 20°C. In addition, we confirmed that [Na+]idid not change significantly during 20 min of normothermic Ca2+-free perfusion. Creatine kinase release during normothermic Ca2+ repletion in the 20°C groups was ∼10% and in the 25°C groups 75% of the release in the normothermia group. Recovery of rate-pressure product was ∼50% in the 20°C groups versus 0% in the normothermia group. In conclusion, hypothermic Ca2+/Mg2+-free perfusion results in a significant increase of [Na+]i, which does not contribute to the extent of the Ca2+ paradox on normothermic Ca2+ repletion.

Carbofuran-induced alterations (in vivo) in high-energy phosphates, creatine kinase (CK) and CK isoenzymes

1991 ◽  
Vol 65 (4) ◽  
pp. 304-310 ◽  
Author(s):  
Ramesh C. Gupta ◽  
John T. Goad ◽  
Wade L. Kadel
Keyword(s):  
Creatine Kinase ◽  
High Energy ◽  
High Energy Phosphates

Cardioprotective Effects of Propofol and Sevoflurane in Ischemic and Reperfused Rat Hearts 

1999 ◽  
Vol 91 (5) ◽  
pp. 1349-1349 ◽  
Author(s):  
Sanjiv Mathur ◽  
Parviz Farhangkhgoee ◽  
Morris Karmazyn
Keyword(s):  
High Energy ◽  
Left Ventricular ◽  
High Energy Phosphates ◽  
Constant Flow Rate ◽  
Rat Hearts ◽  
Reperfusion Period ◽  
Coronary Syndromes ◽  
Cardioprotective Effects ◽  
Developed Pressure

Background Sodium ion-hydrogen ion (Na(+)-H(+)) exchange inhibitors are effective cardioprotective agents. The N(+)-H(+) exchange inhibitor HOE 642 (cariporide) has undergone clinical trials in acute coronary syndromes, including bypass surgery. Propofol and sevoflurane are also cardioprotective via unknown mechanisms. The authors investigated the interaction between propofol and HOE 642 in the ischemic reperfused rat heart and studied the role of adenosine triphosphate-sensitive potassium (K(ATP)) channels in the myocardial protection associated with propofol and sevoflurane. Methods Isolated rat hearts were perfused by the Langendorff method at a constant flow rate, and left ventricular function and coronary pressures were assessed using standard methods. Energy metabolites were also determined. To assess the role of K(ATP) channels, hearts were pretreated with the K(ATP) blocker glyburide (10 microM). Hearts were then exposed to either control buffer or buffer containing HOE 642 (5 microM), propofol (35 microM), sevoflurane (2.15 vol%), the K(ATP) opener pinacidil (1 microM), or the combination of propofol and HOE 642. Each heart was then subjected to 1 h of global ischemia followed by 1 h of reperfusion. Results Hearts treated with propofol, sevoflurane, pinacidil, or HOE 642 showed significantly higher recovery of left ventricular developed pressure and reduced end-diastolic pressures compared with controls. The combination of propofol and HOE 642 provided superior protection toward the end of the reperfusion period. Propofol, sevoflurane, and HOE 642 also attenuated the onset and magnitude of ischemic contracture and preserved high-energy phosphates (HEPs) compared with controls. Glyburide attenuated the cardioprotective effects of sevoflurane and abolished the protection observed with pinacidil. In contrast, glyburide had no effect on the cardioprotection associated with propofol treatment. Conclusion HOE 642, propofol, and sevoflurane provide cardioprotection via different mechanisms. These distinct mechanisms may allow for the additive and superior protection observed with the combination of these anesthetics and HOE 642.

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