Effects of deprivation of oxygen and glucose on the neural activity and the level of high energy phosphates in the hippocampal slices of immature and adult rat

1989 ◽  
Vol 48 (1) ◽  
pp. 11-18 ◽  
Author(s):  
Shinji Kawai ◽  
Masahiko Yonetani ◽  
Hajime Nakamura ◽  
Yasuhiro Okada
Keyword(s):  
Neural Activity ◽  
Hippocampal Slices ◽  
High Energy ◽  
High Energy Phosphates ◽  
Adult Rat

Manipulating the intracellular environment of hippocampal slices: pH and high-energy phosphates

1989 ◽  
Vol 28 (1-2) ◽  
pp. 83-91 ◽  
Author(s):  
Tim S. Whittingham ◽  
Eduardo Warman ◽  
Hussein Assaf ◽  
Thomas J. Sick ◽  
Joseph C. LaManna
Keyword(s):  
Hippocampal Slices ◽  
High Energy ◽  
High Energy Phosphates ◽  
Intracellular Environment

Energy metabolism and neural activity during deprivation of oxygen and/or glucose in the hippocampal slices of immature and adult rat

1992 ◽  
Vol 17 ◽  
pp. 69
Author(s):  
Makoto Nabetani ◽  
Yukihiro Yamada ◽  
Shinji Kawai ◽  
Masahiko Yonetani ◽  
Satoshi Takada ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Neural Activity ◽  
Hippocampal Slices ◽  
Adult Rat

scholarly journals Role of cation gradients in hypercontracture of myocytes during simulated ischemia and reperfusion

1993 ◽  
Vol 264 (6) ◽  
pp. H1896-H1906 ◽  
Author(s):  
M. Nishida ◽  
S. Borzak ◽  
B. Kraemer ◽  
J. P. Navas ◽  
R. A. Kelly ◽  
...  
Keyword(s):  
Ventricular Myocytes ◽  
Extracellular Fluid ◽  
High Energy ◽  
Ischemia And Reperfusion ◽  
High Energy Phosphates ◽  
Twitch Contraction ◽  
Adult Rat ◽  
Simulated Ischemia ◽  
The Relationship

We examined the relationship between transsarcolemmal cation gradients and hypercontracture of cardiac myocytes in ischemia and reperfusion using adult rat ventricular myocytes superfused with buffer mimicking normal or ischemic extracellular fluid. Contractile performance of electrically stimulated cells was recorded by an optical video system simultaneously with measurements of intracellular Ca2+ concentration ([Ca2+]i) using fura-2 or intracellular pH (pHi) using 2',7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein. While cells were exposed to simulated ischemia buffer, the transsarcolemmal H+ gradient was abolished, [Ca2+]i transient stopped, and twitch contraction of myocytes ceased. Upon reperfusion with normal buffer, H+ gradient was quickly restored, Ca2+ transients restarted with transient increase in systolic Ca2+, and twitch contraction restarted with development of hypercontracture, which continued after [Ca2+]i returned to preischemic level even in the presence of near-normal concentrations of high-energy phosphates. When the transsarcolemmal proton, Na+, and Ca2+ gradients were altered so that Na+ entry via Na(+)-H+ exchange and Ca2+ entry via Ca(2+)-Na+ exchange were made less favorable, the transient systolic overshoot of Ca2+ at reperfusion and development of hypercontracture was largely avoided. These results suggest that Na+ and then Ca2+ entry via the Na(+)-H+ and Na(+)-Ca2+ exchangers, respectively, probably contribute to the increase in [Ca2+]i and hypercontracture of myocytes at time of reperfusion in this model.

31P-NMR studies of isolated adult heart cells: effect of myoglobin inactivation

1991 ◽  
Vol 261 (4) ◽  
pp. H1155-H1163 ◽  
Author(s):  
R. K. Gupta ◽  
B. A. Wittenberg
Keyword(s):  
Sodium Nitrite ◽  
High Energy ◽  
Heart Cells ◽  
High Energy Phosphates ◽  
High Energy Phosphate ◽  
Nmr Studies ◽  
Adult Rat ◽  
Inhibition Of Glycolysis ◽  
Rat Heart Cells ◽  
External Ph

31P nuclear magnetic resonance (NMR) studies of isolated adult rat heart cells revealed that the cells maintained high-energy phosphates for up to 6 h in polyamide hollow fibers perfused with well-oxygenated nutrient medium. Glucose plus pyruvate superfused heart cells maintained [phosphocreatine]/[ATP] at 1.4 +/- 0.1, internal pH at 7.09 +/- 0.04 (external pH = 7.25), and intracellular free Mg2+ at 0.51 +/- 0.04 mM. In glucose-containing media, hypoxia was accompanied by a reversible decrease in intracellular ATP and phosphocreatine of approximately 50% and 80%, respectively, while the intracellular free Mg2+ was reversibly increased by 40%. However, inhibition of glycolysis by iodoacetate in aerobic pyruvate-containing medium did not significantly alter high-energy phosphate content. Inactivation of intracellular myoglobin with 1-2 mM sodium nitrite, which reduces the steady-state respiratory oxygen consumption rate by 30%, caused a significant (30%) decrease in intracellular phosphocreatine peak, which was reversed upon removal of sodium nitrite. The nitrite-induced decrease in phosphocreatine was also observed in iodoacetate-treated myocytes but not in oligomycin-treated cells. These results indicate that functional myoglobin enhances high-energy phosphate synthesis in well-oxygenated myocytes.

Reducing lactate accumulation does not attenuate lethal ischemic injury in isolated perfused rat hearts

1996 ◽  
Vol 270 (1) ◽  
pp. H38-H44 ◽  
Author(s):  
R. S. Vander Heide ◽  
J. A. Delyani ◽  
R. B. Jennings ◽  
K. A. Reimer ◽  
C. Steenbergen
Keyword(s):  
Cell Injury ◽  
Lactate Production ◽  
Myocardial Cell ◽  
High Energy ◽  
High Energy Phosphates ◽  
Glycogen Depletion ◽  
Lactate Accumulation ◽  
Adult Rat ◽  
Rat Hearts ◽  
Myocardial Cell Injury

The role of lactate accumulation in lethal ischemic myocardial cell injury was assessed by partially depleting hearts of glycogen before ischemia by using glucagon. Isolated adult rat hearts were perfused with glucose-free Krebs-Henseleit buffer containing acetate as substrate. After stabilization, treated hearts were perfused briefly (3 min) with buffer containing 2 micrograms/ml glucagon to reduce tissue glycogen stores, followed by 10 min of perfusion with control buffer, and 60 or 90 min of global ischemia. Before the onset of ischemia, glucagon-treated hearts contained 40% less glycogen than untreated hearts, but myocardial function and tissue levels of high-energy phosphates, lactate, and glucose 6-phosphate were similar. Lactate production during ischemia in the glucagon-treated hearts was 50% less than in untreated hearts. However, there was no decrease in the amount of creatine kinase release during reperfusion after either 60 or 90 min of ischemia. Thus although partial glycogen depletion reduced lactate accumulation during ischemia, this did not decrease the amount of lethal myocardial cell injury.

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