Mitochondrial dehydrogenase activity affects adaptation of cardiac oxygen consumption to demand

1993 ◽  
Vol 264 (2) ◽  
pp. H448-H453 ◽  
Author(s):  
J. B. Hak ◽  
J. H. Van Beek ◽  
M. H. Eijgelshoven ◽  
N. Westerhof
Keyword(s):  
Oxygen Consumption ◽  
Response Time ◽  
Dehydrogenase Activity ◽  
Calcium Uptake ◽  
High Energy ◽  
Mitochondrial Calcium ◽  
High Energy Phosphates ◽  
Mean Response Time ◽  
The Mean ◽  
Mitochondrial Calcium Uptake

The effect of regulation of mitochondrial dehydrogenase activities on the mean response time of mitochondrial oxygen consumption, which characterizes the delay between changes in ATP hydrolysis and changes in oxygen consumption, was investigated in isolated rabbit hearts and perfused with Tyrode solution at 28 degrees C. Perfusion with ruthenium red (RR) blocks mitochondrial calcium uptake and thus decreases mitochondrial dehydrogenase activities. Perfusion with pyruvate increases pyruvate dehydrogenase activity. The mean response time was 11.8 +/- 0.7 s (means +/- SE) during control, 12.2 +/- 1.2 s during perfusion with 0.9 microgram/ml RR, and 20.7 +/- 3.4 s during perfusion with 2.1 micrograms/ml RR. Blockade with 0.9 microgram/ml RR, which is presumably partial, did not slow the response, suggesting that mitochondrial calcium uptake may not be rate limiting. Strong blockade of mitochondrial calcium uptake increases the mean response time, presumably due to decreased calcium activation of the mitochondrial dehydrogenases. Perfusion with pyruvate significantly decreased the mean response time to 10.0 +/- 1.4 s compared with 11.9 +/- 0.7 s during perfusion with glucose. This decrease with pyruvate is not compatible with a shift to regulation by high-energy phosphates but may reflect increased mitochondrial oxidative capacity caused by increased NADH levels.

Mitochondrial calcium uptake and oxygen consumption in cystic fibrosis

Nature ◽  
1979 ◽  
Vol 278 (5701) ◽  
pp. 276-277 ◽  
Author(s):  
ROBERT J. FEIGAL ◽  
BURTON L. SHAPIRO
Keyword(s):  
Cystic Fibrosis ◽  
Oxygen Consumption ◽  
Calcium Uptake ◽  
Mitochondrial Calcium ◽  
Mitochondrial Calcium Uptake

Adaptation speed of cardiac mitochondrial oxygen consumption decreases with higher heart rate

1993 ◽  
Vol 265 (6) ◽  
pp. H1893-H1898 ◽  
Author(s):  
M. H. Eijgelshoven ◽  
J. B. Hak ◽  
J. H. Van Beek ◽  
N. Westerhof
Keyword(s):  
Skeletal Muscle ◽  
Heart Rate ◽  
Oxygen Consumption ◽  
Response Time ◽  
Metabolic Demand ◽  
Average Delay ◽  
Mitochondrial Oxygen Consumption ◽  
Atp Production ◽  
Mean Response Time ◽  
The Mean

The purpose of the present study was to determine whether the mean response time of cardiac mitochondrial oxygen consumption after a step in metabolic demand is constant in heart muscle, as has already been found for skeletal muscle. The mean response time reflects the average delay between the change in ATP hydrolysis due to a heart rate step and mitochondrial ATP production. Isolated rabbit hearts with a water-filled balloon in the left ventricle were perfused according to Langendorff with a constant flow of Tyrode solution at 28 degrees C. The mean response time increased significantly from 7.6 s for a step in heart rate from 60 to 70 min-1 to 12.1 s for a step from 60 to 120 min-1. The mean response times for heart rate steps downward from 120 min-1 were all approximately 12 s, but for the step from 120 to 140 min-1 the response time was 16.8 s. These results demonstrate that the mean response time of cardiac mitochondrial oxygen consumption in most cases increases with heart rate. These findings are in contrast to those obtained in skeletal muscle, where the response time at which ATP synthesis adapts to a change in work load is constant.

scholarly journals Development of Perceptual Inhibition in Adolescents—a Critical Period?

Symmetry ◽  
2021 ◽  
Vol 13 (3) ◽  
pp. 457
Author(s):  
Isabel María Introzzi ◽  
María Marta Richard’s ◽  
Yesica Aydmune ◽  
Eliana Vanesa Zamora ◽  
Florencia Stelzer ◽  
...  
Keyword(s):  
Response Time ◽  
Executive Functions ◽  
Critical Period ◽  
Search Task ◽  
Probability Distributions ◽  
Linear Trajectory ◽  
Gaussian Functions ◽  
Mean Response Time ◽  
The Mean ◽  
One Year

Recent studies suggest that the developmental curves in adolescence, related to the development of executive functions, could be fitted to a non-linear trajectory of development with progressions and retrogressions. Therefore, the present study proposes to analyze the pattern of development in Perceptual Inhibition (PI), considering all stages of adolescence (early, middle, and late) in intervals of one year. To this aim, we worked with a sample of 275 participants between 10 and 25 years, who performed a joint visual and search task (to measure PI). We have fitted ex-Gaussian functions to the probability distributions of the mean response time across the sample and performed a covariance analysis (ANCOVA). The results showed that the 10- to 13-year-old groups performed similarly in the task and differ from the 14- to 19-year-old participants. We found significant differences between the older group and all the rest of the groups. We discuss the important changes that can be observed in relation to the nonlinear trajectory of development that would show the PI during adolescence.

Dinuclear nitrido-bridged ruthenium complexes bearing diimine ligands

2017 ◽  
Vol 46 (41) ◽  
pp. 14256-14263 ◽  
Author(s):  
Julie Urgiles ◽  
Sarah R. Nathan ◽  
Samantha N. MacMillan ◽  
Justin J. Wilson
Keyword(s):  
Calcium Uptake ◽  
Ruthenium Complexes ◽  
Ligand Substitution ◽  
Mitochondrial Calcium ◽  
Substitution Reactions ◽  
Uptake Inhibition ◽  
Diimine Ligands ◽  
Mitochondrial Calcium Uptake ◽  
Ligand Substitution Reactions

Nitrido-bridged ruthenium complexes are synthesized via ligand substitution reactions and evaluated for mitochondrial calcium uptake inhibition.

Mitochondrial calcium uptake during ischemia is regulated by cytosolic ATP:ADP ratio

2003 ◽  
Vol 114 (2) ◽  
pp. 304 ◽  
Author(s):  
A. Wakata ◽  
A.E. Belous ◽  
C.D. Knox ◽  
J.M. Pierce ◽  
I.B. Nicoud ◽  
...  
Keyword(s):  
Calcium Uptake ◽  
Mitochondrial Calcium ◽  
Mitochondrial Calcium Uptake

OXYGEN AND MITOCHONDRIAL CALCIUM UPTAKE CAPACITY REGULATE THE INCIDENCE OF APOPTOSIS IN EPITHELIAL CELLS

Shock ◽  
2004 ◽  
Vol 21 (Supplement) ◽  
pp. 28
Author(s):  
Xueling Ma ◽  
Stefan Baeder ◽  
Weidong Du ◽  
Marion E. Schneider
Keyword(s):  
Epithelial Cells ◽  
Calcium Uptake ◽  
Mitochondrial Calcium ◽  
Uptake Capacity ◽  
Mitochondrial Calcium Uptake

Abstract 284: Loss of Micu3 Confers Cardioprotection Against Cardiac Injury

2020 ◽  
Vol 127 (Suppl_1) ◽  
Author(s):  
Bao Puente ◽  
Junhui Sun ◽  
Maria Fergusson ◽  
Julia Liu ◽  
Anna Kosmach ◽  
...  
Keyword(s):  
Cardiac Function ◽  
Infarct Size ◽  
Reperfusion Injury ◽  
Calcium Uptake ◽  
Cardiac Injury ◽  
Mitochondrial Calcium ◽  
Wild Type ◽  
Ischemic Reperfusion ◽  
Mitochondrial Calcium Uptake

Background: Mitochondrial calcium flux and signaling is integral to cardiac function and contraction. However, during pathologic conditions such as ischemic/reperfusion injury, mitochondrial calcium overload can induce the opening of the mitochondrial permeability transitioning pore (PTP), resulting in the collapse of mitochondrial membrane potential, ATP depletion, and generation of reactive oxygen species, all together leading to cell death. Hence, modulation of mitochondrial calcium and inhibition of the PTP is a promising target for cardioprotection and prevention of cardiomyocyte death. The mitochondrial calcium uniporter (MCU) complex mediates rapid mitochondrial calcium uptake. MICU3 is a regulator of the MCU complex and has been shown to be a highly potent stimulator of MCU-dependent calcium uptake in neuronal cells. We found that MICU3 is expressed in hearts and we therefore investigated the role of MICU3 in the heart. We examined the role of MICU3 in the development of hypertrophy and in a separate study we examined the response to ischemic-reperfusion (I/R) injury. Given its role in regulating mitochondrial calcium uptake, we hypothesized that loss of MICU3 confers protection against cardiac injury. Methods: Mice with global deletion of Micu3 (Micu3 -/- ) were created utilizing CRISPR-Cas9 technology. Adult knockout and littermate wild type mice were treated with Isoproterenol (15mg/kg/day) for two weeks to induce hypertrophy. Echocardiograms were performed at baseline and after treatment to assess changes in left ventricular size and function. I/R injury was studied using Langendorff ex vivo perfused heart system, exposing knockout and wild type hearts to 20 minutes of ischemia and 90 minutes of reperfusion. Hemodynamic data and infarct size were collected and compared. Student t-test and 2-way ANOVA were used for statistical analysis. Result: Micu3 -/- mice had normal cardiac function at baseline. There was no sex difference in cardiac function. Micu3 -/- mice continued to show normal function after 2 weeks of treatment with Isoproterenol, whereas wild type mice exhibited depressed function (median FS 35% vs. 24% p = 0.0001, EF 64% vs. 50% p = 0.0001). Wild type mice developed LV dilation from baseline (median 4.15mm vs. 4.57mm, p = 0.0014), whereas LV dimension remained stable in Micu3 -/- mice (median 4.12mm vs. 4.18mm, p= 0.9892). Micu3 - /- mice were also protected from I/R injury. Compared to wild types, Micu3 -/- hearts demonstrated less contractile dysfunction at end reperfusion (median rate pressure product 62% vs. 41%, p = 0.002), and significantly smaller infarct size (median 33% vs. 53%, p = 0.0001). Conclusion: Loss of MICU3 confers cardioprotection against ischemic reperfusion injury and Isoproterenol induced cardiac dysfunction.

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