Myocardial infrastructure in the Isolated Rabbit Heart Exposed to Dopamine, Dobutamine, Isoprenaline, G‐Strofanthin, Xamoterol and Hypoxia

Kjaerulf-Jensen, H; Korsgaard, Niels; Lindeberg, H; Vigholt-Sørensen, E

doi:10.1111/j.1600-0773.1992.tb00988.x

Cited by 2 publications

(3 citation statements)

References 7 publications

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“…The mitochondrial volume is ϳ40% of that of a cardiomyocyte. The matrix volume, which is not static, occupies 29% of the mitochondrial volume in the OXPHOS state and can swell by 44% in leak states and in hypoxia (47). ⌬⌿ was similar for both groups [Ϫ200 mV (leak) and Ϫ170 mV (OXPHOS)].…”

Section: Discussionmentioning

confidence: 96%

“…Approximately 35-40% of the cardiomyocyte volume is occupied by mitochondria (6). The mitochondrial matrix volume in transitions between OXPHOS and leak states is dynamic, accounting for 29% and 44% of the mitochondrial volume, respectively (47). We therefore estimate matrix volumes to be 0.2 and 0.31 l/mg tissue in respective OXPHOS and leak states.…”

Section: Methodsmentioning

confidence: 99%

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Mitochondrial inefficiencies and anoxic ATP hydrolysis capacities in diabetic rat heart

Pham

Loiselle

Power

et al. 2014

American Journal of Physiology-Cell Physiology

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As ~80% of diabetic patients die from heart failure, an understanding of diabetic cardiomyopathy is crucial. Mitochondria occupy 35-40% of the mammalian cardiomyocyte volume and supply 95% of the heart's ATP, and diabetic heart mitochondria show impaired structure, arrangement, and function. We predict that bioenergetic inefficiencies are present in diabetic heart mitochondria; therefore, we explored mitochondrial proton and electron handling by linking oxygen flux to steady-state ATP synthesis, reactive oxygen species (ROS) production, and mitochondrial membrane potential (ΔΨ) within rat heart tissues. Sprague-Dawley rats were injected with streptozotocin (STZ, 55 mg/kg) to induce type 1 diabetes or an equivalent volume of saline (control, n = 12) and fed standard rat chow for 8 wk. By coupling high-resolution respirometers with purpose-built fluorometers, we followed Magnesium Green (ATP synthesis), Amplex UltraRed (ROS production), and safranin-O (ΔΨ). Relative to control rats, the mass-specific respiration of STZ-diabetic hearts was depressed in oxidative phosphorylation (OXPHOS) states. Steady-state ATP synthesis capacity was almost one-third lower in STZ-diabetic heart, which, relative to oxygen flux, equates to an estimated 12% depression in OXPHOS efficiency. However, with anoxic transition, STZ-diabetic and control heart tissues showed similar ATP hydrolysis capacities through reversal of the F1F0-ATP synthase. STZ-diabetic cardiac mitochondria also produced more net ROS relative to oxygen flux (ROS/O) in OXPHOS. While ΔΨ did not differ between groups, the time to develop ΔΨ with the onset of OXPHOS was protracted in STZ-diabetic mitochondria. ROS/O is higher in lifelike OXPHOS states, and potential delays in the time to develop ΔΨ may delay ATP synthesis with interbeat fluctuations in ADP concentrations. Whereas diabetic cardiac mitochondria produce less ATP in normoxia, they consume as much ATP in anoxic infarct-like states.

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Section: Discussionmentioning

confidence: 96%

Section: Methodsmentioning

confidence: 99%

Mitochondrial inefficiencies and anoxic ATP hydrolysis capacities in diabetic rat heart

Pham

Loiselle

Power

et al. 2014

American Journal of Physiology-Cell Physiology

View full text Add to dashboard Cite

show abstract

“…However, it is a very specific and constant value for any particular species making its variability a reliable measure of adaptation. Mitochondrial content was unchanged after chronic hypoxia in the adult guinea pig at 3,100 m (Kayar et al, 1987) and flounder heart at 25% oxygen saturation (Lennard et al, 1992) and in rabbit heart following acute anoxia (Kjaerulf Jensen et al, 1992), whereas, it was significantly elevated in cattle born and raised at 4,250 m (Ou et al, 1970).…”

Section: Discussionmentioning

confidence: 99%

Quantitative electron microscopic study of the hypoxic fetal sheep heart

et al. 1999

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In order to determine the effects of chronic, high-altitude hypoxia on the ovine fetal heart, we exposed pregnant ewes to 3,820 m beginning at 30 days gestation. We previously showed that following Ϸ110 days of hypoxia the fetal heart showed significant reduction in cardiac output (76% of control) and contractility, and elevated levels of citrate synthase and lactate dehydrogenase. To investigate ultrastructural influences on these observed physiologic changes at altitude, we hypothesized that the volume densities of myofibrils and mitochondria, and glycogen content would be reduced in the ovine fetal heart and that this may contribute to contraction and cardiac output deficits in hypoxia. Mitochondria and myofibril volume density were determined by standard point-counting techniques and glycogen content was determined by biochemical analysis. The glycogen content from the hypoxic right ventricle (4.8 Ϯ 0.3%) was significantly lower than in control right ventricle (6.8 Ϯ 0.5%) and both left ventricles (hypoxia, 7.2 Ϯ 0.5; control, 7.8 Ϯ 0.4%). Total mitochondrial volume density was also significantly reduced following hypoxia (15.5 Ϯ 0.7%) compared to controls (16.9 Ϯ 0.4%). As is common in the ovine fetal heart, the myofibril volume density of the right ventricle from both groups was significantly higher than the left ventricle (RV, 58.6 Ϯ 1.6; LV 54.3 Ϯ 0.9%). However, it was not different between control and high altitude. In support of our hypothesis, we may speculate that deficits in the quantity of myocyte glycogen and mitochondria contribute to the observed reduction in cardiac output and contractility, despite the upregulation of citrate synthase and lactate dehydrogenase. In contrast, myofibril volume density was unchanged.

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Myocardial infrastructure in the Isolated Rabbit Heart Exposed to Dopamine, Dobutamine, Isoprenaline, G‐Strofanthin, Xamoterol and Hypoxia

Cited by 2 publications

References 7 publications

Mitochondrial inefficiencies and anoxic ATP hydrolysis capacities in diabetic rat heart

Mitochondrial inefficiencies and anoxic ATP hydrolysis capacities in diabetic rat heart

Quantitative electron microscopic study of the hypoxic fetal sheep heart

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