Cardiac mitochondrial activity in acute and chronic cyanosis

Park, C. Dick; Mela, Leena; Wharton, Robert; Reilly, James B.; Fishbein, Paul G.; Aberdeen, Eoin

doi:10.1016/0022-4804(73)90022-x

Cited by 26 publications

(1 citation statement)

References 7 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Thus, the effects of hypoxia could parallel organ pathology in CS. Notably, state 3 respiratory rate in cardiac mitochondria has been found to increase more than 100% during acute in vivo hypoxemia and to stabilize at more than 40% above baseline during chronic in vivo hypoxemia [34]. A similar observation has been made following hypoperfusion [35], [36], and comparable effects were also observed when demand was increased by endurance training [37], [38].…”

Section: Discussionsupporting

confidence: 54%

The Acute Phase of Experimental Cardiogenic Shock Is Counteracted by Microcirculatory and Mitochondrial Adaptations

et al. 2014

View full text Add to dashboard Cite

The mechanisms contributing to multiorgan dysfunction during cardiogenic shock are poorly understood. Our goal was to characterize the microcirculatory and mitochondrial responses following ≥10 hours of severe left ventricular failure and cardiogenic shock. We employed a closed-chest porcine model of cardiogenic shock induced by left coronary microembolization (n = 12) and a time-matched control group (n = 6). Hemodynamics and metabolism were measured hourly by intravascular pressure catheters, thermodilution, arterial and organ specific blood gases. Echocardiography and assessment of the sublingual microcirculation by sidestream darkfield imaging were performed at baseline, 2±1 and 13±3 (mean±SD) hours after coronary microembolization. Upon hemodynamic decompensation, cardiac, renal and hepatic mitochondria were isolated and evaluated by high-resolution respirometry. Low cardiac output, hypotension, oliguria and severe reductions in mixed-venous and hepatic O2 saturations were evident in cardiogenic shock. The sublingual total and perfused vessel densities were fully preserved throughout the experiments. Cardiac mitochondrial respiration was unaltered, whereas state 2, 3 and 4 respiration of renal and hepatic mitochondria were increased in cardiogenic shock. Mitochondrial viability (RCR; state 3/state 4) and efficiency (ADP/O ratio) were unaffected. Our study demonstrates that the microcirculation is preserved in a porcine model of untreated cardiogenic shock despite vital organ hypoperfusion. Renal and hepatic mitochondrial respiration is upregulated, possibly through demand-related adaptations, and the endogenous shock response is thus compensatory and protective, even after several hours of global hypoperfusion.

show abstract

Section: Discussionsupporting

confidence: 54%

The Acute Phase of Experimental Cardiogenic Shock Is Counteracted by Microcirculatory and Mitochondrial Adaptations

et al. 2014

View full text Add to dashboard Cite

show abstract

Development and Adaptation of Heart Mitochondrial Respiratory Chain Function in Fetus and in Newborn

Goodwin

Mela

Deutsch

et al. 1976

Advances in Experimental Medicine and Biology

View full text Add to dashboard Cite

The effect of oxygen on growth and development of the chick embryo

Metcalfe

Stock

Ingermann

1984

Respiration and Metabolism of Embryonic Vertebrates

View full text Add to dashboard Cite

When eggs are incubated in 60% O 2 , the weight of the 18-day embryo is greater than that of the control incubated in 21 % O 2 , Conversely, when O 2 availability is reduced by covering part of the eggshell, embryonic growth is retarded. The weight of the embryo at day 18 correlates with the surface area of its egg, as does the diffusing capacity for O 2 and the calculated chorioallantoic capillary surface area. Furthermore, during the last few days of chorioallantoic respiration in 21 % O 2 , the embryo becomes hypoxemic and its rate of growth slows. We propose that the O 2 tension in blood leaving the chorioallantoic capillaries limits the rate of growth of the chick embryo until the onset of pulmonary respiration.Oxygen may exert its effect on growth indirectly by altering the activity of a particular group of cells that controls embryonic growth rate. Alternatively, the availability of O 2 may directly determine the rate of energy production in individual embryonic tissues; an increase in the available energy would translate into accelerated growth. The concentration of adenosine triphosphate (ATP) in the nucleated embryonic erythrocytes is responsive to changes in O 2 availability.Under normoxic conditions erythrocytic [ATP] declines between the fourteenth and eighteenth days of incubation. This is consistent with the observation that the chick embryo becomes relatively hypoxemic during the last third of its development until air breathing begins. Incubation in 70% O 2 markedly attenuates the fall in [A TP]. If the erythrocyte is characteristic of other embryonic tissues with regard to the basic mechanisms of ATP production, the growth-accelerative effect of hyperoxia may be mediated by an increased rate of ATP generation.Our work with chick embryos began when we used them to study capillary growth and its control. Work in other laboratories had shown that when hen's eggs are incubated in environments with a high partial pressure of O 2 (P 02)' development of the large chorioallantoic vessels is retarded, and the vascularity of the yolk sac and the embryonic tissues is diminished compared to eggs incubated in room air (Remotti, 1933;Flemister and Cunningham, 1940;Allen, 1963). These earlier Seymour, R.S., (ed.) Respiration and metabolism of embryonic vertebrates.

show abstract

Cardiac mitochondrial activity in acute and chronic cyanosis

Cited by 26 publications

References 7 publications

The Acute Phase of Experimental Cardiogenic Shock Is Counteracted by Microcirculatory and Mitochondrial Adaptations

The Acute Phase of Experimental Cardiogenic Shock Is Counteracted by Microcirculatory and Mitochondrial Adaptations

Development and Adaptation of Heart Mitochondrial Respiratory Chain Function in Fetus and in Newborn

The effect of oxygen on growth and development of the chick embryo

Contact Info

Product

Resources

About