Metabolism of the artificially arrested heart and of the gas-perfused heart

Lochner, W.; Arnold, G.; Müller-Ruchholtz, E. R.

doi:10.1016/0002-9149(68)90114-8

Cited by 83 publications

(17 citation statements)

References 27 publications

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“…21 These studies provide further evidence that ischaemic injury may be initiated in the mitochondrion due to increased O 2 2 † production from the distal ETC, and that preventing electrons from reaching these sites better preserves respiratory chain activity and attenuates O 2 2 † production. Therefore, hypothermia, in addition to preserving the myocardial content of high-energy phosphates, 46,47 may also protect via temperature-sensitive blockade of electron transport during cold ischaemia. 21 Cardiac protection mediated by blocking electron transport during ischaemia is also reflected in the improved coronary flow and higher O 2 extraction in the amobarbital group on reperfusion.…”

Section: Discussionmentioning

confidence: 99%

WITHDRAWN: Inhibited mitochondrial respiration by amobarbital during cardiac ischemia improves redox state and reduces matrix Ca2+ overload and ROS release☆

Aldakkak

Stowe

Chen

et al. 2007

Cardiovascular Research

173

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Aim Damage to the mitochondrial electron transport chain (ETC) occurs during ischaemia. Blockade of electron flow in the ETC just before ischaemia with the reversible complex I inhibitor amobarbital protects isolated mitochondria against ischaemic damage and preserves oxidative phosphorylation and cytochrome c content. We hypothesized that brief amobarbital perfusion just before ischaemia would improve cardiac recovery and decrease infarct size after ischaemia and reperfusion (IR) ] were significantly reduced, NADH-FAD redox state was preserved and cardiac function was markedly improved in the amobarbital group; infarct size was smaller in the amobarbital group compared to the untreated group. Conclusion Temporary blockade of mitochondrial complex I activity by amobarbital protects hearts by reducing production of O 2 2 † and mtCa 2þ loading during IR injury.

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Section: Discussionmentioning

confidence: 99%

WITHDRAWN: Inhibited mitochondrial respiration by amobarbital during cardiac ischemia improves redox state and reduces matrix Ca2+ overload and ROS release☆

Aldakkak

Stowe

Chen

et al. 2007

Cardiovascular Research

173

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“…It was shown in KCL-arrested rat hearts that the level of oxygen consumption at the moment of arrest determines the resting uptake value of oxygen. The higher the active oxygen utilization, the higher will be the arrested values (9). This would mean for this study that the complete cessation of blood flow induces a higher oxygen deficiency in the subendocardial than in the subepicardial layers.…”

Section: Discussionmentioning

confidence: 90%

Temporal and spatial development of infarcts in porcine hearts

et al. 1984

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We investigated the temporal and spatial development of infarcts in porcine hearts to evaluate the time-dependent beneficial effect of reperfusion on infarct size. The left anterior descending coronary artery (LAD) was occluded in 17 pigs for different periods of time followed by 4 hours of reperfusion. Transmural needle biopsies subdivided into subendocardial and subepicardial halves were taken from the ischemic apex after 60 min of ischemia to determine the tissue concentrations of ATP and NAD. The myocardium-at-risk was assessed with a fluorescent dye injected into the right atrium at the end of the experiments, just after the LAD had been reoccluded. The excised hearts were cut into slices parallel to the heart basis. The ischemic myocardium was measured by planimetry of the non-fluorescent areas whereas the infarcted tissue was determined with the NBT stain and related to the area-at-risk. Ischemic cell death started in the jeopardized left ventricular subendocardial septum after about 30 min of ischemia. The further progress involved the right subendocardial septum and the subendocardium of the left anterior free wall. Already after 75 min of ischemia most of the myocytes-at-risk were irreversibly injured. Infarctions reached their final extent after 90-120 min of ischemia. These results indicate that in hearts without a significant collateral blood flow reperfusion can only reduce infarct size if its initiated within 60-75 min of ischemia. Like in canine hearts infarctions progress from the ischemic subendocardium towards the outer layers.

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“…Since the tissue level of CrP is an inverse function of the myocardial 0 2-consumption [17] and thus of the work of the myocardium [6,18], it would be tempting to explain the increase in CrP by a temporary relief of the mechanical work of the ischemically stressed musculature. But this rather long-lasting supernor mal degree of phosphorylation of creatine -the ratio CrP/tCr rose from 0.4 under control conditions to 0.7 -was also found in whole hearts which recovered from asphyxia and which performed normal circulatory work [8,9,12].…”

Section: Discussionmentioning

confidence: 99%

Metabolic and Structural Recovery of Left Ventricular Canine Myocardium from Regional Complete Ischemia

Isselhard¹,

Lauterjung²,

Witte³

et al. 1975

Eur Surg Res

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The capacity for recovery of the normothermic left ventricular myocardium from a regional complete ischemia (RCI) was investigated using changes in the myocardial metabolic status (ATP, ADP, AMP, creatine phosphate (CrP), free creatine, glycogen, glucose, lactate) and alterations of the morphology as parameters. In dogs, an area of the anterior wall of the left ventricular myocardium was temporarily deprived completely of its blood supply by 5–7 overlapping ligatures extending into the heart cavity. The metabolites of the adenylic acid-CrP system returned to normal tissue levels after 30 and 60 min of RCI within 14 and 35 days of recovery, respectively; restoration averaged 82% after 100 min, 74% after 140 min, and 38% after 180 min of RCI after 5 weeks of recovery. At the same time glycogen amounted to 163% after 100 min, 114% after 140 min, and 65% after 180 min of RCI. The biochemical data correlated well with the structural changes in the affected myocardium, especially with the amount of de- and regenerating heart muscle cells. These obviously were functionally defect and were not comparable with normal structured and functioning heart muscle cells.

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Metabolism of the artificially arrested heart and of the gas-perfused heart

Cited by 83 publications

References 27 publications

WITHDRAWN: Inhibited mitochondrial respiration by amobarbital during cardiac ischemia improves redox state and reduces matrix Ca2+ overload and ROS release☆

WITHDRAWN: Inhibited mitochondrial respiration by amobarbital during cardiac ischemia improves redox state and reduces matrix Ca2+ overload and ROS release☆

Temporal and spatial development of infarcts in porcine hearts

Metabolic and Structural Recovery of Left Ventricular Canine Myocardium from Regional Complete Ischemia

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