Stunning: A Radical Re-view

Hearse, David J.

doi:10.1007/978-1-4613-1517-9_3

Cited by 38 publications

(15 citation statements)

References 197 publications

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“…However, the declining glycolytic activity after 3 h of hypothermic perfusion may indicate an exacerbation of energy deficiency, which should be accompanied by excessive noradrenaline and DOPEG liberation into the extracellular space [15]. On the other hand, the addition of glucose to the perfusate has been found to almost completely prevent the release of noradrenaline and DOPEG in normothermia, irrespective of oxygen pressure [16]. Thus, the reduced glycolytic activity may produce sufficient metabolic energy to prevent excessive noradrenaline liberation.…”

Section: Discussionmentioning

confidence: 95%

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Concentrations of catecholamines in transplanted hearts after extracorporeal perfusion and cold storage

et al. 1995

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Using different perfusion regimes and orthograde implantation, some investigators have found sufficient heart function after extracorporeal perfusion of hearts for 24 and even 72 h. However, we found no significant improvement of perfused hearts compared to cold stored hearts after a 9-h extracorporeal period. A possible explanation for this finding could be the excessive liberation of catecholamines during ischemia, as has been demonstrated in isolated perfused hearts. Therefore, the aim of this study was to investigate whether concentrations of noradrenaline and dihydroxyphenylglycol (DOPEG)--a noradrenaline metabolite-increased pathologically during continuous extracorporeal heart perfusion for 5 h in pigs, in comparison to hearts stored at 4 degrees C. The venoarterial differences in noradrenaline and DOPEG were not significantly different in the two groups. Concentrations of lactate and pyruvate decreased substantially after 3-h hypothermic perfusion. The lactate/pyruvate ratio remained at a value of 25-35. Only after the end of the extracorporeal circulation did this ratio reach a value of 40-65. In our model, these findings demonstrate that the excessive liberation of catecholamines is not a reason for heart failure after cold storage or perfusion.

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Section: Discussionmentioning

confidence: 95%

“…Free radicals are synthesized in the physiological cell metabolism, e.g., in purine metabolism, in HaberWeiss and Fenton reactions, and in the metabolism of unsaturated fatty acids [16]. But the cells have sufficient mechanisms for protection against the deleterious effects of these highly reactive molecules [17].…”

Section: Discussionmentioning

confidence: 99%

Concentrations of catecholamines in transplanted hearts after extracorporeal perfusion and cold storage

et al. 1995

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“…Depending on the site of action, a troponin-mediated Ca2+ sensitivity has been described (33,38), as well as a Ca" sensitivity of the myofilaments (27,77), or likewise, a Ca2+ response of the myofilaments (60). The definition, as provided by the individual authors, is used in this review.…”

Section: Ca2+ Sensitivitymentioning

confidence: 99%

“…Myocardial stunning is, however, still ill-defined (8,38). Contractile dysfunction in stunned myocardium could be due to either decreased myofilament Ca2+ sensitivity or decreased [Ca2+Ii transients (55).…”

Section: Acute Ischemia and Postischemic Reperfusionmentioning

confidence: 99%

EMD 57033: A Novel Ca²⁺ Sensitizing Agent

Schipke¹,

Korbmacher²

1996

Cardiovascular Drug Reviews

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“…That free radicals mediate myocardial ischemia-reperfusion injury [7][8][9] is still debated mainly because free radicals generated at ischemia and reperfusion are difficult to measure directly [10,11]. Preconditioning may reduce injury by decreasing free radical production during reperfusion [12][13][14].…”

Section: Introductionmentioning

confidence: 99%

Acetylcholine Attenuates Cardiomyocyte Oxidant Stress during Simulated Ischemia and Reoxygenation

et al. 2001

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We wanted to determine whether oxygen radicals open the mitochondrial ATP-dependent potassium channels (K_ATP) during an ischemic period to reduce cell death and oxidant stress. Chick embryonic cardiomyocytes were used. Cell viability was quantified with propidium iodide (5 µM), and free radicals was measured using 2′,7′-dichlorofluorescin diacetate. Preconditioning was produced by 10 min of simulated ischemia followed by 10 min of reoxygenation. Acetylcholine (1 mM), infused for 10 min instead of preconditioning, reduced cell death similarly (24 ± 5%, n = 7 and 18 ± 2%, n = 7, respectively, vs. controls, 49 ± 6%, n = 8). In control series, 60 min of simulated ischemia and 3 h of reoxygenation generated free radicals more than 300% above the baseline (ischemia: 3.63 ± 0.58, reoxygenation: 3.66 ± 0.47, n = 8). Preconditioning and acetylcholine markedly attenuated the oxidant stress during simulated ischemia (1.18 ± 0.41, n = 6 and 1.34 ± 0.60, n = 7 vs. controls 3.63 ± 0.58, n = 8) and re-oxygenation (1.23 ± 0.36, n = 6 and 1.50 ± 0.59, n = 7 vs. controls 3.66 ± 0.47, n = 8). The protection of acetylcholine was abolished with pretreatment with the antioxidant thiol reductant 2-mercaptopropionyl glycine and posttreatment with 5-hydroxydecanoate, a selective mitochondrial K_ATP channel antagonist (37 ± 7%, n = 7). These results demonstrate that oxygen radicals open mitochondrial K_ATP channels, which mediates the acetylcholine-induced preconditioning effect, and that stimulation of this signaling pathway attenuates oxidant stress.

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Stunning: A Radical Re-view

Cited by 38 publications

References 197 publications

Concentrations of catecholamines in transplanted hearts after extracorporeal perfusion and cold storage

Concentrations of catecholamines in transplanted hearts after extracorporeal perfusion and cold storage

EMD 57033: A Novel Ca²⁺ Sensitizing Agent

Acetylcholine Attenuates Cardiomyocyte Oxidant Stress during Simulated Ischemia and Reoxygenation

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Stunning: A Radical Re-view

Cited by 38 publications

References 197 publications

Concentrations of catecholamines in transplanted hearts after extracorporeal perfusion and cold storage

Concentrations of catecholamines in transplanted hearts after extracorporeal perfusion and cold storage

EMD 57033: A Novel Ca2+ Sensitizing Agent

Acetylcholine Attenuates Cardiomyocyte Oxidant Stress during Simulated Ischemia and Reoxygenation

Contact Info

Product

Resources

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EMD 57033: A Novel Ca²⁺ Sensitizing Agent