Mitochondrial enzymatic alterations produced in the myocardium by anoxic cardiac arrest

Gomes, Otoni Moreira; Pedroso, F. I.; Pereira, Sónia; Ayoub, Ali; Kwang, W.T.; Bittencourt, D; Zerbini, E.J.

doi:10.1016/s0022-5223(19)40500-x

Cited by 11 publications

(2 citation statements)

References 15 publications

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“…Even severe mitochondrial damage as observed after 60 minutes of normothermic anoxia may be restored by a 50 minute reperfusion period. However, according to the findings of O'Connor and Gomes (9,4), mitochondrial function may not be normalized in spite of normal structure. Furthermore, the loss of adeninenucleotides caused by the ischemia is repleted only slowly during the postischemic period (2,3,6).…”

Section: Discussionmentioning

confidence: 97%

Recovery of the Heart after Normothermic Ischemia Part I: Ultrastructural Findings during Postischemic Reperfusion

Mulch¹,

Schaper²,

Hh³

et al. 1979

Thorac cardiovasc Surg

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The influence of controlled ischemia on myocardial ultrastructure was investigated in isolated, metabolically supported canine hearts. Recovery of functionally normal tissue as indicated by the reversibility of morphological alterations was observed up to 60 minutes of anoxia. It was shown that prolonged reperfusion of the empty beating heart supports the recovery of normal cellular ultrastructure. Severe ischemic damage of mitochondria due to ischemia of 60 minutes was almost completely reversible after a reperfusion period of 50 minutes.

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Section: Discussionmentioning

confidence: 97%

Recovery of the Heart after Normothermic Ischemia Part I: Ultrastructural Findings during Postischemic Reperfusion

Mulch¹,

Schaper²,

Hh³

et al. 1979

Thorac cardiovasc Surg

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“…Lochner (15), Burdette (5), Wedell (21), and Gomes (8) have also found that 60 minutes of normothermic ischemia is a critical time span for the postischemic recovery of mitochondria.…”

Section: Discussionmentioning

confidence: 97%

Recovery of the Heart after Normothermic Ischemia: Part II: Myocardial Function during Postischemic Reperfusion

Mulch¹,

Schaper²,

Gottwik³

et al. 1979

Thorac cardiovasc Surg

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Contraction and relaxation of the canine myocardium were examined during normothermic ischemia in an isolated heart model. Decrease in the development of tension depends on the duration of ischemia. Deficient functional recovery was observed after ischemic periods extending beyond 30 minutes, in spite of reperfusion periods of over 1 hour. A decrease in compliance was observed during the anoxic period, but a persistent defect of relaxation occurred only after 60 minutes of ischemia. After this period there was also a disturbance in the autoregulative mechanisms of coronary perfusion and an uncoupling of O2-consumption and mechanical efficiency. A prolonged reperfusion period of the heart beating empty allowed ultrastructural recovery of the damaged myocardium. In contrast, functional recovery of the myocardium, as determined by several parameters of contraction and relaxation, did not correlate with ultrastructural recovery and was not improved by prolonged reperfusion.

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Experimental Evaluation of Coronary Infusates in Dogs

Raju¹,

Gibson²,

Heath³

et al. 1975

Arch Surg

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Mitochondrial enzymatic alterations produced in the myocardium by anoxic cardiac arrest

Cited by 11 publications

References 15 publications

Recovery of the Heart after Normothermic Ischemia Part I: Ultrastructural Findings during Postischemic Reperfusion

Recovery of the Heart after Normothermic Ischemia Part I: Ultrastructural Findings during Postischemic Reperfusion

Recovery of the Heart after Normothermic Ischemia: Part II: Myocardial Function during Postischemic Reperfusion

Experimental Evaluation of Coronary Infusates in Dogs

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