[On the theory of cocarboxylase action. II. Origin and fundamentals of a two-center mechanism of thiamine pyrophosphate action from research on models and enzymatic measuremets].
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Biomedical subjects
Publications and source records attributed to G Hübner.
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In the skeletal muscle of a patient with bilateral ptosis suggestive of progressive external ophthalmoplegia (PEO), but without ragged red fibres, electron microscopy revealed a moderate proliferation of mitochondria in nearly all fibres. A focal absence of cytochrome c oxidase and of mitochondrial ATPase was demonstrated histochemically in 3.2% and 1.4% respectively of the fibres. In 0.9% of the fibres both enzymes were deficient. In addition, mitochondrial ATPase, the ATP-synthesizing enzyme latent in controls, showed activation already before addition of an uncoupler. This indicates loosely coupled oxidative phosphorylation. The findings point to a complex derangement of mitochondrial function. Immunocytochemistry of cytochrome c oxidase favours the assumption that the defect is based on a highly diminished content of immunoreactive enzyme protein.
This article is a short review of newer findings concerning the physiological and biochemical bases of the heart's tolerance to ischemia. The following themes are discussed. I. Energy-pool, energy-demand, and efficiency of anaerobic metabolism, the essential determinants of reanimation time and the heart's tolerance to ischemia. II. Experimental results of ischemic heart arrest and the heart arrest induced by a sodium-poor calcium-free, procaine-containing cardioplegic solution, developed by the author. III. Equivalents of function, metabolism and structure during the anaerobic period of the myocardium. IV. The myocardium's capability to recover in dependence on the metabolic state of ischemia and summary of the most important points of gaining a long time of tolerated ischemia. V. Survey and prospects.
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