Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.3.5.1 (succinate dehydrogenase)
 8,177 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The contractile, histochemical, morphological and electrophysiological properties of two rat laryngeal muscles, the cricothyroid and posterior cricoarytenoid, have been measured. Both muscles act during respiration to maintain upper airway patency and an even distribution of air in the lungs. The cricothyroid and posterior cricoarytenoid are fast-twitch muscles, having contraction times of 3.4 and 7.2 ms respectively, high myosin ATPase activity, abundant sarcoplasmic reticulum (with average volumes of 9% and 15%, respectively, of the fibre volume) and T-system membrane (with average areas of 0.4 and 0.5 micron 2 micron -3 of fibre). The large areas of T-tubule membrane are reflected in the average specific membrane capacities of 6.5 muF cm-2 to 10.5 muF cm-2, which are high considering the small diameter of the fibres (20-30 micron). Of the two muscles, the posterior cricoarytenoid has the faster contraction time and the more abundant sarcoplasmic reticulum content. In addition, the posterior cricoarytenoid is less resistant to fatigue and demonstrates lower succinic dehydrogenase activity. The fatigability of this muscle, coupled with its general lack of functional reserve, suggest that its failure may contribute to upper airway obstruction during respiratory distress.
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PMID:The contractile properties, histochemistry, ultrastructure and electrophysiology of the cricothyroid and posterior cricoarytenoid muscles in the rat. 621 35

We report a case of a 6-week-old male who was admitted to the hospital for respiratory distress. An echocardiogram revealed a poorly functioning left ventricle with an ejection fraction of 18% and dilated cardiomyopathy with noncompaction of the left ventricle. A muscle biopsy was performed to identify the cause of his cardiomyopathy, which revealed succinate dehydrogenase deficiency. The patient was medically managed for dilated cardiomyopathy and eventually died due to congestive heart failure.
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PMID:Succinate dehydrogenase deficiency associated with dilated cardiomyopathy and ventricular noncompaction. 1708 68