title: [Morphogenesis of metabolic lesions in skeletal muscles: strategy for limitation of the lesions].
abstract: The data obtained in this study suggest an integrated cascade of destructive and compensatory reactions triggered by disruption of metabolic equilibrium in skeletal muscle cells. Actual parameters of the pathologic process are determined by the intensity and dynamics of the injurious stimulus rather than by its specific nature and also depend on the adaptive potential of target muscular fibers. General analysis of experimental pathologic processes differing in dynamics of injurious impacts permitted to distinguish chronic and acute variants of the development of pathologic changes and the respective spectra of structural reactions. Acute injuries (contracture and lysis) appear to roughly fall into the two categories, confined and extended. De novo restoration of complicated cell architecture being rather "expensive", limitation of damage acquires special significance. Many of the confined destructive events may be regarded as "adaptive" in respect to a higher organizational level. In chronic pathologic processes, gradual accumulation of structural and energetic disturbances leaves time for adaptive rearrangements to develop. The most prominent adaptive reactions are at first confined to mitochondrial compartment and thereafter give place to its structural decompensation. Increasing fragmentation of mitochondrial reticulum may be "preventive" in that it contributes to isolation and removal of its irreversibly damaged parts and can therefore be considered as the first ("metabolic") phase of the damage restriction strategy. Under the threat of total demolition of a skeletal muscle fiber, its "mechanical" fragmentation associated with local destruction of the contractile apparatus becomes of primary importance along with extracellular factors participating in fast removal and reparation of the damaged fragment. Insufficiency of these reactions or extreme character of the impact promotes the spread of the lesion over the entire fiber or its large part. Extended forms of damage are associated with intense infiltration by inflammatory cells and, after elimination of cell debris, produce a structural defect compensated by newly formed regenerating fibers and connective tissue expansion.
authors.forename: L M
authors.initials: LM
authors.lastname: Nepomniashchikh
authors.forename: M A
authors.initials: MA
authors.lastname: Bakarev
mesh_terms: D000818:Animals; D006801:Humans; D008854:Microscopy, Electron; D008931:Mitochondria, Muscle / Q000648:ultrastructure; D018482:Muscle, Skeletal / Q000378:metabolism / Q000648:ultrastructure*; D009135:Muscular Diseases / Q000378:metabolism / Q000473:pathology*