Morphological alterations in skeletal muscle of spontaneously hypertensive rats.

Invest Clin

Institute of Experimental Medicine, Section of Muscle Adaptation, Central University of Venezuela, Caracas, Venezuela.

Published: March 2008

AI Article Synopsis

  • The study compared the extensor digitorum longus (EDL) and soleus muscles of spontaneously hypertensive rats (SHR) to normal Wistar Kyoto (WKY) rats, focusing on muscle fiber types and capillary structure.
  • There were no differences in the distribution of muscle fiber types or capillary density; however, a reduction in the size of IIB fibers in SHR was noted.
  • Ultrastructural examination revealed significant capillary abnormalities in SHR, such as enlarged endothelial cell cross-sections and irregular capillary membranes, along with signs of muscle damage and necrosis, indicating mild myopathy and focal fibrosis in these hypertensive rats.

Article Abstract

The Extensor digitorum longus (EDL) and the soleus muscles of spontaneously hypertensive rats (SHR) were studied in comparison with those of their normal counterparts, the Wistar Kyoto (WKY) rats. Quantitative assessment of capillaries and muscle fibre typing was done with optical microscopy, while the study of capillary abnormalities was performed by ultrastructural observation. There were no differences in fibre type proportion or in capillarity indexes between the SHR and the control rats. A reduction in the area of IIB fibres was found in the EDL muscle of the hypertensive animals. The ultrastructural study showed abnormalities in the capillaries of both muscles in SHR, the cross section of the endothelial cells was enlarged; there was irregular distribution of caveolae and pinocytic vesicles, the capillary basement membrane showed irregular width, with parts engrossed and reduplicated. Some pericytes were prominent. There were macrophages present in the interstitial space. In some muscle fibres there was disorganization of the sarcomere structure, swelling of the sarcotubular system, abundant autophagic vacuoles, and proliferative satellite cells. There were abundant collagen fibrils. The presence of cellular rests, autophagic vacuoles and loss of sarcolemma indicated necrosis. It can be concluded, that in SHR, muscle capillaries showed alterations that may be the substrate of functional rarefaction, although anatomical rarefaction (number reduction) could not be demonstrated. In EDL and soleus muscles of SHR, signs of a mild myopathy with focal fibrosis were present.

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