Ultrastructure of failing myocardium due to induced chronic mitral insufficiency in dogs.
Left ventricular failure was produced in dogs by inducing mitral insufficiency and the cardiac muscle was examined for ultrastructural changes in thsese failing hearts after 5-10 months of mitral insufficiency. The left ventricular failure was established by haemodynamic measurements, chest X-ray and examination of the heart. In the failing heart, the increased number of mitochondria showed close approximation with the sarcolemmal membrane in the T-tubules as well as in the intercalated discs (ID); this is in contrast to what is seen in normal hearts, where T-tubules were mostly coupled with sarcoplasmic reticulum. It is possible that in the heart failing on account of mitral insufficiency mitochondria may be taking over the function of the sarcoplasmic reticulum. Although ID were jumbled up in the failing heart, the intercellular gap and specialized membrane junctions (gap and tight junctions, desmosomes) were quite comparable to normal, indicating that intercellular communication at ID in this type of heart failure is probably maintained. Nuclear chromatin in the failing heart was condensed and lined the inner nuclear membrane. Microbodies with a single limiting membrane were frequent and so were lipofuscin granules. The latter could be an end product of degenerative mitochondria. Golgi bodies in the failing heart were also present in locations away from the nucleus.
D000818:Animals; D004285:Dogs; D005260:Female; D008297:Male; D008854:Microscopy, Electron; D008870:Microtubules / Q000648:ultrastructure; D008928:Mitochondria / Q000648:ultrastructure; D008944:Mitral Valve Insufficiency / Q000473:pathology*; D009206:Myocardium / Q000648:ultrastructure*; D012519:Sarcoplasmic Reticulum / Q000648:ultrastructure