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[Light and electron microscopic studies of cardiac pathomorphology in swine due to transport fatigue (porcine stress syndrome)].

作者信息

Johannsen U, Menger S

出版信息

Arch Exp Veterinarmed. 1980;34(6):797-816.

PMID:7212934
Abstract

Optical light microscopy and electron microscopy were used to examine 22 or eleven hearts of pigs which had been killed in a state of extreme fatigue due to transport. Samples were taken and fixed within five minutes from stunning. The following histological findings were obtained: Glycogen depletion of the myocardiac fibres was conspicuous in most cases, usually with high glycogen levels in Purkinje's fibres. Discrete, easily overseeable changes of scattered fibres or groups of fibres in the form of granular or hyaline degeneration were recorded from 73 per cent of the cases, with degeneration having been granular in 59 per cent and hyaline in 54 per cent. Fibre oedema was rare and recordable from only two cases. Changing prestatic hyperaemia was established from terminal vessels, while no visible alterations were found in capillary endothelia by optical light microscopy. The following results were gained by means of electron microscopy: Glycogen depletion was accompanied by differently pronounced expansion of parts of both the sarcoplasmic reticulum and T-system. Unchanged mitochondria were detected together with incipient mitochondrial swelling to different degrees, accompanied by cristolysis, in certain rare instances, as well as by partial or total homogenisation of interior mitochondrial structures, in more frequent cases. Z-strips were widened in eight cases. Limited decomposition of fibrils in some myocardiac cells was observed in samples of three animals. There were signs of usually moderate interfibrillar and perinuclear oedema and of predominantly inconspicuous capillary endothelia. Most of the changes were reversible and less strongly pronounced, and they were likely to suggest the presence of disorders in energy metabolism and impairment of stimulus conduction. They are interpreted as secondary myocardiopathy, caused by haemodynamic-hypoxic factors, following primary insufficiency of peripheral circulation.

摘要

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