ABSTRACT
Human pancreas tissue was studied electron microscopically during various stages of shock. The subcellular changes of exocrine pancreas affect in particular endoplasmic reticulum (ER), mitochondria, cytoplasm, and nuclei. Alterations correlate with duration and severity of shock, causing cell death in prolonged or severe manifestations of shock. This is obviously due to release of enzymes from zymogen granules; the ensuing damage cannot be distinguished from autodigestive pancreatitis. Lesions of exocrine pancreas cells are of multifactorial origin, arising from general shock-induced hypoxia, but also from local ischemia due to disturbed microcirculation provoking intravasal coagulation. Beyond these main causes, intracellular disorders of metabolism, obstruction of lymph drainage, and nervous factors may be of influence. As the cases surveyed in this paper had no fatal outcome - except for one patient - the changes described can be defined as non-lethal or as reversible.
Subject(s)
Pancreas/ultrastructure , Shock/pathology , Acute Disease , Adult , Aged , Humans , Male , Microscopy, Electron , Middle Aged , Pancreas/pathologyABSTRACT
The pancreas was examined histologically in 146 cases of patients dying of shock. The finding of morphological evidence of disseminated intravascular coagulation (DIC) in the pancreas supports the opinion that the pancreas in highly sensitive to disturbances of blood perfusion. The presence of DIC combined with a variety of pathological lesions in the exocrine ad endocrine pancreas was sufficiently characteristic to justify use of the term " shock pancreatitis". The relative scarcity of data hitherto available on pathological changes in the pancreas caused by shock can be ascribed to changes in the management of shock. It is concluded that the pancreatic lesions described in this study could influence the outcome in shock treated by modern methods of resuscitation.
Subject(s)
Pancreas/pathology , Pancreatitis/pathology , Shock/pathology , Disseminated Intravascular Coagulation/etiology , Disseminated Intravascular Coagulation/pathology , Humans , Islets of Langerhans/pathology , Pancreatitis/etiology , Shock/complicationsABSTRACT
An light and electronmicroscopic study of the rabbit hepatocytes during shock after experimental histamine release by Polymyxin-B-sulphate was made. As soon as five minutes after the histamine liberation the endoplasmatic reticulum becomes dissociated and the mitochondria show a spherical transformation. When the shock lasts up to one hour the changes are more intensive. The rest of deteriorated mitochondria and the endoplasmic membranes are expelled from the cells into the sinusoid lumina in form of myelinic figures. The hepatocyte microvilli swell up at first, and later, from the fifteenth minute after the beginning of shock they disappear which results in the flattening of the plasma membrane or its complete dissapearance in some places. Endothelial cells suffer similar alterations and they also acquire cytoplasmic protrusions. The findings lead to the conclusion that the changes of hepatocytes during shock after histamine liberation are primarily due to the direct influence of released histamine, and secondarily to the influence of hypoxia produced during the shock state.
Subject(s)
Liver/ultrastructure , Shock/pathology , Animals , Endoplasmic Reticulum/ultrastructure , Endothelium/ultrastructure , Female , Histamine , Male , Microscopy, Electron , Microvilli/ultrastructure , Mitochondria, Liver/ultrastructure , Rabbits , Time FactorsSubject(s)
Histamine Release , Kupffer Cells/ultrastructure , Anaphylaxis/pathology , Animals , Female , Male , RabbitsABSTRACT
The therapeutic influence of the spider Latrodectus tredecimguttatus poison on the progressive muscular dystrophy in rats caused by the method of Mendell's et al., as well as on the genetic dystrophy in mice, was examined. It was shown that the poison produces a functional and histological improvement, wheras the weight of the dystrophic muscles was not affected.
