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The Korean Journal of Pathology 1985;19(3): 255-289.
Ultrastructural Changes in the Exocrine and Endocrine Cells of Rat Pancreas in Endotoxin Shock.
Kun Young Kwon, Chai Hong Chung, Tae Joong Sohn
1Department of Pathology, Keimyung University School of Medicine, Taegu, Korea.
2Department of Pathology, Kyungpook University School of Medicine, Taegu, Korea.
This study was carried out to investigate the morphological changes in the exocrine and endocrine glands of rat pancreas treated with endotoxin. Thirty-five male Sprague-Dawley rats, maintained on a stock diet, weight 200.0 gm. average. were divided into two experimental groups. Group 1. Control group. Five rats. Intraperitoneal infections of 0.3 ml normal saline only. Group 2. Endotoxin-treated group. Thirty rats. 7.6 mg of endotoxin per kg. of body weight was administered intraperitoneally. Each of 5 experimental animal was sacrificed 30 minutes, 1, 2, 4, 6 and 8 hours after endotoxin treatment, followed by examinations of histochemical, light and electron microscopy of both transmission and scanning modes. The results were as follows: A. Light microscopic findings: A mild interstitial edema and hyperemia were noted 1-hour after endotoxin treatment. Cytoplasmic vacuolization at 2-hour level(2-hours after endotoxin administration), diminished staining quality of both endocrine and exocrine cells at 6-hour level. B. Electron microscopic examination: a. Transmission electron microscopy. The acinar cells of pancreas showed a mildly increased pre-lysosome at 30-minute level. At 1-hour level, appearance of secondary lysosome was noted in addition to the findings of mitochondrial swelling and decreased cristae; disarray and vacuolization of the RER; vacuolar change of Golgi apparatus. At 6-hour level, post-lysosomes. The changes in the endocrine glands were similar to the findings of exocrine glands just described with time lag of 1 to 2 hours. The endothelial cells of capillaries show swelling and pinocytotic vesicle formation, protrusion of the cytoplasmic processes into the capillary lumen and increased heterochromatin at 1-hour level. These findings became more prominent as time lapses. The lumen of the endothelium tends to be narrowed, filled with fibrin and other blood cell components which later terminated with occasional complete occlusion by the formation of thrombi. b. Histochemical study: Primary lysosomes of the control group revealed a strong reaction of the acid phosphatase whereas the endotoxin treated group with less reactivity limited in the peripheral zones of the lysosomes. Secondary lysosomes with partial reactions. However, the pre-lysosomes and post-lysosomes failed to demonstrate any acid phosphatase activity at all. c. Scanning electron microscopy. The endothelial cells of the capillaries, arterioles and venules demonstrated increased microvillous activity, broad bled formation, cytoplasmic protrusion into the luminal spaces and microthrombi formation at 1-hour level. Six-hour level onward there noted a junctional disruption and partial detachment from the subendothelium of the wall. It can be concluded, therefore: When the endotoxin enters the blood stream, it elicits endothelial injury followed by both exudation with resultant edema of the surrounding tissue and concomitant vascular occlusions due to thrombosis. This vascular occlusion, in turn, causes ischemic degenerative change of the cells of exocrine and endocrine glands of the pancreas which are followed by digestions of degradational materials from the injured cells through the lysosomal phagocytic system. Besides the above pathogenetic pathway, one can not rule out the possibility of the direct effects of the endotoxin to the cells of exocrine and endocrine cells of the pancreas also so rendered.