To study in vivo effect of methylcobalamin (CH3-B12) on the peripheral nerve structures, rats with experimental diabetes induced by streptozotocin were administered with daily intramuscular injection of CH3-B12 (500 microgram/kg) for 16 weeks. By isolated nerve fiber studies, CH3-B12-treated diabetic rats showed less incidence of paranodal demyelination as an early sign of segmental demyelination than non-treated diabetic rats. From morphometrical analysis on sural nerves, the reduction in the density of myelinated nerve fibers, nerve fiber size and axon size of myelinated fibers was definitely protected in treated diabetic rats. The results suggested that continuous treatment with CH3-B12 had an ameliorative effect on the peripheral nerve lesions in experimental diabetic neuropathy.
Experimental aganglionosis was produced successfully in a colonic segment proximal to the peritoneal reflection by intraluminal filling under tension of the colorectum of rats with 0.01% corrosive sublimate in normal saline solution. Where the length of aganglionic segment was more than 3 cm, ileus appeared and megacolon proximal to a narrow segment was observed. Histologically and histochemically, a total denervation state was observed in the aganglionic segment, in contrast to findings in narrow segments of Hirschsprung's disease, in which intramural extraneous nerves are known to be increased. The fact that a definite narrow segment like that seen in Hirschsprung's disease appeared at the portion of the colon in which experimental aganglionosis was produced indicates that a narrow colonic segment certainly can be produced without presence of any intramural extraneous nerves, although the possibility that the presence of such nerves may exaggerate the narrowing cannot be denied. The fact that the cases in which length of aganglionosis was less than 2.5 cm did not have an ileus suggests that there may be some contributing factors other than aganglionosis in the etiology of Hirschsprung's disease of ultrashort segment, if this entity of the disease really exists. Aperistalsis observed in experimental aganglionic segments and that observed in aganglionotic segments of Hirschsprung's disease seem to be based on a common main factor, i.e., absence of the nonadrenergic, noncholinergic nerves.
Fecal fat excretion, fecal mass, fecal fat concentration, and the coefficient of fat absorption were evaluated in 31 normal Japanese subjects with a mean fat consumption of 61.8 g and compared with the values in 43 Japanese patients with chronic pancreatitis (CP) with a fat consumption of 40.2 g. Fecal fatty acids were analyzed by the gas chromatographic method. Fecal fat excretion by normal individuals was 1.7 +/- 1.0 (Mean +/- SD) g/day (range, 0.4-4.9 g/day). Steatorrhea was therefore defined as fecal fat excretion that exceeded 5.0 g/day. The patients with CP were divided into three groups: non-steatorrhea (fecal fat < 5.0 g/day), chemical steatorrhea (fecal fat > or = 5 g/day and no appearance of fatty stool), and manifest steatorrhea (evaluated from the appearance of fatty stool). In addition, we investigated the correlation between fecal fat excretion and pancreatic exocrine function, obtained by the pancreozymin-secretin (or secretin) test in 24 controls and 30 CP patients. Fecal fat excretion by CP patients was 9.1 +/- 8.8 g/day, which was significantly higher (P < 0.01) than that of controls. There were 28 (65%) CP patients with steatorrhea. Of these, 15 (35%) showed chemical steatorrhea and 13 (30%) manifest steatorrhea. In CP patients, the fecal mass (250.5 +/- 133.6 g vs control, 125.6 +/- 52.5 g), fecal fat concentration (3.40 +/- 2.16 g% vs control, 1.48 +/- 0.89 g%), and coefficient of fat absorption (77.3 +/- 20.2% vs control, 97.2 +/- 1.7%) all showed significant differences from the controls.(ABSTRACT TRUNCATED AT 250 WORDS)
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