[Changes in the gallbladder, bile ducts and liver after sectioning of the sphincter of Oddi].
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Biomedical subjects
Publications and source records attributed to S Kruś.
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We compared the morphology of the hepatic artery intima which is free of atherosclerosis, with that of the typically atherosclerosis-prone coronary artery. The study group comprised material collected from 116 autopsies. Subjects were aged between 1 month and 90 years. Specimens were collected from grossly normal arterial segments. An already known fact was confirmed: the presence and remarkable intensity of non-atherosclerotic intimal thickening in the coronary arteries since the beginning of life. On the contrary, hepatic artery intimal thickening was incidental during the first 4 decades of life and regular later on. During all the decades intimal thickness was decreased in the hepatic artery in comparison to the coronary artery. Initial atherosclerosis was noted during the 4th decade of life in the coronary artery and during the 8th and 9th decades in the hepatic artery. Intimal thickness was always lower in women compared to men. These findings reveal a positive correlation between the intensity of intimal hyperplasia and the incidence of atherosclerosis. The intimal pattern is of limited value in the determination of an unidentified subject age who underwent an autopsy. The thickness of the hepatic artery intima, which surpasses 200 microns indicates that the subject is at least 40 years of age, while initial atherosclerosis--the 8th or 9th decades of life.
Evident difference in the occurrence of atherosclerosis between hepatic and coronary arteries justifies the search for local preconditions of this disease. In this study we compared the internal elastic membrane morphology of both arteries. It appeared to be mono- or polylinear (laminar) and continuous in the hepatic artery. This was in contrast to its fragmentation in the coronary artery since the beginning of life. Thus, the condition of the internal elastic membrane may play an important role in the development of non-atherosclerotic intimal thickening. Continuous elastica could make the migration of medial myocytes into the intima more difficult (hepatic artery). On the other hand, fragmented coronary artery elastica seems to facilitate this migration. In turn, intimal thickening is less or more advanced, respectively.
Since hepatic arteries are free of atherosclerosis any possible wall structure change may be attributed to age. We determined the media of hepatic and coronary arteries in view of this assumption. We measured its thickness and myocytic density (per 1 mm2 of cross-section) from specimens collected from autopsied subjects, aged up to 90 years. The media gradually thickens with age, although values noted during particular decades remain statistically insignificant. The myocytic density (in 1 mm2) was almost constant throughout life. The latter observation is incompatible, in comparison with data reported by other authors (diminution was expected).
The present series comprises 36 cases of mesangial glomerulonephritis in children aged from six months to 14 years. On the basis of morphological criteria, types with considerable and slight mesangial proliferation were distinguished. Slight mesangial proliferation was more typical of younger children. Clinically they showed more often the nephrotic syndrome (sometimes difficult to differentiate from lipoid nephrosis). Older children developed mesangial proliferation rather of greater intensity: renal insufficiency and erythruria predominated in this group.
The cumulative toxicity of alpha and gamma forms of crystalline indomethacin was studied on Wistar rats treated with these compounds in increasing doses for 24--32 days. The toxic effect of alpha and gamma forms is significantly cumulative. When administration of indomethacin is many times repeated doses 3--4 times lower than those applied once are sufficient to cause death. Indomethacin causes ulcers of small intestinal and cecal mucosa, with perforation. The alpha and gamma crystalline forms of indomethacin did not differ in the degree of cumulation of the toxic effect and intensity of morphological lesions.
The chloroform--induced renal tubular necrosis is associated with the rise of serum urea, creatinine and potassium. The highest values, observed 24 hours after chloroform administration, are respectively: 75 mg% (norm 32 mg%), 1.75 mg% (norm 0.25 mg%), 6.1 mEq/1 (norm 4.4 mEq/1). They gradually decreased with the progress of renal regeneration. These transient, rather little biochemical deviations justify the good conditions and eventual survival of chloroform-poisoned mice. The contribution of possible glomerular lesions to the disturbed renal function is taken into consideration.
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