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간디스토마 감염가토(感染家兎)의 Vitamin A 부하(負荷)에 관한 연구

간디스토마 감염가토(感染家兎)의 Vitamin A 부하(負荷)에 관한 연구
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Loading of vitamin A in rabbits infected by Clonorchis sinensis
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연세대학교 대학원
Clonorchis sinensis principally lives in the bile bucts absorbing nutritional substances and leading to chronic peribiliary inflammation due to mechanical irritation. During infection of Clonorchis sinensis, nightblindness frequently appears due to deficiency of vitamin A (vit. A). Levine (1958) observed one case of nightblindness in the experimental infection of Amphimerus pseudofelineus of cat. However, Bercovitz(1931) reported previously the symptom could disappear on inducing the excretion of bile from the duct. Lewis(1942) observed that the serum vit. A decreased when residual vit. A in the liver tissue was exhausted. Kim (1964), recently, reported that vit. A loading in infected animal caused the temporary raising of serum value. The object of the present study is to confirm the fate of vit. A which was absorbed from the intestinal wall of the rabbit infected with Clonorchis sinensis and to clarify the mechanism of the vit. A deficiency. Materials and Methods Animals: White rabbits(1.6∼2.0kg) were used as experimental animals and were fed similarly. Metacercariae: Metacercariae of Clonorchis sinensis were collected by digestion method from fresh water fish caught from an endemic area (Iri Chollabuk-Do). About 1,500 of the larvae were given orally, and 6 weeks after the infection egg-out-put was confirmed by stool examination. Vitamin A: Water soluble(U.S. vitamin corportion). For loading 15,000㎍ of vit. A was given orally and 3,000 ㎍ intravenously. In order to calculate the vit. A, Georgy modification of Dann & Evelyn method was applied for serum vit. A, and Oser, Melnick Pader's method for tissue vit. A. 3∼4 gm of liver tissue weighed and sliced into small pieces and followed by the regular procedure. A number of Clonorchis sinensis from the bile duct were washed with saline several times and followed the same procedure. Vit. A in bile juice and urine was measured by the same method, except replacing the 0.5 N alcoholic potassium hydroxide into 95% ethyl alcohol in order to coagulate the protein substances. Blood was taken from the heart at hunger condition at intervals of two hours in the first part and three hours in the second part(13 hours after the vit. A was given). the separated serum was kept at freezing temperature. Results The average serum vit. A in healthy rabbits was 71.1㎍% and infected group was 30.8 ㎍% 7 weeks after the infection. When vit. A was given to non-infected group (15,000㎍), the serum value increased to high level(198.1, 264.6, 222.4 ㎍%) from 7 to 16 hours. the decrease started after 19 hours and recovered to original lvel after 25 hours. In the infected group, though there were individual differences, the value of vit. A in the serum increased to high level (296.8, 351.3, 320.7 ㎍%) from 7 to 16 hours after the administration of vit. A and showed acute decrease at 19 hours to 160.6㎍%, but still held high titre, 85.9 ㎍% even 25 hours after the loading. In general, there was no difference of the ability of vit. A absorption between the infected and non-infected group, but the value of vit. A in the serum after the loading was much higher in the infected group than in non-infected. The amount of vit. A in liver parenchyma was also calculated before and after vit. A was given. In the infected rabbits, the weight of the liver parenchyma increased to about 1.6 times as in the normal rabbit due to dilatation, rupture of the capillary bile ducts, necrosis of liver parenchyma and degeneration of the cells. However the amount of vit. A in the liver parenchyma was 61.84 ㎍/gm in the normal group and only 13.82㎍/gm in infected group. 7 hours after vit. A was given in the normal group the amount increased to about 1.7 times (104.53㎍/gm), but in infected group there were no differences comparing the value before the loading, 16.56 ㎍/gm after 3 hours, 12.81 ㎍/gm after 7 hours. In order to clarify the reason of the low value of vit. A in the liver parenchyma of infected group, whether it was due to the loss of vit. A by means of bile juice or consumption by the liver fluke itself, the bile juice and parasites were examined. Bile juice was taken from common duct hourly(normal rabbit 13 ml, moderatry infected rabbit 9 ml, heavily infected rabbit 3 ml), but no vit. A was detected even from the vit. A loaded group and the vit. A could not be found from the parasite itself collected from biliary ducts numbering 600 and 1,800. Since the storing ability of liver parenchyma in the infected group was lower than in the normal group, the process of the rapid decrease along with time elapes was one of the subjects to be clarified. The amount of vit. A in kidney tissue, urine, and feces were measured comparing the normal group. Since it took much time to get sufficient amount of stool from the rabbit, the animals were sacrificed after a certain given time, and stool was taken from the lower colon. In the kidney a slight amount of vit. A was detected, bud there was no difference between the normal and infected group. 36 hours after the vit. A loading, the amount of vit. A in urine of normal rabbits were 22.7 ㎍ in average, whereas it was 82.7 ㎍ in the infected group. The data shows that loss of vit. A from urine in the infected group is about 4 times that of the normal group. The amount of vit. A in feces showed no difference between the two groups. It is presumed a considerable amount of vit. A is excreted without absorption from the small intestine. Conclusion In conclusion, it is considered that the reason of vit. A deficiency in the infection of Clonorchis sinensis is due to the decrease of storing ability of the liver and rapid excretion from kidney, and not by the absorbability of vit. A form the intestinal wall.
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2. 학위논문 > 1. College of Medicine (의과대학) > 박사
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