Wataru Ohta

Scanning electron microscopy of the bile ductule.

SummaryScanning electron microscopy of a liver biopsy specimen from a patient 6 months after the onset of acute hepatitis revealed a normal appearing bile ductule. The bile ductule was 13 μm in outer diameter and 1.5–2.7 μm in inner diameter. The ductular lumen was surrounded by two ductular cells and ampullary dilated at the canalicular side. In the lumen, intracytoplasmic diverticles were observed with an orifice d ameter of 0.9 μm. About 15 microvilli 0.4–0.6 μm in length and 0.1 μm in thickness were observed on 1 μm2 of luminal surface. The number of microvilli was calculated to be approximately 1,500 per ductular cell. A single cilium 0.15 μm in diameter at the base and 0.10 μm at the trunk, and 7–15 μm in length was found on each ductular cell. The cilium arose from p. recess at the canalicular side of the ductular cell, and the free-end was on the bile-duct side. The cilia seemed to play an important role in bile flow to the duct. Sometimes between the ductular cells at the edge of the basal portion a cell was intercalated with thin processes. Such thin processes were not observed on ductular cells.

Kupffer cell hyperplasia in liver diseases. Demonstration by scanning electron microscopy of biopsy samples.

SummaryKupffer cells were observed in liver biopsy tissues of 9 cases of liver diseases by scanning electron microscopy to prove Kupffer cell proliferation numerically. Kupffer cell count per 0.01 mm2 of cracked surface of liver lobule was 1.2 ± 0.3 in the convalescent stage of a mild acute hepatitis case and 1.2 ± 0.1 in a chronic persistent hepatitis case with slight inflammation. Wheras it was increased to 2.4–5.5 (p<0.01) in the convalescent stage of moderate to severe acute hepatitis cases, 1.8 ± 0.1 (p< 0.05) in a chronic active hepatitis case, 2.5 ± 0.3 (p< 0.001) in an alcoholic portal fibrosis case and 2.2 ± 0.4 (p< 0.001) in a liver cirrhosis case. Kupffer cell count per mm3 of liver lobule was estimated roughly 3,500 in the convalescent stage of a mild acute hepatitis case and in a mild chronic persistent hepatitis case and 7,000 to 16,000 in the convalescent stage of moderate to severe acute hepatitis cases.

Effects of Octapressin on Portal Venous Pressure

octapressinの門脈圧下降作用を追求する目的で,2例の肝硬変症例および2例の慢性肝炎症例に,同剤の微量緩速点滴静注を行なった.同剤の注入開始後1～2分で閉塞肝静脈圧の下降が始まり,10分以内に減少率14～45%の下降を示した.同剤の注入量は0.4～1.8単位であったが,下降率は注入量に比例せず,むしろ,投与前の閉塞肝静脈圧の高い症例ほど,大きい減少率を示した.末梢動脈血圧は,13～41%上昇し,脈拍数は28～35%減少した.閉塞肝静脈圧は,同剤注入中止後約30分で前値に復した.副作用として,軽度の腹痛,顔面蒼白,尿意を認めたが,格別の処置なく消失した.

On portal hypertension and pancytopenia observable in the course of virus hepatitis

ConclusionIt is true that there are cases having complication of splenomegaly and portal hypertension due to intra-hepatic pre-sinusoidal block after the onset of infectious hepatitis, but in the observation over a long period the cases with complication of pancytopenia prove to be only two cases out of ten. Moreover, in the three cases out of four, pancytopenia occurred after the distortion of lobular architecture.From these findings it would be most rational to assume that portal hypertension, splenomegaly and pancytopenia observable after virus hepatitis are simply one series of symptoms of changes occurring in the liver, spleen, portal venous system and bone marrow in the course of progress to liver cirrhosis. In addition, the fact that in the examinations of 80 cases of liver cirrhosis the cases showing pancytopenia prove to be 31% and that the incidence of such a complication increases with advance in age indirectly supports our assumption.