• Journal of Yeungnam Medical Science
• /
• v.16 no.2
• /
• pp.181-192
• /
• 1999

Background: Nitric oxide, a vasodilator synthesized from L-arginine by vascular endothelial cells, accounts for the biological activity of endothelium derived relaxing factor. Previous studies demonstrated that nitric oxide inhibitor, $N^{\omega}$-Nitro-L-Arginine(NNA) diminished the hyperdynamic splanchnic and systemic circulation in portal hypertensive rats The present study was done to determine the role of nitric oxide in the development of hyperdynamic circulations in the prehepatic portal hypertensive rat model produced by partial portal vein ligation. Methods: The portal hypertensive rats were divided into water ingestion group and NNA ingestion group. After partial portal vein ligation, NNA ingestion group and water ingestion group received NNA 1mg/kg/day and plain water through the mouth for 14 days, respectively. Cardiac output, mean arterial pressure, organ blood flow and porto-systemic shunting were measured by radioisotope labeled microsphere methods. Vascular resistances were calculated by standard equation. Results: There were significant decreases in mean arterial pressure, increases in cardiac output and cardiac index, and decreases in total systemic and splanchnic vascular resistance in portal hypertensive rats compared to normal control group (p<0.01). Compared to the water ingestion group, significantly increased mean arterial pressure with decreased cardiac output and cardiac index were developed in the NNA ingestion group. Total systemic and splanchnic vascular resistance were significantly increased in the NNA ingestion group compared to water ingestion group (p<0.05). But, there was no significant difference in portal pressure between the two groups. Conclusion: The hemodynamic results of this study indicate that hyperdynamic circulation in prehepatic portal hypertensive rat mode1 was attenuated by ingestion of NNA. Nitric oxide may play an important role in the development of hyperdynamic circulation with splanchnic vasodilation in chronic portal hypertension.

• Journal of the korean academy of Pediatric Dentistry
• /
• v.27 no.1
• /
• pp.70-76
• /
• 2000

Congenital biliary atresia with progressive sclerosis of the intra- and extra-hepatic duct system occurs in 1 : 10,000 live births, and has a poor prognosis with an expected survival of less than 5 years. Etiology of biliary atresia is unclear, however, it is believed a genetic or developmental cause. The clinical characteristics include pronounced jaundice, hepatosplenomegaly, pruritus, steatorrhea, xanthomas, growth retardation, portal hypertension, bleedings, ascites and respiratory infections. Oral manifestations have seldom been reported in patients with biliary atresia, but there may be enamel hypoplasia, delayed tooth eruption, and green teeth. Early diagnosis and surgical intervention have decreased morbidity. returned growth and development to normal and improved the prognosis for survival. Authors report the clinical and radiologic characteristics, proper managements about two cases with biliary atresia.

• Journal of Chest Surgery
• /
• v.5 no.2
• /
• pp.107-112
• /
• 1972

Recently we experienced a case of the portal hypertension, extrahepatlc origin in the National Medical Center, Seoul. The case was a male aged 19 who was undergone the elective splenorenal shunt with splenectomy 9 years ago and emergency ligation of the coronary vein because of recurred variceal rupture 6 years later and had recurring esophageal varices with bleeding this time.At the age of 10 he had been occasionally suffering from nasal bleeding and visited to our Pediatric department, when there was encountered for the first time the splenomegaly, esophageal varices in the lower third esophagus on the esophagogram, and stenosis and kinking of the portal vein with rich collateral circulation on the splenoportography without hepatic functional impairment.The elective splenorenal shunt with splenectomy was undergone under the diagnosis of portal hypertension due to congenital anomaly of the portal vein and postoperatlvely no troubles had been obtained until postoperative 1st attack of massive hematemesis due to esophagenl variceal rupture recurred about 6 years later which was confirmed by control esophagogram and it was resulted by stenosis of previous anastomotic site of the splenorenal shunt.Then emergency ligation of the coronary vein was only made for bleeding control and no episodes of hematemesis had been encountered thereafter until April 1972 about 3 years after the 2nd operation, when hematemesis recurred again. In this time, recurring esophageal varices were noted in the lower third esophagus on the control esophagogram and he was employed side to end mesocaval shunt as the final step of portal decompression,and following results were obtained. 1] No postoperatlve troubles as leg edema or pain: Postoperatively leg elevation and elastic bandage on the both legs were employed until discharge. 2] During operation the portal pressure was 300 mm $H_2O$ and immediately lowered to 170 mm $H_2O$ after shunt.