• The Korean Journal of Pharmacology
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• v.23 no.1
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• pp.15-23
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• 1987

To elucidate the mechanism of splanchnic hyperemia associated with chronic portal hypertension, we have investigated the alteration in visceral reflexes in conjuction with circulatory hemodynamics in portal ligated portal hypertension in cats. When capsaicin, bradykinin and vasopressin were injected via splenic artery of sham cat, respectively, they caused not only reflex excitation of systemic arterial pressure, but also elevation of splenic venous pressure with unchanged heart rates. Simultaneously, they evoked the sympathetic efferent excitation of liver (spleno-hepatic reflex) as well as of spleen (spleno-splenic reflex). Similarly, capsaicin upon pledging on the liver surface evoked a significant increase in the pressor reflex with hepatic nerve excitation (hepato-hepatic reflex). After portal ligation, the splenic venous pressure was gradually elevated in association with decrease in systemic arterial pressure. However, the excitation of pressor reflex was enhanced on the and day, thereafter, being returned to the control, and the reflexly induced spleno-splenic, spleno-hepatic and hepato-hepatic sympathetic excitations were significantly diminished on the 8th day following portal vein ligation. In conclusion, it is suggested that sympathetic reflexes to spleen and liver are specifically intervened by the same central pathways and furthermore, the diminution of these viscero-visceral reflex excitations after portal ligation may be related to the intestinal hyperemia.

• The Korean Journal of Pharmacology
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• v.24 no.1
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• pp.63-70
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• 1988

Alterations in splanchnic circulatory hemodynamics along with reactivities to the alpha adrenoceptor agonists were assessed in association with the preventive effects of propranolol 10 days after portal ligation. Decreases in precapillary resistance (Ra) and postcapillary resistance (Rv) along with increases in mesenteric blood flow (MBF) and capillary pressure (CP) were observed in conjunction with an increment of splenic pulp pressure (SPP). Dose-dependent increase in Rv in response to noradrenaline, increases in Ra and RV to adrenaline, and increases in superior mesenteric arterial pressure (SMAP), Ra and Rv to phenylephrine observed in sham group were significantly attenuated by portal vein stenosis. In PPL-3 group (propranolol 3 mg/kg, i.p. three times daily for 10 days), MBF was significantly decreased in association with decrease in mesenteric venous pressure (MVP) when compared with those of protal ligated (PL) group, and decreased Ra and Rv in PL group were recovered toward the values of sham group. Likewise, in PPL-1 group (propranolol 5 mg/kg, i.p. once daily for 10 days), the pressor response of Rv to adrenaline was recovered up to the level of sham group. Thus, it is suggested that decreases in Ra and Rv in association with increases in MBF and CP may have a close relevance to the increased SPP, and the changes in circulatory hemodynamics and vascular reactivities were effectively reversed by longterm propranolol treatment. Based on these results, it is concluded that these changes observed in portal hypertension are closely related with the altered functions of the adrenoceptors in the splanchnic vascular beds.

• Journal of Chest Surgery
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• v.27 no.8
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• pp.710-713
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• 1994

The Budd-Chiari syndrome is a rare type of portal hypertension caused by complete or incomplete obstruction of the hepatic vein or the corresponding portion of the inferior vena cava or both. In this case, the obstruction was located just beneath the diaphragm, above the right hepatic vein opening, which was confirmed by vena cavography preoperatively. Budd-Chiari syndrome with stenosis or thrombosis of the inferior vena cava may be cured by prosthetic bypass to the right atrium. This case is caused by thrombus of unknowed primary origin. Combined mesoatrial and cavoatrial shunt should be encouraged in this specific situation. Postoperatively, there were marked fall of venous pressure and symptoms and signs improved remarkably.