TY - JOUR
T1 - Pathogenesis of Precirrhotic Portal Hypertension in Alcohol-Fed Baboons
AU - Miyakawa, Happei
AU - Iida, Shinji
AU - Leo, Maria A.
AU - Greenstein, Robert J.
AU - Zimmon, David S.
AU - Lieber, Charles S.
PY - 1985
Y1 - 1985
N2 - To study mechanisms and anatomic correlates of precirrhotic portal hypertension, we measured portal pressure either at laparotomy (in the portal vein) or by hepatic vein catheterization (wedge pressure) in 24 pairs of baboons fed 50% of energy either as ethanol or isocaloric carbohydrate (controls) for 4 mo–9 yr. On liver biopsy 7 had simple fatty liver; none had portal pressure exceeding the control range (2.7–13.0 cmH2O). The remaining 17 alcoholfed baboons had fibrous tissue deposition around the terminal hepatic venules and adjacent sinusoids. The mean portal pressure was significantly increased (15.0 ± 1.4 cmH2O) compared with the value in baboons with fatty liver (9.6 ± 0.9 cmH2O) and in controls (8.0 ± 0.6 cmH2O), with 8 animals exceeding the control range. Estimated hepatic blood flow was unchanged. Alcohol feeding resulted in increased hepatocyte size in both the fatty liver and fatty liver with fibrosis group; however, portal pressure did not correlate with alterations of cell size, liver volume, hepatic triacylglycerol, and protein contents. By contrast, for veins of comparable size, there was a significant correlation (r = 0.6666, p < 0.01) between the thickness of the perivenular fibrous rim and portal pressure. Perivenular fibrosis was commonly associated with adjacent perisinusoidal fibrosis and this lesion also correlated with portal pressure. Furthermore, i f one postulates that increased cell size causes enhanced pressure with secondary fibrosis, the latter should have first occurred “upstream,” in the mid and portal zones. Sequential biopsy specimens, however, showed that fibrosis first appeared in the perivenular areas, suggesting that, in most instances, increased pressure is in fact secondary to the perivenular fibrosis.
AB - To study mechanisms and anatomic correlates of precirrhotic portal hypertension, we measured portal pressure either at laparotomy (in the portal vein) or by hepatic vein catheterization (wedge pressure) in 24 pairs of baboons fed 50% of energy either as ethanol or isocaloric carbohydrate (controls) for 4 mo–9 yr. On liver biopsy 7 had simple fatty liver; none had portal pressure exceeding the control range (2.7–13.0 cmH2O). The remaining 17 alcoholfed baboons had fibrous tissue deposition around the terminal hepatic venules and adjacent sinusoids. The mean portal pressure was significantly increased (15.0 ± 1.4 cmH2O) compared with the value in baboons with fatty liver (9.6 ± 0.9 cmH2O) and in controls (8.0 ± 0.6 cmH2O), with 8 animals exceeding the control range. Estimated hepatic blood flow was unchanged. Alcohol feeding resulted in increased hepatocyte size in both the fatty liver and fatty liver with fibrosis group; however, portal pressure did not correlate with alterations of cell size, liver volume, hepatic triacylglycerol, and protein contents. By contrast, for veins of comparable size, there was a significant correlation (r = 0.6666, p < 0.01) between the thickness of the perivenular fibrous rim and portal pressure. Perivenular fibrosis was commonly associated with adjacent perisinusoidal fibrosis and this lesion also correlated with portal pressure. Furthermore, i f one postulates that increased cell size causes enhanced pressure with secondary fibrosis, the latter should have first occurred “upstream,” in the mid and portal zones. Sequential biopsy specimens, however, showed that fibrosis first appeared in the perivenular areas, suggesting that, in most instances, increased pressure is in fact secondary to the perivenular fibrosis.
KW - CAB
KW - NS
KW - THV
KW - chromotrope aniline blue
KW - not significant
KW - terminal hepatic venules
UR - http://www.scopus.com/inward/record.url?scp=0021964831&partnerID=8YFLogxK
U2 - 10.1016/S0016-5085(85)80146-3
DO - 10.1016/S0016-5085(85)80146-3
M3 - Article
C2 - 3964762
AN - SCOPUS:0021964831
SN - 0016-5085
VL - 88
SP - 143
EP - 150
JO - Gastroenterology
JF - Gastroenterology
IS - 1
ER -