[Morphology of portal hypertension at the early stage of liver damage induced by CCl4: an experimental study with dogs].
OBJECTIVE
To explore the morphological basis of portal hypertension happened at the early stage of liver damage.


METHODS
Sixteen mongrel dogs were injected intraperitoneally with carbon tetrachloride (CCl(4)) once a week for 4 weeks and then once every 4 days, totally for 7 weeks. Before the experiment and 7 weeks after the beginning of experiment, small pieces of liver tissues were taken through a median upper abdominal incision and underwent HE staining, Masson's staining, and immunohistochemistry with alpha-smooth muscle actin (alpha-SMA) to label the activated astrocyte (hepatic stellate cell, HSC), and transmission electron microscopy. The portal vein pressure was measured by puncture of gastroepiploic vein. The diameter of spleen was measure too.


RESULTS
Since the second weeks after the experiment, the dogs showed vomiting, diarrhea, anorexia, weight loss, and varicose vein in the abdominal wall. One dog died of toxic enteritis 3 weeks after the beginning of experiment. 7 weeks after the injection of CCl(4), the average portal vein pressure of the rest 115 dogs was 22.7 cm H(2)O +/- 1.5 cm H(2)O, significantly higher than that before the experiment (12.2 cm H(2)O +/- 1.9 cm H(2)O, 1cm H(2)O = 0.098 kPa, P < 0.05). The long diameter of spleen of the 15 dogs was 24.4 +/- 3.1 cm, significantly greater than that before the experiment (18.7 cm +/- 2.4 cm, P < 0.05). Seven weeks after the injection of CCl(4) the appearance of liver did not change remarkably among the dogs, however, the spleens of the dogs showed swelling and stagnation of blood. No obvious ascites was seen. HE staining showed slight liver damage, such as fatty degeneration of liver cells; Masson's staining and electron microscopy showed typical sinusoid capillarization. alpha-SMA immunohistochemistry stain showed increased number of activated HSCs. Immunohistochemistry showed a number of alpha-SMA positive cells in the hepatic lobules. Portal hypertension was successfully induced in 15 dogs.


CONCLUSIONS
At the early stage of liver damage the possible cause of portal hypertension is the increased resistance of blood stream due to sinusoid capillarization and activation of HSC.
Zhang
Ri-Ping
RP
Department of General Surgery of the Second Clinical Hospital, Harbin Medical University, Harbin 150001, China.
Zhang
Wei-Hui
WH
Xue
Dong-Bo
DB
Wei
Yun-Wei
YW
D000818:Animals; D002251:Carbon Tetrachloride / Q000633:toxicity; D002252:Carbon Tetrachloride Poisoning; D056486:Chemical and Drug Induced Liver Injury; D004285:Dogs; D005260:Female; D006975:Hypertension, Portal / Q000139:chemically induced / Q000473:pathology*; D008099:Liver / Q000473:pathology; D008102:Liver Circulation / Q000502:physiology*; D008106:Liver Cirrhosis, Experimental / Q000139:chemically induced / Q000473:pathology*; D008107:Liver Diseases / Q000473:pathology; D008297:Male
D002251:Carbon Tetrachloride