Effects of Low Flow Portal Vein Arterialization for Hepatic Ischemic Damage Compared with Groups of Administrating Calcium Antagonists

Yasuhiro Sumi, Hajime Hirose^*, Kenichi Sakamoto^*, Takuya Yamada^*, Masatomo Hayashi^*, Yoshifumi Katagiri^** and Atsuyoshi Onitsuka^**

Department of Surgery, Tosei National Hospital, First Department of Surgery, Gifu University School of Medicine^*, Department of Surgery, Gifu Red Cross Hospital^**

Purpose: Ischemia during hepatectomy, for example continuous clamping of hepatoduodenal ligament, is a cause of postoperative hepatic failure. To prevent ischemia, portal vein arterialization (PVA) is usually performed. We have reported that PVA producing a 25% total hepatic blood flow (THBF) rate was sufficient for hepatic energy metabolism and that carbon dioxide tension in the arterial blood influenced hepatic hemodynamics. Low flow PVA (LFPVA) unables portal vein cannulation and allows bleeding easy to be easily controlled. However, LFPVA may reduce hepatic energy metabolism. We decided to investigate whether the use of calcium antagonists could be used to improve hepatic hemodynamics. Material & Method: LFPVA and the administration of calcium antagonists (diltiazem: group D, nicardipine: group N, no administration: group C) was performed in 18 mongrel dogs to investigate the maintenance of hepatic energy metabolism. A LFPVA flow rate equal to 15% of the THBF was selected. LFPVA was performed from the right femoral artery to the portal vein trunk using a roller pump after ligating the hepatic arteries and clamping the portal vein using a portocaval shunt for 120 minutes. Calcium antagonists were continuously administered through the portal vein beginning 30 minutes before the initiation of LFPVA and throughout perfusion. Results: The mean aortic pressure (mAoP) decreased significantly after the LFPVA in all three groups. However, the mAoP decreased only slightly in the D group. Portal venous pressure did not changed in any of the groups. Portal venous resistance was lower in the N group than in the C group. No differences in oxygen delivery and consumption were observed among the three groups. ATP decreased in all 3 groups, but the changes were not significant. The AKBR of each group was low due to the LFPVA. However, the mean AKBR value of C group was lower than 0.4. The AKBR in the D group was significantly higher than that of C group after 120 minutes of LFPVA. Histological examination showed hepatocellular damage in groups D and N to be sligh, and the functions of the sinusoidal endothelial cells were protected. Conclusions: The administration of calcium antagonists during LFPVA is effective for maintaining hepatic energy metabolism and hemodynamics. However, different calcium antagonists afforded different protective effects.

Key words
portal vein arterialization, hepatic ischemia, calcium antagonists

Reprint requests
Yasuhiro Sumi Department of Surgey, Tosei National Hospital 762-1 Nagasawa, Shimizucho, Suntogun, Shizuoka, 411-0905 JAPAN

Accepted
October 31, 2001

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