Intraoperative Direct Measurement of Hepatic Arterial... : Liver Transplantation (original) (raw)

Original Articles

Intraoperative Direct Measurement of Hepatic Arterial Buffer Response in Patients With Or Without Cirrhosis

Aoki, Taku1; Imamura, Hiroshi1,*; Kaneko, Junichi1; Sakamoto, Yoshihiro1; Matsuyama, Yutaka2; Kokudo, Norihiro1; Sugawara, Yasuhiko1; Makuuchi, Masatoshi1

1_From the Department of Surgery, Division of Hepato-Biliary- Pancreatic and Transplantation Surgery, Graduate School of Medicine, University of Tokyo, Tokyo, Japan._

2_From the Department of Biostatistics, School of Health Sciences and Nursing, University of Tokyo, Tokyo, Japan._

*Address reprint requests to Hiroshi Imamura, MD, Division of Hepato-Biliary-Pancreatic and Transplantation Surgery, Department of Surgery, Graduate School of Medicine, University of Tokyo,7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-8655, Japan.

Email:[email protected]

Telephone: 81 3-3815-5411 ext. 33321; FAX: 81 3-5684-3989

Supported by grants from the Public Trust Surgery Research Fund and from the Public Trust Fund for the Promotion of Surgery.

Published online in Wiley InterScience (www.interscience.wiley.com).

Abstract

The hepatic arterial buffer response (HABR) is an intrinsic regulatory mechanism of the hepatic artery (HA) that compensates for reductions in portal venous (PV) blood flow. Whether this response is maintained in patients with cirrhosis (LC) is unclear. The aim of the present study was to examine whether HABR is maintained in patients with LC using direct blood flow measurements. PV and HA blood flow were intraoperatively measured and compared in patients with (LC group, n = 39) or without (control group, n = 22) cirrhosis at baseline (baseline HABR) and after PV clamping (acute HABR) using an ultrasound transit-time flowmeter. In contrast to the proportional relationship between the baseline PV and HA blood flow observed in the control group, HA blood flow and the HA-PV flow ratio increased when PV blood flow decreased in the LC group, suggesting that the baseline HABR had already been activated. Acute HABR, evaluated by the absolute and relative changes in HA blood flow and by the buffer capacity, was blunted in the LC group ( P < 0.001, P < 0.01, and P = 0.01, respectively). An association between the degree of acute HABR impairment and the level of baseline HABR activation (HA-PV flow ratio) could not be confirmed in the LC group. In conclusion, the baseline HABR appears to be continuously activated in patients with LC; this phenomenon probably results in the impairment of the acute HABR.