Response of Hepatic Microcirculation Following Hemodynamic Changes: An Experimental Study Using Laser Doppler Flowmetry in Dog.
- Author:
Shin HWANG
1
;
Sung Gyu LEE
Author Information
1. Department of Surgery, University of Ulsan College of Medicine and Asan Medical Center, Seoul, Korea.
- Publication Type:Original Article
- Keywords:
Hepatic microcirculation;
Liver transplantation;
Brain death;
Laser doppler flowmetry;
Hemodynamics
- MeSH:
Animals;
Arterial Pressure;
Blood Pressure;
Brain Death;
Cadaver;
Central Venous Pressure;
Denervation;
Dobutamine;
Dogs*;
Dopamine;
Hemodynamics*;
Humans;
Laser-Doppler Flowmetry*;
Liver;
Liver Transplantation;
Microcirculation*;
Tissue Donors;
Vasoconstriction
- From:Journal of the Korean Surgical Society
1999;57(6):771-781
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Management of a cadaveric donor with hemodynamic stability is essential for successful liver transplantation. Since the liver is susceptible to ischemic insult and since the blood pressure of a brain-dead patient is usually hypotensive, donor management should be performed on the bases of the hemodynamic characteristics of brain death and physiologic control of hepatic blood flow. In this study, the response of hepatic microcirculation was evaluated in six dogs in which hepatic innervation was sequentially altered and change of blood pressure and corresponding therapy for brain-dead donor was simulated. METHODS: The hepatic microcirculation in a dog model was measured by using laser Doppler flowmetry (LDF). Factors affecting the LDF signal were set as the mean arterial pressure (MAP), the central venous pressure (CVP), and the infusion of vasopressors. RESULTS: Common hemodynamic responses in dogs with innervated and sequentially denervated livers were as follows: First, buffering of the hepatic arterial flow was observed when the MAP was in the range of 60-120 mmHg. Second, a CVP of upto 12-13 cm saline did not decrease the LDF signal. Third, dopamine and dobutamine doses of up to 20 microgram/Kg/min offset the prehepatic flow resistance with elevation of the MAP against splanchnic vasoconstriction. Attenuation of hepatic arterial buffering was the only difference following hepatic denervation. Meanwhile, hepatic arterial buffering seemed not to be working when the MAP fell below 60 mmHg. CONCLUSIONS: Although dysfunction of the hepatic nerve in a brain-dead condition has not been evaluated, common responses from an innervated and sequentially denervated liver may be observed inthe livers of donors in a brain-dead state. The results of this experiment suggest that there is a certain control mechanism for hepatic blood flow, independent of hepatic innervation. Even though these results cannot be applied directly to clinical treatment, they will would provide clues about the control mechanism for hepatic blood flow for the management of brain-dead liver donors.
