• F Jakab, I Sugár, Z Ráth, P Nagy, and J Faller.
• Department of Surgery, Semmelweis University Medical School, Budapest, Hungary.
• Acta Chir Hung. 1994 Jan 1; 34 (1-2): 69-78.

AbstractThe relationship between the changes in portal venous and hepatic arterial blood flows, e.g. the interaction of the two vascular systems in the liver always was a much disputed question, although it has tremendous significance in the practice of transplantation, and the explanation has been known since 1981, when Lautt published the so-called "adenosine washout theory" /9/. According to our earlier observations the decrease of portal pressure of flow generally and consistently led to an increase in hepatic artery flow. At the same time, changes in hepatic artery flow or pressure seemed to produce only inconsistent effects on the portal circulation. In the present experiments liver transplantations were carried out on mongrel dogs by Starzl's method /14/. Electromagnetic flow probes were placed on the hepatic artery and the portal vein before removal of recipient's liver, and after completion of all vascular anastomoses of newly inserted liver, e.g. in the recirculatory phase of OLTX. The flow probes were connected to Hellige electromagnetic flowmeter, portal venous and systemic arterial pressures were recorded too. The control HAF was 241 +/- 23 ml/min, the average PVF was 517 +/- 47 ml/min before removal of the recipient's liver. In the recirculatory phase the HAF increased to 414 +/- 39 ml/min, by 71 +/- 12% (p < 0.001). The PVF decreased in most animals after OLTX. The decrease was in average -40.2 +/- 3.5% (p < 0.001). The THBF calculated by adding the HAF and PVF showed a small, but not significant decrease during recirculation. The control THBF was 758 +/- 50 ml or 39.0 +/- 3.1 ml/min/kg. In the recirculatory phase 754 +/- 48 ml/min HBF could be measured, respectively. The systemic arterial pressure slightly decreased, portal vein pressure rose in most animals after OLTX, accordingly there was a substantial increase of portal inflow resistance and of prehepatic arteriolar resistance, decrease of hepatic arterial resistance. The decrease of PVF after OLTX can be explained by a progressive fluid accumulation in the liver parenchyma and increased sinusoidal and portal inflow resistance. The prolonged and continuous increase of hepatic artery flow during recirculatory phase of OLTX may be due to the decrease of portal flow. The exact mechanism, by which a change in portal flow leads to arteriolar dilatation, can be most probably explained by "adenosine washout theory" of Lautt.

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