Effects of Nitric Oxide Donor on Hepatic Arterial Buffer Response in Anesthetized Pigs
Department of Clinical Physiology, Nagasaki University, Nagasaki, Japan.Journal of Investigative Surgery (Impact Factor: 1.16). 08/2010; 23(4):183-9. DOI: 10.3109/08941931003596885
The effects of systemic administration of exogenous nitric oxide (NO) donor on hepatic arterial buffer response (HABR) have not yet been studied in an anesthetized model. In this study, 28 anesthetized pigs received administration of sodium nitroprusside (SNP) or nitroglycerin (NTG) as exogenous NO donors. Pressure-flow (P-Q) relationships in the hepatic artery defined the pressure at zero flow (P(Qha = 0)) and flow-dependent resistance (R). The magnitude of HABR was evaluated by comparing the change in hepatic arterial blood flow (DeltaQha) divided by the change in portal venous blood flow (DeltaQpv), using the index of change in blood flow (DeltaQha/DeltaQpv). Mean arterial pressure decreased from baseline (95.6 +/- 3.8 mmHg) to SNP condition (68.3 +/- 1.9 mmHg) and decreased from baseline (92.7 +/- 4.4 mmHg) to NTG condition (66.2 +/- 1.7 mmHg). Mean index of change in blood flow (DeltaQha/DeltaQpv) was also significantly increased from baseline (0.19 +/- 0.12) to SNP condition (0.28 +/- 0.17; p = .009) and from baseline (0.18 +/- 0.17) to NTG (0.28 +/- 0.20; p < .05). In conclusion, systemic administration of SNP and NTG increases HABR with reduced hepatic arterial tone under decreased mean arterial pressure, presumably via exogenous NO enhancing another regulatory system and reducing the pressure gradient for sinusoidal washout.
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ABSTRACT: The characteristics of the hepatic macrocirculation, i.e., the parallel portal-venous and arterial blood supply, is of utmost relevance for liver surgery. With extended hepatectomy or transplantation of a reduced-size liver the remaining or transplanted liver tissue is overperfused because the liver fails to regulate the portal-venous inflow. This portal hyperperfusion is responsible for the initiation of liver cell proliferation but represents at the same time one of the substantial events in the pathogenesis of the small-for-size syndrome. Portal-venous hyperperfusion, the so-called hepatic arterial buffer response, which describes the semi-reciprocal relationship between the portal-venous and hepatic arterial blood flows, leads to an arterial hypoperfusion of the small-for-size liver. In this article experimental and clinical data are discussed which underline the high but so far overseen relevance of this arterial underperfusion in the development of a small-for-size syndrome.Der Chirurg 10/2011; 83(3):238-46. DOI:10.1007/s00104-011-2179-4 · 0.57 Impact Factor
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