Article

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
Source: PubMed

ABSTRACT

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.

0 Followers
 · 
4 Reads
  • [Show abstract] [Hide abstract]
    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.
    No preview · Article · Oct 2011 · Der Chirurg
  • [Show abstract] [Hide abstract]
    ABSTRACT: Objective: To investigate the association of passive hepatic arterial buffer response (HABR) with recovery of liver function and early biliary complications after liver transplantation. Methods: The early hepatic arterial flow and portal venous flow were monitored in 60 patients subject to liver transplantation before operation and 1 d and 2 d after operation, and HABR was evaluated. According to HABR findings, patients were divided into HABR group (HABR existence) and No-HABR group (HABR impairment). Based on results of liver function tests, B ultrasonography and endoscopic retrograde cholangio-pancreatography (ERCP), the association of HABR with recovery of liver function and early biliary complications after liver transplantation was analysed. Results: There were 30 patients in HABR group and No-HABR group each. The time of recovery of liver function and duration of hospital stay in HABR group were significantly shorter than those in No-HABR group (P<0.05), and the liver function parameters of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and total bilirubin (TBIL) in HABR group were better recovered (P<0.05). The prevalence of early biliary complications in HABR group was significantly lower than that in No-HABR group (P<0.05). Conclusion: HABR can be evaluated by monitoring of hepatic arterial flow and portal venous flow after liver transplantation, and the intact passive HABR may promote recovery of liver function and decrease the prevalence of early biliary complications.
    No preview · Article · Jun 2012 · Journal of Shanghai Jiaotong University (Medical Science)
  • [Show abstract] [Hide abstract]
    ABSTRACT: The reduction of endogenous nitric oxide (NO) production during hepatic ischemia-reperfusion injury, generally via a reduction in endothelial NO synthase activity, leads to liver injury. We hypothesized that administration of an exogenous NO donor into the portal vein may ameliorate hepatic blood flow reduction after a period of ischemia. A total of 90 min of ischemia (portal vein and hepatic artery) was applied in 15 anesthetized pigs, using the Pringle method under sevoflurane anesthesia. All animals were administered either saline (control group, n = 8) or sodium nitroprusside (SNP, n = 7) as exogenous NO donor drugs into the portal vein, 30 min before and after ischemia. The portal venous blood flow and hepatic artery blood flow were measured continuously using transonic flow probes attached to each vessel. Endogenous NO (NOx = NO2- + NO3-) production was measured every 10 min using a microdialysis probe placed in the left lobe of the liver. In the SNP group, portal venous flow remained unchanged and hepatic artery flow significantly increased compared to baseline. Although the production of liver tissue NOx transiently decreased to 60% after ischemia, its level in the SNP group remained higher than the control saline group. Regional administration of SNP into the portal vein increases hepatic arterial flow during ischemia reperfusion periods without altering mean systemic arterial pressure. We speculate that administration of an exogenous NO donor may be effective in preventing liver injury via preservation of total hepatic blood flow.
    No preview · Article · Aug 2015 · Journal of Investigative Surgery