Buffer Response (buffer + response)

Distribution by Scientific Domains
Medical Sciences85%

Kinds of Buffer Response

  • arterial buffer response
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  • hepatic arterial buffer response
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    Selected Abstracts

    POST-HARVEST RIPARIAN BUFFER RESPONSE: IMPLICATIONS FOR WOOD RECRUITMENT MODELING AND BUFFER DESIGN,

    JOURNAL OF THE AMERICAN WATER RESOURCES ASSOCIATION, Issue 1 2006
    Michael K. Liquori
    ABSTRACT: Despite the importance of riparian buffers in providing aquatic functions to forested streams, few studies have sought to capture key differences in ecological and geomorphic processes between buffered sites and forested conditions. This study examines post-harvest buffer conditions from 20 randomly selected harvest sites within a managed tree farm in the Cascade Mountains of western Washington. Post-harvest wind derived treefall rates in buffers up to three years post-harvest averaged 268 trees/km/year, 26 times greater than competition-induced mortality rate estimates. Treefall rates and stem breakage were strongly tied to tree species and relatively unaffected by stream direction. Observed treefall direction is strongly biased toward the channel, irrespective of channel or buffer orientation. Fall direction bias can deliver significantly more wood recruitment relative to randomly directed treefall, suggesting that models that utilize the random fall assumption will significantly underpredict recruitment. A simple estimate of post-harvest wood recruitment from buffers can be obtained from species specific treefall and breakage rates, combined with bias corrected recruitment probability as a function of source distance from the channel. Post-harvest wind effects may reduce the standing density of trees enough to significantly reduce or eliminate competition mortality and thus indirectly alter bank erosion rates, resulting in substantially different wood recruitment dynamics from buffers as compared to unmanaged forests. [source]

    Hepatic arterial buffer response in patients with advanced cirrhosis

    HEPATOLOGY, Issue 3 2002
    Veit Gülberg
    Hepatic arterial buffer response (HABR) is considered an important compensatory mechanism to maintain perfusion of the liver by hepatic arterial vasodilation on reduction of portal venous perfusion. HABR has been suggested to be impaired in patients with advanced cirrhosis. In patients with hepatopetal portal flow, placement of a transjugular intrahepatic portosystemic shunt (TIPS) reduces portal venous liver perfusion. Accordingly, patients with severe cirrhosis should have impaired HABR after TIPS implantation. Therefore, the aim of this study was to investigate the effect of TIPS on HABR as reflected by changes in resistance index (RI) of the hepatic artery. A total of 366 patients with cirrhosis (Child-Pugh class A, 106; class B, 168; class C, 92) underwent duplex Doppler ultrasonographic examination with determination of RI and maximal flow velocity in the portal vein before and 1 month after TIPS placement. Portosystemic pressure gradient was determined before and after TIPS placement. In 29 patients with hepatofugal portal blood flow, RI was significantly lower than in 337 patients with hepatopetal flow (0.63 ± 0.02 vs. 0.69 ± 0.01; P < .001). TIPS induced a significant decrease of the RI in patients with hepatopetal flow (RI, 0.69 ± 0.01 before vs. 0.64 ± 0.01 after TIPS; P = .001) but not in patients with hepatofugal flow (RI, 0.63 ± 0.02 before vs. 0.63 ± 0.02 after TIPS; NS). This response was not dependent on the Child-Pugh class. In conclusion, our results suggest that some degree of HABR is preserved even in patients with advanced cirrhosis with significant portal hypertension. [source]

    Regulatory processes interacting to maintain hepatic blood flow constancy: Vascular compliance, hepatic arterial buffer response, hepatorenal reflex, liver regeneration, escape from vasoconstriction

    HEPATOLOGY RESEARCH, Issue 11 2007
    W. Wayne Lautt
    Constancy of hepatic blood flow (HBF) is crucial for several homeostatic roles. The present conceptual review focuses on interrelated mechanisms that act to maintain a constant HBF per liver mass. The liver cannot directly control portal blood flow (PF); therefore, these mechanisms largely operate to compensate for PF changes. A reduction in PF leads to reduced intrahepatic distending pressure, resulting in the highly compliant hepatic vasculature passively expelling up to 50% of its blood volume, thus adding to venous return, cardiac output and HBF. Also activated immediately upon reduction of PF are the hepatic arterial buffer response and an HBF-dependent hepatorenal reflex. Adenosine is secreted at a constant rate into the small fluid space of Mall which surrounds the terminal branches of the hepatic arterioles, portal venules and sensory nerves. The concentration of adenosine is regulated by washout into the portal venules. Reduced PFreduces the washout and the accumulated adenosine causes dilation of the hepatic artery, thus buffering the PF change. Adenosine also activates hepatic sensory nerves to cause reflex renal fluid retention, thus increasing circulating blood volume and maintaining cardiac output and PF. If these mechanisms are not able to maintain total HBF, the hemodynamic imbalance results in hepatocyte proliferation, or apoptosis, by a shear stress/nitric oxide-dependent mechanism, to adjust total liver mass to match the blood supply. These mechanisms are specific to this unique vascular bed and provide an excellent example of multiple integrative regulation of a major homeostatic organ. [source]

    A distinct nitric oxide and adenosine A1 receptor dependent hepatic artery vasodilatatory response in the CCl4 -cirrhotic liver

    LIVER INTERNATIONAL, Issue 7 2010
    Alexander Zipprich
    Abstract Increase of portal venous vascular resistance is counteracted by decrease of hepatic arterial vascular resistance (hepatic arterial buffer response). This process is mediated by adenosine in normal livers. In cirrhosis, hepatic arterial vascular resistance is decreased but the involvement of adenosine in this process is unknown. The aim of our study was to identify the signalling pathway responsible for the decreased hepatic arterial resistance in cirrhotic livers. Methods: Cirrhosis was induced by CCl4. Using a bivascular liver perfusion dose,response curves to adenosine of the HA were performed in the presence and the absence of pan-adenosine blocker (8-SPT), A1 blocker (caffeine) or nitric oxide synthase-blocker (l -NMMA) after preconstriction with an ,1-agonist (methoxamine). Western blot of the HA were used to measure the density of the A1 and A2a receptors. Results: Adenosine caused a dose dependent relaxation of the hepatic artery of both cirrhotic and control animals that were blocked in both groups by 8-SPT (P<0.02). The response to adenosine was greater in cirrhotic rats (P=0.016). Both l -NMMA (P=0.003) and caffeine reduced the response to adenosine in cirrhotic but not in control animals. Western blot analysis showed a higher density of A1 and a lower density of A2a receptor in cirrhotic animals (P<0.05). Conclusion: The adenosine-induced vasodilatation of the HA is increased in cirrhotic rats suggesting a role for adenosine-NO in the decreased hepatic arterial vascular resistance found in cirrhosis. This significantly greater response in cirrhosis by the A1 receptor follows the same pathway that is seen in hypoxic conditions in extra-hepatic tissues. [source]

    Adenosine restores the hepatic artery buffer response and improves survival in a porcine model of small-for-size syndrome,

    LIVER TRANSPLANTATION, Issue 11 2009
    Dympna M. Kelly
    The aim of the study is to define the role of the HABR in the pathophysiology of the SFS liver graft and to demonstrate that restoration of hepatic artery flow (HAF) has a significant impact on outcome and improves survival. Nine pigs received partial liver allografts of 60% liver volume, Group 1; 8 animals received 20% LV grafts, Group 2; 9 animals received 20% LV grafts with adenosine infusion, Group 3. HAF and portal vein flow (PVF) were recorded at 10 min, 60 min and 90 min post reperfusion, on POD 3 and POD 7 in Group 1, and daily in Group 2 and 3 up to POD 14. Baseline HAF and PVF (ml/100g/min) were 29 ± 12 (mean ± SD) and 74 ± 8 respectively, with 28% of total liver blood flow (TLBF) from the HA and 72% from the PV. PVF peaked at 10 mins in all groups, increasing by a factor of 3.8 in the 20% group compared to an increase of 1.9 in the 60% group. By POD 7-14 PVF rates approached baseline values in all groups. The HABR was intact immediately following reperfusion in all groups with a reciprocal decrease in HAF corresponding to the peak PVF at 10 min. However in the 20% group HAF decreased to 12 ± 8 ml/100 g/min at 90 min and remained low out to POD 7-14 despite restoration of normal PVF rates. Histopathology confirmed evidence of HA vasospasm and its consequences, cholestasis, centrilobular necrosis and biliary ischemia in Group 2. HA infusion of adenosine significantly improved HAF (p < .0001), reversed pathological changes and significantly improved survival (p = .05). An impaired HABR is important in the pathophysiology of the SFSS. Reversal of the vasospasm significantly improves outcome. Liver Transpl 15:1448,1457, 2009. © 2009 AASLD. [source]