Erratum

Dirsch, Olaf; Madrahimov, N.; Chaudri, Naved; Deng, Meihong; Madrahimova, Fotima; Schenk, Andrea; Dahmen, Uta

doi:10.1097/tp.0b013e31816631f9

Cited by 34 publications

(27 citation statements)

References 22 publications

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“…Focal outflow obstruction results in confluent centrilobular necrosis in the early postoperative phase (Dirsch et al 2008) and focal inflow obstruction leads to focal warm ischemia. This focal warm ischemic injury may also induce an injury in the nonischemic liver through autocrine and paracrine pathways.…”

Section: Introductionmentioning

confidence: 99%

HMGB1 in ischemic and non-ischemic liver after selective warm ischemia/reperfusion in rat

Liu

Dirsch

Fang

et al. 2011

Histochem Cell Biol

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High mobility group box 1 (HMGB1) acts as an early mediator in inflammation and organ injury. Ischemia reperfusion (I/R) injury induces HMGB1 translocation and expression in ischemic areas. However, it is unknown whether selective warm liver I/R injury also induces the expression of HMGB1 in non-ischemic lobes. The present study aimed to test the hypothesis that selective liver I/R injury also causes HMGB1 translocation and up-regulates its expression in non-ischemic liver areas. In the present study, selective I/R injury was induced by clamping the median and left lateral liver lobes for 90 min followed by 0.5, 6 and 24 h reperfusion. We used male inbred Lewis rats; six animals for each point in time and six animals for the normal control group. Selective hepatic I/R injury induced morphological changes not only in ischemic lobes but also in non-ischemic lobes. HMGB1 translocation and expression was increased in a time-dependent manner in the ischemic lobes, and increased in with delayed onset in the non-ischemic lobes. Serum HMGB1 levels were increased after reperfusion. Furthermore, liver I/R injury up-regulated the expression of HMGB1 receptors (Toll-like receptor 4 and receptor for advanced glycation end products and pro-inflammatory cytokines (Tumor necrosis factor-alpha and interleukin-6) in both ischemic lobes, however, the up-regulation of these cytokines was more prominent in the ischemic lobes. In conclusion, selective warm I/R induces a substantial "sympathetic/bystander" effect on the non-ischemic lobes in terms of HMGB1 translocation and local cytokine production.

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Section: Introductionmentioning

confidence: 99%

HMGB1 in ischemic and non-ischemic liver after selective warm ischemia/reperfusion in rat

Liu

Dirsch

Fang

et al. 2011

Histochem Cell Biol

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“…The vessel diameter and length of the perfused vessels per observation area can be measured by OPS (19). The previously described procedure of OPS video acquisition was followed strictly (5). Linearly polarized light of OPS, penetrated the liver surface (approximately 1 mm in diameter) to a depth of approximately 500 lm (20).…”

Section: Surgical Proceduresmentioning

confidence: 99%

“…Donor and graft preparation: The RMHV was exposed and isolated from the liver mass before ligation with one silk 6-0 suture (Resorba, Nuremberg, Bavaria, Germany), as described previously (5). Congestion of the corresponding drainage territory was recorded macroscopically by digital camera (Nikon CoolPix5800, Nikon, Tokyo, Japan).…”

Section: Surgical Proceduresmentioning

confidence: 99%

“…We previously performed right median hepatic vein (RMHV) ligation in combination with 50% partial hepatectomy (PH) in rats to mimic the clinical situation of focal hepatic venous outflow obstruction in a small-for-size liver after PH (5). Confluent necrosis and sinusoidal dilatation were observed in the outflow obstructed liver territory at the early postoperative stage.…”

Section: Introductionmentioning

confidence: 99%

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Hepatic Arterial Perfusion Is Essential for the Spontaneous Recovery From Focal Hepatic Venous Outflow Obstruction in Rats

Huang

Deng

Jin

et al. 2011

American Journal of Transplantation

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We previously observed that focal hepatic venous outflow obstruction recovered spontaneously by the formation of sinusoidal canals in a rat model of portal hyperperfusion. We aimed to investigate whether the lack of hepatic arterial perfusion aggravates parenchymal damage, decelerates recovery and influences the formation of sinusoidal canals after focal hepatic venous outflow obstruction. Rats were subjected to arterialized versus nonarterialized syngeneic liver transplantation after ligating the right median hepatic vein in the donor. Hepatic damage, microcirculation, regeneration and vascular remodeling were evaluated. In arterialized-recipients, confluent necrosis interspersed with viable periportal islands of hepatocytes, and vascularized sinusoidal canals with visible blood flow, surrounded by normal sinusoidal structure, were visible on postoperative day (POD) 2. Complete parenchymal recovery was consequently established by resorption of necrosis and hepatocyte proliferation, detected in viable portal islands and border zone. Lack of hepatic arterial perfusion caused complete necrosis in the obstruction zone without viable hepatocytes in the periportal area on POD2. Hepatocyte proliferation was only visible in the border zone. On POD28, perfused vascular structures, without neighboring normal sinusoidal structures, were observed in the scar-like area. Hepatic arterial perfusion determined the extent of hepatic necrosis, the formation of vascularized sinusoidal canals and the parenchymal recovery, after focal hepatic venous outflow obstruction.

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“…Over time, these dilated sinusoidal structures undergo vascularization and transformation into sinusoidal canals-also showing CD34 expression of endothelial cells, cf. Dirsch et al (2008). This finding highlights the plasticity of the sinusoidal meshwork and indicates that permanent changes in flow are accompanied by structural changes in the sinusoidal endothelial cells.…”

Section: Transversely Isotropic Permeability and Remodelingmentioning

confidence: 74%

Modeling function–perfusion behavior in liver lobules including tissue, blood, glucose, lactate and glycogen by use of a coupled two-scale PDE–ODE approach

Ricken

Werner

Holzhütter

et al. 2014

Biomech Model Mechanobiol

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This study focuses on a two-scale, continuum multicomponent model for the description of blood perfusion and cell metabolism in the liver. The model accounts for a spatial and time depending hydro-diffusion-advection-reaction description. We consider a solid-phase (tissue) containing glycogen and a fluid-phase (blood) containing glucose as well as lactate. The five-component model is enhanced by a two-scale approach including a macroscale (sinusoidal level) and a microscale (cell level). The perfusion on the macroscale within the lobules is described by a homogenized multiphasic approach based on the theory of porous media (mixture theory combined with the concept of volume fraction). On macro level, we recall the basic mixture model, the governing equations as well as the constitutive framework including the solid (tissue) stress, blood pressure and solutes chemical potential. In view of the transport phenomena, we discuss the blood flow including transverse isotropic permeability, as well as the transport of solute concentrations including diffusion and advection. The continuum multicomponent model on the macroscale finally leads to a coupled system of partial differential equations (PDE). In contrast, the hepatic metabolism on the microscale (cell level) was modeled via a coupled system of ordinary differential equations (ODE). Again, we recall the constitutive relations for cell metabolism level. A finite element implementation of this framework is used to provide an illustrative example, describing the spatial and time-depending perfusion-metabolism processes in liver lobules that integrates perfusion and metabolism of the liver.

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Erratum

Cited by 34 publications

References 22 publications

HMGB1 in ischemic and non-ischemic liver after selective warm ischemia/reperfusion in rat

HMGB1 in ischemic and non-ischemic liver after selective warm ischemia/reperfusion in rat

Hepatic Arterial Perfusion Is Essential for the Spontaneous Recovery From Focal Hepatic Venous Outflow Obstruction in Rats

Modeling function–perfusion behavior in liver lobules including tissue, blood, glucose, lactate and glycogen by use of a coupled two-scale PDE–ODE approach

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