Intra-abdominal pressure development after different temporary abdominal closure techniques in a porcine model.

Background: Decompressive laparotomy followed by temporary abdominal closure (TAC) is an established prophylaxis and treatment for abdominal compartment syndrome. The herein presented study aimed at the comparison of volume reserve capacity and development of intra-abdominal hypertension after forced primary abdominal closure and different TAC techniques in a porcine model.

Methods: Eight anesthesized and mechanically ventilated domestic pigs underwent a standardized midline laparotomy.

Curcumin attenuates oxidative stress and inflammatory response in the early phase after partial hepatectomy with simultaneous intraabdominal infection in rats.

Background: Curcumin is a nontoxic, hepatoprotective antioxidant. It has been shown to efficiently scavenge oxygen free radicals, increase intracellular glutathione concentrations, and prevent lipid peroxidation in rat hepatocytes. Moreover, it has strong anti-inflammatory effects.

Erythropoietin reduces necrosis in critically ischemic myocutaneous tissue by protecting nutritive perfusion in a dose-dependent manner.

Background: Erythropoietin (Epo), the primary regulator of erythropoiesis, has recently been shown to exert antiinflammatory and antiapoptotic properties in neuronal and myocardial tissue. We herein studied whether Epo pretreatment can reduce cell death and ischemic necrosis in a chronic in vivo model.

Methods: C57BL/6 mice were treated daily for 3 consecutive days with either 500 IU EPO/kg body weight (bw) (group Epo 500, n = 8) or 5000 IU EPO/kg bw (group Epo 5000, n = 8) administered intraperitoneally 24 hours before surgery.

Metalloporphyrins, used for HO-1 inhibition, themselves affect hepatic microcirculation, liver function, and hepatocellular integrity.

Background: Metalloporphyrins (MPs) are broadly used in the studies of the role of the heme oxygenase (HO)-1 system in different stress models. However, possible side effects of the MP administration itself have to be further investigated.

Methods: Sin IV mesoporpyhrin IX (SnMP; 10 micromol/kg body weight), tin protoporpyhrin IX (SnPP; 50 micromol/kg body weight), or chromium mesoporpyhrin IX (CrMP; 40 micromol/kg body weight) were administered to Sprague-Dawley rats (each group, n=5).

Inhibition of 3-hydroxy-3-methyl-glutaryl-coenzyme A reductase reduces leukocyte recruitment and hepatocyte apoptosis in endotoxin-induced liver injury.

Background: Endotoxemia is well known to be associated with an excessive host response to bacteria or microbial compounds, resulting in systemic inflammation and organ injury. The aim of the present study was to examine the effects of simvastatin on endotoxemic liver injury.

Methods: Male C57BL/6J mice were challenged intraperitoneally with 0.

In vivo biocompatibility and vascularization of biodegradable porous polyurethane scaffolds for tissue engineering.

Scaffolds for tissue engineering should be biocompatible and stimulate rapid blood vessel ingrowth. Herein, we analyzed in vivo the biocompatibility and vascularization of three novel types of biodegradable porous polyurethane scaffolds. The polyurethane scaffolds, i.

Role of the perforin/granzyme cell death pathway in D-Gal/LPS-induced inflammatory liver injury.

Cytotoxic T lymphocytes and their granule components, such as perforin and granzyme, play an important role in the defense of hepatic infections caused by different pathogens. Moreover, it has been shown in vitro that hepatocytes can initiate cell death via a perforin-dependent mechanism. Although it is well known that hepatocellular apoptosis in D-galactosamine/lipopolysaccharide (D-Gal/LPS)-associated liver failure is mediated by TNF-alpha-dependent Fas/FasL cytotoxicity, there is no information on the role of perforin-mediated mechanisms in vivo.

p38 MAPK regulates ischemia-reperfusion-induced recruitment of leukocytes in the colon.

Background: Our objective was to examine the role of p38 mitogen-activated protein kinase (MAPK) in ischemia-reperfusion (I/R)-induced recruitment or leukocytes in the colon.

Methods: C57/Bl6 mice were subjected to 30 minutes of ischemia by clamping the superior mesenteric artery followed by 2 hours of reperfusion. Animals were pretreated with the selective p38 MAPK inhibitors SB 239063 and SKF 86002 before induction of I/R.

Ex vivo analysis of rotational stiffness of different osteosynthesis techniques in mouse femur fracture.

The various molecular mechanisms of cell regeneration and tissue healing can best be studied in mouse models with the availability of a wide range of monoclonal antibodies and gene-targeted animals. The influence of the mechanical stability of individual stabilization techniques on the molecular mechanisms of fracture healing has not been completely elucidated yet. Although during recent years several osteosynthesis techniques have been introduced in mouse fracture models, no comparative study on fracture stabilization is available yet.

Rapamycin, but not cyclosporine A, inhibits vascularization and incorporation of implanted surgical meshes.

Incisional hernias are a frequent complication of upper abdominal wall interventions, especially in patients undergoing liver transplantation with subsequent immunosuppressive therapy. Therefore, we analyzed in this study the manner in which the incorporation of a surgical mesh for hernia repair is affected by the immunosuppressant drugs rapamycin and cyclosporine A (CsA). For this purpose, Ultrapro meshes were implanted into the dorsal skinfold chambers of rapamycin- and CsA-treated hamsters.

Rho-kinase inhibitor attenuates cholestasis-induced CXC chemokine formation, leukocyte recruitment, and hepatocellular damage in the liver.

Background: In the present experimental study, we analyzed the role of Rho-kinase during obstructive cholestasis by studying the effect of the Rho-kinase inhibitor Y-27632 on hepatic CXC chemokine formation, leukocyte recruitment and hepatocellular damage.

Materials And Methods: C57BL/6 mice underwent bile duct ligation (BDL) to induce obstructive cholestasis. Mice were pretreated with Y-27632 (1 and 10mg/kg) or the vehicle PBS.

Simvastatin protects against cholestasis-induced liver injury.

Background: Bile duct obstruction is associated with hepatic accumulation of leukocytes and liver injury. The aim of this study was to evaluate the effect of simvastatin on cholestasis-induced liver inflammation and tissue damage.

Experimental Approach: C57BL/6 mice were treated with simvastatin (0.

Improvement of vascularization of PLGA scaffolds by inosculation of in situ-preformed functional blood vessels with the host microvasculature.

Objective: We analyzed, in vivo, whether the establishment of blood supply to implanted scaffolds can be accelerated by inosculation of an in situ-preformed microvascular network with the host microvasculature.

Background: A rapid vascularization is crucial for the survival of scaffold-based transplanted tissue constructs.

Methods: Poly-lactic-glycolic acid scaffolds were implanted into the flank of balb/c or green fluorescent protein (GFP)-transgenic mice for 20 days to create in situ a new microvascular network within the scaffolds.

Erythropoietin protects critically perfused flap tissue.

Objective: The objective of this study was to analyze whether erythropoietin (EPO) protects from necrosis of critically perfused musculocutaneous tissue and the mechanisms by which this protection is achieved.

Background: EPO is the regulator of erythropoiesis and is used to treat patients with anemia of different causes. Recent studies suggest that EPO has also other tissue-protective effects, irrespective of its erythropoietic properties.

Multiple doses of erythropoietin impair liver regeneration by increasing TNF-alpha, the Bax to Bcl-xL ratio and apoptotic cell death.

Background: Liver resection and the use of small-for-size grafts are restricted by the necessity to provide a sufficient amount of functional liver mass. Only few promising strategies to maximize liver regeneration are available. Apart from its erythropoiesis-stimulating effect, erythropoietin (EPO) has meanwhile been recognized as mitogenic, tissue-protective, and anti-apoptotic pleiotropic cytokine.

A new model for studying the revascularization of skin grafts in vivo: the role of angiogenesis.

Background: Models of skin graft revascularization are based mostly on histologic evaluations but lack the possibility of analyzing the vascular biology in vivo. The aim of the present study was therefore to develop an animal model that allows continuous monitoring of the microcirculation during skin graft healing.

Methods: Skin and subcutaneous tissue were removed from the back of dorsal skinfold chamber preparations in mice, leaving one layer of striated muscle and subcutaneous tissue as a wound bed (n = 5).

A new model for chronic in vivo analysis of the periosteal microcirculation.

Objective: Microvascular perfusion is indispensable for the growth and remodulation of membrane bone. Trauma, inflammation and surgical interventions may alter periosteal perfusion. However, there is not much known about periosteal perfusion in membrane bones.

Hepatocellular apoptosis is mediated by TNFalpha-dependent Fas/FasLigand cytotoxicity in a murine model of acute liver failure.

There is increasing evidence that the active contribution of hepatocytes to liver disease is strongly dependent on local cytokine environment. It has been shown in vitro that TNFalpha can enhance hepatocyte FasLigand (FasL)-mediated cytotoxicity. Here, we demonstrate that TNFalpha-induced apoptosis was associated with Fas and FasL upregulation and that a FasL-neutralizing antibody prevented TNFalpha-induced apoptosis.

Erythropoietin enhances oxygenation in critically perfused tissue through modulation of nitric oxide synthase.

The aim of this study was to investigate the effect of human recombinant erythropoietin (EPO) on the microcirculation and oxygenation of critically ischemic tissue and to elucidate the role of endothelial NO synthase in EPO-mediated tissue protection. Island flaps were dissected from the back skin of anesthetized male Syrian golden hamsters including a critically ischemic, hypoxic area that was perfused via a collateralized vasculature. Before ischemia, animals received an injection of epoetin beta at a dose of 5,000 U/kg body weight with (n = 7) or without (n = 7) blocking NO synthase by 30 mg/kg body weight L-NAME (Nomega-nitro-L-arginine methyl ester hydrochloride).

Local preconditioning by thermal stress accelerates microvascular thrombus formation.

Heme oxygenase 1 (HO-1) has been shown to suppress microvascular thrombus formation. Because stress conditioning induces HO-1 and, in addition, the anticoagulant thrombomodulin and thrombospondin 1, we studied the effect of hyperthermic and hypothermic local stress conditioning on microvascular thrombus formation. For local stress conditioning, the hindlimb of Sprague-Dawley rats was subjected to local heating (42.

Nutritive perfusion of pancreatic endocrine tissue during hemorrhagic hypotension: how differ islets in situ from islet isografts?

Although the exocrine gland frequently has I/R-associated complications such as posttransplant pancreatitis, hypoxia-induced dysfunction of pancreatic endocrine tissue is rarely observed. However, sympathetic hypersensitivity is accused of impaired endocrine function observed in human pancreatic grafts. These tissue-confined differences in susceptibility might be attributed to a distinct islet-specific regulatory control of blood flow (BF).

Cholestatic liver damage is mediated by lymphocyte function antigen-1-dependent recruitment of leukocytes.

Background: The role of specific adhesion molecules in cholestasis-induced leukocyte recruitment in the liver is not known. Therefore, the aim of our experimental study was to evaluate the role of lymphocyte function antigen-1 (LFA-1) in cholestatic liver injury.

Methods: C57BL/6 mice underwent bile duct ligation for 12 hours.

Development of a stable closed femoral fracture model in mice.

Background: Mice have become of increasing interest as experimental model for fracture studies. Due to their small size, most studies use simple pins for fracture stabilization, although insufficient rigidity of fixation critically affects fracture healing. Herein, we studied whether longitudinal fracture compression by an intramedullary screw represents a standardized, stable osteosynthesis technique in mice, and whether it may accelerate fracture healing.

Primary and secondary capture of platelets onto inflamed femoral artery endothelium is dependent on P-selectin and PSGL-1.

Platelets constitute a key role in vascular injuries, however, the detailed mechanisms behind platelet-endothelial cell and platelet-leukocyte interactions in the femoral artery are not yet fully elucidated. We used intravital fluorescence microscopy of the femoral artery in C57BL/6 mice to study primary and secondary capture of platelets onto endothelial cells as well as onto adherent platelets and leukocytes in vivo. By use of monoclonal antibodies, the role of P-selectin and P-selectin glycoprotein ligand 1 (PSGL-1) in these adhesive interactions in mice exposed to endotoxin was determined.

Epigallocatechin-3-gallate inhibits estrogen-induced activation of endometrial cells in vitro and causes regression of endometriotic lesions in vivo.

Background: Epigallocatechin-3-gallate (EGCG), the major component of green tea, is a pleiotropic substance, which may inhibit tumor growth via multiple intracellular signaling pathways. Herein, we studied whether EGCG may also be effective in the treatment of endometriosis.

Methods: We investigated the effect of EGCG on activation by estradiol (E(2)), proliferation and vascular endothelial growth factor (VEGF) expression of isolated hamster endometrial stromal cells and glandular cells in vitro using the water-soluble tetrazolium (WST)-1 colorimetric assay and western blot analysis.