A time-dependent balance between endothelins and nitric oxide regulating portal resistance after endotoxin

1996 ◽  
Vol 271 (5) ◽  
pp. H1953-H1961 ◽  
Author(s):  
B. H. Pannen ◽  
M. Bauer ◽  
J. X. Zhang ◽  
J. L. Robotham ◽  
M. G. Clemens
Keyword(s):  
Nitric Oxide ◽  
Escherichia Coli ◽  
Portal Pressure ◽  
Time Dependent ◽  
Epifluorescence Microscopy ◽  
Synthesis Inhibitor ◽  
Before And After ◽  
Etb Receptor ◽  
Escherichia Coli Lipopolysaccharide ◽  
Zero Flow

To test whether endothelins are involved in the regulation of portal resistance after endotoxin pretreatment and whether their effects are modulated by nitric oxide (NO), rats received intraperitoneal injections of Escherichia coli lipopolysaccharide (LPS, 1 mg/kg body wt) or saline. Six and twenty-four hours later, livers were isolated and perfused. Analyses of portal pressure-flow (P-Q) relationships and epifluorescence microscopy were performed before and after administration of 1) the NO synthesis inhibitor N omega-nitro-L-arginine methyl ester (L-NAME, 10(-3) M), followed by L-arginine (2 x 10(-3) M), or 2) the endothelin ETA/ETB-receptor antagonist bosentan (2 x 10(-4) M), followed by L-NAME (10(-3) M). LPS pretreatment increased all measures of resistance, which included total portal resistance, zero flow, incremental resistance (slopes of P-Q relationship), and sinusoid resistance. L-NAME had no effect in sham controls but increased all measures of resistance at 6 h after LPS and increased total and incremental resistance 24 h after LPS. L-Arginine reversed these changes. Bosentan reduced total and sinusoid resistance slightly in control livers and caused substantial reductions in all measures of resistance at 6 and 24 h after LPS; these were partially reversed after L-NAME at 6 but not at 24 h. Our data support the hypothesis that a critical balance between endothelin-mediated vasoconstrictor influences and NO-mediated vasodilator influences controls portal resistance after endotoxin pretreatment.

scholarly journals Forsythiaside attenuates Escherichia coli lipopolysaccharide-induced liver acute inflammatory response in chicken

2019 ◽  
Vol 17 ◽  
pp. 205873921982679 ◽  
Author(s):  
Jingwen Bai ◽  
Xiaoting Wang ◽  
Meiqi Hao ◽  
He Li ◽  
Guangdong Cheng ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Escherichia Coli ◽  
Inflammatory Response ◽  
Mrna Expression ◽  
Control Group ◽  
Interleukin 17 ◽  
Acute Inflammatory Response ◽  
Total Proteins ◽  
Necrosis Factor Alpha ◽  
Escherichia Coli Lipopolysaccharide

This study investigated the effects of forsythiaside on the acute inflammatory response induced by Escherichia coli lipopolysaccharide (LPS) in liver of broiler chickens. Fifteen-day-old chickens were randomly assigned to three groups (n = 20 for each group, orally treated with 0, 30, or 60 mg/kg BW of forsythiaside) for 7 days. At 21 days of age, the chickens were intravenously injected with either LPS (200 μg/kg BW) or sterile saline (200 μg/kg BW, control group). All the chickens were humanely euthanized by cervical dislocation 2 h after the LPS injection. The results showed that the injection of LPS induced some indexes, including total proteins, nitric oxide (NO), interleukin-1beta (IL-1β), interleukin-6 (IL-6), and interleukin-17 (IL-17) production ( P < 0.05) and increased the mRNA expression of LPS-induced tumor necrosis factor-alpha (LITAF), IL-1β, IL-17, IL-6, and inducible nitric oxide synthase (iNOS) ( P < 0.05). Forsythiaside supplementation alleviated the LPS-induced inflammatory response by inhibiting the production of total proteins, NO, LITAF, IL-1β, IL-17, and IL-6 and down-regulating the mRNA expression of pro-inflammatory cytokines and iNOS. In conclusion, forsythiaside is a potential treatment for LPS-induced liver acute inflammation in chicken.

Endotoxin pretreatment enhances portal venous contractile response to endothelin-1

1996 ◽  
Vol 270 (1) ◽  
pp. H7-H15 ◽  
Author(s):  
B. H. Pannen ◽  
M. Bauer ◽  
J. X. Zhang ◽  
J. L. Robotham ◽  
M. G. Clemens
Keyword(s):  
Contractile Response ◽  
Portal Pressure ◽  
Normal Liver ◽  
Portal Circulation ◽  
Cell Velocity ◽  
Before And After ◽  
Red Blood Cell Velocity ◽  
Regression Slopes ◽  
Escherichia Coli Lipopolysaccharide ◽  
Krebs Buffer

To test whether endotoxin pretreatment modulates the portal hemodynamic response to endothelin (ET)-1 and phenylephrine (PE), two potent vasoconstrictors in the portal circulation of the normal liver, rats received intraperitoneal injections of Escherichia coli lipopolysaccharide (LPS; 1 mg/kg body wt) or saline. Livers were isolated after 6 or 24 h and perfused with Krebs buffer containing 5% autologous erythrocytes. Analyses of portal pressure-flow (P-Q) relationships and epifluorescence video microscopy were performed before and after ET-1 (10(-9) M) or PE (10(-5) M) administration. LPS pretreatment increased total portal resistances (Rt), zero-flow pressures (PQ = 0), and linear regression slopes of P-Q relationships, and decreased the sinusoidal diameters (Ds) and sinusoidal volumetric flow (Qv). The response to ET-1 was enhanced 6 and 24 h after LPS administration, leading to greater increases in Rt, PQ = 0, and slope and more pronounced decreases in Dx, red blood cell velocity (VRBC), and Qv. In contrast, PE effects were similar (PQ = 0, slope, Ds) or even attenuated (Rt, VRBC, Qv) in livers from LPS-treated compared with control animals. Thus endotoxin pretreatment increased the portal contractile response to ET-1 but not to PE. This enhanced ET-1 response appeared to occur at sinusoidal and presinusoidal levels and may contribute to endotoxin-induced hepatic microcirculatory failure.

scholarly journals Optimization of GOPS-Based Functionalization Process and Impact of Aptamer Grafting on the Si Nanonet FET Electrical Properties as First Steps towards Thrombin Electrical Detection

Nanomaterials ◽  
2020 ◽  
Vol 10 (9) ◽  
pp. 1842
Author(s):  
Monica Vallejo-Perez ◽  
Céline Ternon ◽  
Nicolas Spinelli ◽  
Fanny Morisot ◽  
Christoforos Theodorou ◽  
...  
Keyword(s):  
Electrical Properties ◽  
Field Effect Transistors ◽  
Time Dependent ◽  
Epifluorescence Microscopy ◽  
Electrical Detection ◽  
Si Nanowires ◽  
Transmission Electron ◽  
Scanning Transmission ◽  
Before And After ◽  
The Impact

Field effect transistors (FETs) based on networks of randomly oriented Si nanowires (Si nanonets or Si NNs) were biomodified using Thrombin Binding Aptamer (TBA–15) probe with the final objective to sense thrombin by electrical detection. In this work, the impact of the biomodification on the electrical properties of the Si NN–FETs was studied. First, the results that were obtained for the optimization of the (3-Glycidyloxypropyl)trimethoxysilane (GOPS)-based biofunctionalization process by using UV radiation are reported. The biofunctionalized devices were analyzed by atomic force microscopy (AFM) and scanning transmission electron microscopy (STEM), proving that TBA–15 probes were properly grafted on the surface of the devices, and by means of epifluorescence microscopy it was possible to demonstrate that the UV-assisted GOPS-based functionalization notably improves the homogeneity of the surface DNA distribution. Later, the electrical characteristics of 80 devices were analyzed before and after the biofunctionalization process, indicating that the results are highly dependent on the experimental protocol. We found that the TBA–15 hybridization capacity with its complementary strand is time dependent and that the transfer characteristics of the Si NN–FETs obtained after the TBA–15 probe grafting are also time dependent. These results help to elucidate and define the experimental precautions that must be taken into account to fabricate reproducible devices.

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