Hyperdynamic Circulation of Cirrhotic Rats with Ascites: Role of Endotoxin, Tumour Necrosis Factor-α and Nitric Oxide

1997 ◽  
Vol 93 (3) ◽  
pp. 219-225 ◽  
Author(s):  
Chi-Jen Chu ◽  
Fa-Yauh Lee ◽  
Sun-Sang Wang ◽  
LU Rei-Hwa ◽  
Yang-Te Tsai ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Tumour Necrosis Factor ◽  
Plasma Levels ◽  
Tumour Necrosis ◽  
Colorimetric Assay ◽  
Plasma Concentrations ◽  
No Production ◽  
Hyperdynamic Circulation ◽  
Tnf Α ◽  
Necrosis Factor

1. Hyperdynamic circulation observed in portal hypertensive states is characterized by generalized vasodilatation, increased cardiac index and increased systemic and regional blood flows. Endotoxin, tumour necrosis factor-alpha (TNF-α) and nitric oxide (NO) have been reported to be involved in the pathogenesis of hyperdynamic circulation, but the interactions between endotoxin, TNF-α and NO in cirrhotic rats with ascites have never been specifically addressed. 2. This study was designed to determine systemic and portal haemodynamics and plasma levels of endotoxin, TNF-α and nitrate/nitrite in cirrhotic rats with ascites and investigate the relationships between these substances. 3. Plasma concentrations of endotoxin, TNF-α and nitrate/nitrite (an index of NO production) were determined in 25 cirrhotic rats with ascites and 17 control rats using the Limulus assay, ELISA and a colorimetric assay respectively. In addition, haemodynamic studies were performed in another ten cirrhotic rats with ascites and ten control rats. 4. Cirrhotic rats with ascites had hyperdynamic circulation accompanied by increased plasma levels of endotoxin, TNF-α and nitrate/nitrite, as compared with control rats. Significant correlation existed between plasma levels of endotoxin and nitrate/nitrite (r = 0.59, P < 0.0001) and between plasma levels of endotoxin and TNF-α (r = 0.63, P < 0.0001). No correlation was detected between plasma levels of TNF-α and nitrate/nitrite (r = 0.24, P > 0.05). 5. This study suggests that endotoxaemia developed in cirrhotic rats with ascites may stimulate NO formation directly or indirectly via cytokine cascade, and consequently participate in the development and/or maintenance of hyperdynamic circulation.

Differential effect of selective block of α2-adrenoreceptors on plasma levels of tumour necrosis factor-α, interleukin-6 and corticosterone induced by bacterial lipopolysaccharide in mice

1995 ◽  
Vol 144 (3) ◽  
pp. 457-462 ◽  
Author(s):  
G Haskó ◽  
I J Elenkov ◽  
V Kvetan ◽  
E S Vizi
Keyword(s):  
Tumour Necrosis Factor ◽  
Interleukin 6 ◽  
Plasma Levels ◽  
Tumour Necrosis ◽  
Endotoxin Shock ◽  
Bacterial Lipopolysaccharide ◽  
Tumour Necrosis Factor Α ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Abstract The effect of selective block of α2-adrenoreceptors on plasma levels of tumour necrosis factor-α (TNF-α), interleukin-6 (IL-6) and corticosterone induced by bacterial lipopolysaccharide (LPS) was investigated in mice using ELISA and RIA. It was found that the LPS-induced TNF-α response was significantly blunted in mice pretreated with CH-38083, a novel and highly selective α2-adrenoreceptor antagonist (the α2/α1 ratio is >2000). In contrast, LPS-induced increases in both corticosterone and IL-6 plasma levels were further increased by CH-38083. Since it has recently been shown that the selective block of α2-adrenoreceptors located on noradrenergic axon terminals resulted in an increase in the release of noradrenaline (NA), both in the central and peripheral nervous systems, and, in our experiments, that propranolol prevented the effect of α2-adrenoreceptor blockade on TNF-α plasma levels induced by LPS, it seems likely that the excessive stimulation by NA of β-adrenoreceptors located on cytokine-secreting immune cells is responsible for this action. Since it is generally accepted that increased production of TNF-α is involved in the pathogenesis of inflammation and endotoxin shock on the one hand, and corticosterone and even IL-6 are known to possess anti-inflammatory properties on the other hand, it is suggested that the selective block of α2-adrenoreceptors might be beneficial in the treatment of inflammation and/or endotoxin shock. Journal of Endocrinology (1995) 144, 457–462

Chicken amyloid arthropathy: serum amyloid A, interleukin-1β, interleukin-6, tumour necrosis factor-α and nitric oxide profile in acute phase (12th hour)

2013 ◽  
Vol 16 (2) ◽  
pp. 241-247 ◽  
Author(s):  
A. Sevimli ◽  
T. Bübül ◽  
A. Bulübül ◽  
A. Yaǧcı
Keyword(s):  
Nitric Oxide ◽  
Vitamin A ◽  
Tumour Necrosis Factor ◽  
Acute Phase ◽  
Tumour Necrosis ◽  
Serum Amyloid A ◽  
Amyloid A ◽  
Tnf Α ◽  
Amyloid Arthropathy ◽  
Necrosis Factor

Abstract Acute phase response (APR) is part of the early defense system, which is triggered by different stimuli including, infection, trauma, stres, inflammation and neoplasia. The APR complex is a reaction which induces homeostasis and recovery. In this research, serum amyloid A (SAA), interlaukin (IL)-1β, IL-6, tumour necrosis factor alpha (TNF-α) and nitric oxide (NO) levels were measured 12 hours following injection. For this purpose, Thirty-two 5 weeks old laying chicken were allocated into four groups and intra-articular injections of Freund’s adjuvant were used to induce amylod arthropathy in Groups II, III and IV. Vitamin A in group II, and methylprednisolone in group IV were added to enhance and to reduce the severity of amyloidosis, respectively. At the end of the research, it was observed that TNF-α and NO increased significantly (P<0.05) in vitamin A and methylprednisolone groups whereas SAA decreased significantly (P<0.05) in all groups. It was also observed that IL-6 increased (P<0.05) in vitamin A group and decreased in all other gorups however, IL-1β decreased in vitamin A and methylprednisolone groups, while it was increased in the control group. The results of this study suggest that there is a positive correlation between serum TNF-α levels in acute and chronic phase in chickens with amyloid arthropathy.

Steroidogenesis, proliferation and apoptosis in bovine granulosa cells: role of tumour necrosis factor-α and its possible signalling mechanisms

2002 ◽  
Vol 14 (3) ◽  
pp. 141 ◽  
Author(s):  
G. Basini ◽  
G. L. Mainardi ◽  
S. Bussolati ◽  
C. Tamanini
Keyword(s):  
Nitric Oxide ◽  
Tumour Necrosis Factor ◽  
Granulosa Cell ◽  
Granulosa Cells ◽  
Tumour Necrosis ◽  
Tumour Necrosis Factor Α ◽  
Tnf Α ◽  
Proliferation And Apoptosis ◽  
Factor Α ◽  
Necrosis Factor

This study was designed to investigate the presence of bioactive tumour necrosis factor-α (TNF-α) in bovine fluid collected from small (<5 mm) and large (>8 mm) follicles, as well as the production of the cytokine by the granulosa cells collected from the same type of follicles. Moreover, the effectiveness of 10, 1 and 0.1 ng mL-1 of human TNF-α (hTNF-α) in affecting the main parameters of granulosa cell function, progesterone (P4) and oestradiol-17β (E2) production, cell proliferation and apoptosis, was tested. In addition, the study aimed to determine whether the signalling mechanisms of TNF-α in these cells involve cAMP, nitric oxide or prostaglandin E2 (PGE2) and F2α (PGF2α). It emerged that bioactive TNF-α is present in follicular fluid from both types of follicles and can be measured in media conditioned by granulosa cells from large follicles. As for the effects of hTNF-α , it inhibits P4 production in cells from both types of follicles and stimulates E2 output in those from small follicles; it does not affect proliferation, but it stimulates granulosa cell apoptosis. Finally, the effects of hTNF-α on bovine granulosa cells are not mediated by nitric oxide or cAMP, as neither of these substances were affected by treatment with the cytokine; however, in some way, they could be mediated through PGE2 and PGF2α, the production of which was inhibited by TNF-α in cells from small follicles.

Enzymic degradation of plasma arginine using arginine deiminase inhibits nitric oxide production and protects mice from the lethal effects of tumour necrosis factor α and endotoxin

2002 ◽  
Vol 363 (3) ◽  
pp. 581-587 ◽  
Author(s):  
J. Brandon THOMAS ◽  
Frederick W. HOLTSBERG ◽  
C. Mark ENSOR ◽  
John S. BOMALASKI ◽  
Mike A. CLARK
Keyword(s):  
Nitric Oxide ◽  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Arginine Deiminase ◽  
No Production ◽  
Tumour Necrosis Factor Α ◽  
Lethal Effects ◽  
Plasma Arginine ◽  
Factor Α ◽  
Necrosis Factor

Septic shock is mediated in part by nitric oxide (NO) and tumour necrosis factor α (TNFα). NO is synthesized primarily from extracellular arginine. We tested the ability of an arginine-degrading enzyme to inhibit NO production in mice and to protect mice from the hypotension and lethality that occur after the administration of TNFα or endotoxin. Treatment of BALB/c mice with arginine deiminase (ADI) formulated with succinimidyl succinimide polyethylene glycol of Mr 20000 (ADI-SS PEG20000) eliminated all measurable plasma arginine (from normal levels of ∼155μM arginine to 2μM). In addition, ADI-SS PEG20000 also inhibited the production of NO, as quantified by plasma nitrate+nitrite. Treatment of mice with TNFα or endotoxin resulted in a dose-dependent increase in NO production and lethality. Pretreatment of mice with ADI-SS PEG20000 resulted in increased resistance to the lethal effects of TNFα and endotoxin. These observations are consistent with NO production resulting, to some extent, from the metabolism of extracellular arginine. The toxic effects of TNFα and endotoxin may be partially inhibited by enzymic degradation of plasma arginine by ADI-SS PEG20000. Interestingly, pretreatment with ADI-SS PEG20000 did not inhibit the anti-tumour activity of TNFα in vitro or in vivo. This treatment may allow greater amounts of TNFα, as well as other cytokines, to be administered while abrogating side effects such as hypotension and death.

Plasma levels of soluble CD30, tumour necrosis factor (TNF)-α and TNF receptors during primary HIV-1 infection: correlation with HIV-1 RNA and the clinical outcome

AIDS ◽  
1996 ◽  
Vol 10 (13) ◽  
pp. F45-F50 ◽  
Author(s):  
Paolo G. Rizzardi ◽  
Wilma Barcellini ◽  
Giuseppe Tambussi ◽  
Flavia Lillo ◽  
Mauro Malnati ◽  
...  
Keyword(s):  
Clinical Outcome ◽  
Tumour Necrosis Factor ◽  
Plasma Levels ◽  
Tumour Necrosis ◽  
Tnf Receptors ◽  
Soluble Cd30 ◽  
Tnf Α ◽  
Hiv 1 ◽  
Necrosis Factor
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