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Page 1 de 1837 résultats
[Apoptosis and necrosis induced by cyclic mechanical stretching in alveolar type-II-cells--influence of captopril and L-Arginine].
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BACKGROUND
Alveolar type-II(ATII)-cells are exposed to mechanical stretch during breathing and mechanical ventilation. Increased stretch may contribute to lung injury.
METHODS
The influence of three stretching patterns (characterized by frequency [min (-1)] - increase in surface area [%]: S40 - 13,
Lipopolysaccharide and tumor necrosis factor stimulate lung microvascular arginine uptake, a response attenuated by dexamethasone.
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BACKGROUND
Lipopolysaccharide (LPS), tumor necrosis factor-alpha, (TNF), and glucocorticoids can modulate endothelial nitric oxide (NO) production. L-Arginine is the exclusive precursor for NO biosynthesis, suggesting that NO generation and arginine transport are intimately linked.
METHODS
To
The effect of single administration of vascular endothelial growth factor or L-arginine on necrosis and vasculature of the epigastric flap in the rat model.
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OBJECTIVE
Vascular endothelial growth factor (VEGF) and nitric oxide (NO) produce vasodilation, induce angiogenesis, and improve survival of surgical flaps. We used the rat epigastric skin flap to study the effect of a single intra-arterial dose of VEGF or L-arginine, a substrate for NO production,
Neutralization of gamma interferon and tumor necrosis factor alpha blocks in vivo synthesis of nitrogen oxides from L-arginine and protection against Francisella tularensis infection in Mycobacterium bovis BCG-treated mice.
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Peritoneal cells from Mycobacterium bovis BCG-infected C3H/HeN mice produced nitrite (NO2-, an oxidative end product of nitric oxide [NO] synthesis) and inhibited the growth of Francisella tularensis, a facultative intracellular bacterium. Both NO2- production and inhibition of bacterial growth were
In vivo evidence that arginine vasopressin is involved in the adrenocorticotropin response induced by interleukin-6 but not by tumor necrosis factor-alpha in the rat.
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We examined whether arginine vasopressin (AVP) is involved in the adrenocorticotropin (ACTH) response induced by interleukin (IL)-6 or tumor necrosis factor (TNF)-alpha in the rat. To accomplish this, we employed immunoneutralization of brain AVP by injecting anti-AVP antiserum
Time-dependent sensitization of corticotropin-releasing hormone, arginine vasopressin and c-fos immunoreactivity within the mouse brain in response to tumor necrosis factor-alpha.
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Stressor or cytokine treatments, such as interleukin-1beta, promote time-dependent alterations of hypothalamic-pituitary-adrenal functioning, including increased arginine vasopressin stores within corticotropin-releasing hormone (CRH) terminals in the external zone of the median eminence. Likewise,
Interferon-gamma and tumor necrosis factor induce the L-arginine-dependent cytotoxic effector mechanism in murine macrophages.
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We tested several monokines and muramyl dipeptide (MDP) to determine whether they induce the L-arginine-dependent effector mechanism in cultured murine macrophages. Recombinant interferon-gamma (rIFN-gamma) and recombinant tumor necrosis factor (rTNF) synergize to induce nitrite (NO2-) and nitrate
Protective effect of L-arginine against necrosis and apoptosis induced by experimental ischemic and reperfusion in rat liver.
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OBJECTIVE
To study the effect of L-arginine on apoptosis and necrosis induced by 1-h ischemia followed by 3-h reperfusion.
METHODS
Adult Wistar rats underwent 60 min of partial liver ischemia followed by 3-h reperfusion. Eighteen Wistar rats were divided into sham-operated control group (I) (n = 6),
L-arginine enhances nitrative stress and exacerbates tumor necrosis factor-alpha toxicity to human endothelial cells in culture: prevention by propofol.
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Supplementation of L-arginine, a nitric oxide precursor, during the late phase of myocardial ischemia/reperfusion increases myocyte apoptosis and exacerbates myocardial injury, but the underlying mechanism is unclear. During myocardial ischemia/reperfusion, apoptosis of endothelial cells precedes
Tumor necrosis factor alpha activates soluble guanylate cyclase in bovine glomerular mesangial cells via an L-arginine-dependent mechanism.
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Endothelium-derived nitric oxide (NO) causes vasodilatation by activating soluble guanylate cyclase, and glomerular mesangial cells respond to NO with elevations of intracellular guanosine 3',5'-cyclic monophosphate (cGMP). We explored whether mesangial cells can be stimulated to produce NO and
Oral L-arginine can reverse digital necrosis in Raynaud's phenomenon.
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Raynaud's phenomenon is characterized by transient reduction in blood supply through the small arteries in the hands and feet. Severe Raynaud's phenomenon can cause digital necrosis. It has been hypothesized that nitric oxide may have a role in Raynaud's phenomenon. We report two cases in which oral
Oral administration of L-arginine decreases necrosis of the epigastric skin flap in the rat.
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BACKGROUND
We investigated the effect of prolonged oral arginine administration on tissue necrosis and perfusion in the rat skin flap.
METHODS
Twenty-five Sprague-Dawley rats had an 8 x 8 - cm epigastric skin flap elevated and were divided in 2 groups, l-Arginine and Control, which respectively
Full-thickness skin necrosis after arginine extravasation--a case report and review of literature.
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The arginine test is highly useful in the evaluation of short-stature children and adolescents. Extravasation of arginine can cause full-thickness skin necrosis that requires serious surgical intervention with aesthetic and functional sequellea. The authors describe a case of distal forearm skin
NG-methyl-L-arginine inhibits tumor necrosis factor-induced hypotension: implications for the involvement of nitric oxide.
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Clinical assessment of the activity of tumor necrosis factor (TNF) against human cancer has been limited by a dose-dependent cardiovascular toxicity, most frequently hypotension. TNF is also thought to mediate the vascular collapse resulting from bacterial endotoxin. The present studies address the
Prophylactic high-dose N(omega)-monomethyl-L-arginine prevents the late cardiac dysfunction associated with lethal tumor necrosis factor-alpha challenge in dogs.
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We investigated nitric oxide (NO) as a possible cause of the cardiac dysfunction associated with high, lethal doses of tumor necrosis factor-alpha (TNF-alpha) in dogs. Eighty-seven awake, 2-year-old (10-12 kg), purpose-bred beagles were randomized to receive an infusion of saline or
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