5 hydroxytryptamine/necroză

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Overexpression of glyceraldehyde-3-phospahe dehydrogenase is not involved in 5-hydroxytryptamine (5-HT)-induced necrosis in cultured cerebrocortical neurons.

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Cerebrocortical cell cultures were prepared from 1-d-old rats. On post-culture day 6, 5-hydroxytryptamine (5-HT) was added to the medium and cells were exposed for another 3 d. 5-HT elicited cytotoxicity in a dose-dependent manner, and the survival rate of neuronal cells was decreased to 64.9+/-5.0%

The effect of lipopolysaccharide, interleukin-1 and tumour necrosis factor on the hepatic accumulation of 5-hydroxytryptamine and platelets in the mouse.

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1. Injection of lipopolysaccharide (LPS; 0.5-500 microgram kg-1) into mice induced a dose-dependent, slowly developing increase in hepatic content of 5-hydroxytryptamine (5-HT). This sustained increase could not be attributed to an LPS-induced alteration of the pharmacokinetic handling of 5-HT by

Interaction of 5-hydroxytryptamine and tumor necrosis factor-α to pain-related behavior by nucleus pulposus applied on the nerve root in rats.

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METHODS The effects of exogenous 5-hydroxytryptamine (5-HT), tumor necrosis factor(TNF)-α, 5-HT + TNF in combination, and autologous nucleus pulposus (NP) at dorsal root ganglion (DRG) were examined using rat models. OBJECTIVE To examine the interaction of 5-HT with TNF for pain-related behavior in

Serotonin 5-hydroxytryptamine(2A) receptor activation suppresses tumor necrosis factor-alpha-induced inflammation with extraordinary potency.

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The G protein-coupled serotonin 5-hydroxytryptamine (5-HT)(2A) receptor is primarily recognized for its role in brain neurotransmission, where it mediates a wide variety of functions, including certain aspects of cognition. However, there is significant expression of this receptor in peripheral

Production of renal cortical necrosis with serotonin (5-hydroxytryptamine); theoretical relationship to abruptio placentae.

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Loss of Anticontractile Effect of Perivascular Adipose Tissue on Pregnant Rats: A Potential Role of Tumor Necrosis Factor-α.

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The present investigation examined the effect of pregnancy on the anticontractile effect of perivascular adipose tissue (PVAT) on the rat. Ring segments of the aorta, with and without PVAT, were set up in organ baths for isometric tension recording. In both groups, concentration-response curves to

Mechanism of the inhibitory effect of melatonin on tumor necrosis factor production in vivo and in vitro.

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Melatonin is an antioxidant. Since other antioxidants inhibit the production of tumor necrosis factor (TNF) induced by lipopolysaccharide, we investigated its effect on TNF production in vivo and in vitro and on lethality associated with endotoxic shock. Administration of melatonin to mice (5 mg/kg,

Sarpogrelate hydrochloride, an antagonist of 5-hydroxytryptamine receptor, improves skin flap survival and suppresses thrombus formation in injured microvessels of rabbits.

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The authors carried out two studies to examine the effects of the 5-hydroxytryptamine receptor antagonist, sarpogrelate hydrochloride (SH), on flap necrosis. The first study measured survival rates and included histologic examination of random-pattern skin flaps in rabbits. The second study assessed

[Effects of electroacupuncture stimulation of "Neiguan" (PC 6) and "Shenmen" (HT7) on contents of 5-hydroxytryptamine in hypothalamic paraventricular nucleus region and serum in hyperlipidemia rats with acute myocardial infarction].

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OBJECTIVE To observe the effects of electroacupuncture (EA) stimulation of "Neiguan"(PC 6) and "Shenmen" (HT 7) on 5-hydroxytryptamine (5-HT) levels in the paraventricular nucleus (PVN) region of hypothalamus and serum in hyperlipidemia rats with acute myocardial infarction (AMI). METHODS A total of

Role of tumor necrosis factor-alpha in endotoxin-induced lung parenchymal hyporesponsiveness in mice.

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Although changes in airway responsiveness in pulmonary inflammation are commonly related to the action of infiltrated leukocytes, our previous report suggested a direct role of inflammatory cytokines in LPS-induced lung hyporesponsiveness. The aim of this study was to define if cytokines detected in

Tumor necrosis factor causes bronchial hyperresponsiveness in rats.

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We have previously reported that exposure of rats to aerosolized endotoxin (LPS) causes a transient, dose-dependent increase in bronchial responsiveness (BR) to 5 hydroxytryptamine (5HT), 90 min after exposure. In the present study we examined whether LPS induces the release of tumor necrosis factor

Translocation of platelets into Disse spaces and their entry into hepatocytes in response to lipopolysaccharides, interleukin-1 and tumour necrosis factor: the role of Kupffer cells.

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OBJECTIVE Injection into mice of a small dose of either a lipopolysaccharide or interleukin-1 induces a slowly developing accumulation of 5-hydroxytryptamine, predominantly in the liver. We have established that this 5-hydroxytryptamine accumulation is the result of the translocation of platelets to

Active translocation of platelets into sinusoidal and Disse spaces in the liver in response to lipopolysaccharides, interleukin-1 and tumor necrosis factor.

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1. Injection of lipopolysaccharides (LPS) or endotoxin into mice and rats induces a prolonged increase in serotonin (5-hydroxytryptamine: 5HT), predominantly in the liver. 2. The 5HT increase reflects the accumulation of platelets in the sinusoidal and perisinusoidal Disse spaces (spaces between

5-Hydroxytryptamine and thromboxane A2 in ischaemic heart disease.

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Platelet-derived 5-hydroxytryptamine and thromboxane A2 activate vascular smooth muscle cells, blood platelets and myocardial cells, both directly and through mutual amplification. Such an activation triggers: (1) vascular smooth muscle cell mitogenic activity, connective tissue synthetic activity

Induction of acute necrosis in Walker 256 tumors in rats.

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The destructive effect on cells of locally injected hypertonic solutions, resorption of which is delayed by some vasoactive agents, was observed in the skin and subcutis of the rat by Selye and his coworkers who described it as acute conditioned necrosis. The same phenomenon was demonstrated in

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