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Protective action of capsaicin and chilli on haemorrhagic shock-induced gastric mucosal injury in the rat.
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Chilli and its pungent ingredient, capsaicin, have been shown to protect against experimental gastric mucosal injury induced by various necrotizing agents such as ethanol and aspirin and stress. We investigated the effect of capsaicin and long-term ingestion of chilli on haemorrhagic shock-induced
[Surfactant and water balance of lung in intracerebral hemorrhage at conditions of capsaicin blockade of vagus nerve].
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It is known that intracranial hemorrhage (ICH) is accompanied by the development of neurogenic pulmonary edema and insufficiency of surfactant function. The present study was undertaken for evaluation of the role of vagal afferents in the mechanisms of ICH effects on pulmonary surfactant and water
Capsaicin prevents the adrenocorticotropin-induced improvement of cardiovascular function and survival in hemorrhage-shocked rats.
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A volume-controlled hemorrhagic shock was produced in anesthetized rats by intermittent bleeding from an iliac vein over a period of 20-30 min, until the carotid mean arterial pressure (MAP) stabilized around 20-24 mmHg. In this condition, which caused the death of all saline-treated animals within
Prevention of cerebral vasospasm by a capsaicin derivative, glyceryl nonivamide, in an experimental model of subarachnoid hemorrhage.
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BACKGROUND
Cerebral vasospasm after aneurysmal subarachnoid hemorrhage (SAH) remains a major complication in patients suffering from SAH. In our previous study, we reported that stimulating vascular K(+) channel activity prevented the development of cerebral vasospasm. Recent evidence indicates that
Intragastric capsaicin protects against aspirin-induced lesion formation and bleeding in the rat gastric mucosa.
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Previous work has indicated that capsaicin-sensitive afferent neurons are involved in gastric mucosal defense mechanisms. The present study investigated whether stimulation of these neurons by intragastric administration of capsaicin would protect against aspirin-induced mucosal damage in the
Capsaicin-like effect of resiniferatoxin in the rat stomach.
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Neurochemical and functional studies were performed to investigate and to compare the effects of resiniferatoxin and capsaicin in the rat stomach. Neonatal administration of resiniferatoxin (0.6-1.6 mumol/kg subcutaneously (s.c.)) produced a marked decrease in gastric calcitonin gene-related
Sympathoadrenal system in neuroendocrine control of glucose: mechanisms involved in the liver, pancreas, and adrenal gland under hemorrhagic and hypoglycemic stress.
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Glucose homeostasis is maintained by complex neuroendocrine control mechanisms, involving three peripheral organs: the liver, pancreas, and adrenal gland, all of which are under control of the autonomic nervous system. During the past decade, abundant results from various studies on neuroendocrine
Capsaicin protects against ethanol-induced oxidative injury in the gastric mucosa of rats.
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In this study, we investigated the protective effects of capsaicin on gastric mucosal oxidative damage induced by ethanol. Sprague Dawley rats intragastrically received 0.5-10 mg/kg, BW capsaicin or vehicle; 30 min later gastric lesions were induced by intragastric administration of absolute
The indomethacin-induced gastric mucosal damage in rats. Effect of gastric acid, acid inhibition, capsaicin-type agents and prostacyclin.
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In pylorus-ligated rats subcutaneous (s.c.) pentagastrin (325.5 nmol/kg) or histamine (54.3 mumol/kg), but not the cholinergic agent bethanechol (7.6 or 15.2 mumol/kg), increased gastric mucosal injury by s.c. indomethacin (55.8 mumol/kg). Intragastric (i.g.) administration of 0.15 or 0.3 N HCl
Protective effect of lafutidine, a novel H2-receptor antagonist, on reflux esophagitis in rats through capsaicin-sensitive afferent neurons.
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We examined the effect of lafutidine, a novel histamine H(2)-receptor antagonist, on acid reflux esophagitis in rats in relation to capsaicin-sensitive afferent neurons. The esophagitis was induced in rats by ligating both the pylorus and forestomach for 4 h. Lafutidine (1 - 30 mg/kg) and cimetidine
Vascular pathology of large cerebral arteries in experimental subarachnoid hemorrhage: Vasoconstriction, functional CGRP depletion and maintained CGRP sensitivity.
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Subarachnoid hemorrhage (SAH) is associated with increased cerebral artery sensitivity to vasoconstrictors and release of the perivascular sensory vasodilator CGRP. In the current study the constrictive phenotype and the vasodilatory effects of exogenous and endogenous perivascular CGRP were
Effect of lafutidine, a novel histamine H2-receptor antagonist, on monochloramine-induced gastric lesions in rats: role of capsaicin-sensitive sensory neurons.
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BACKGROUND
Lafutidine ((+/-)-2-(furfurylsulfinyl)-N-(4-(4-(piperidinomethyl)-2-pyr idyl)oxy-(Z)-2-butenyl)acetamide) is a novel histamine H2-receptor antagonist and has been shown to exhibit a potent gastroprotective activity in addition to its antisecretory action. In the present study, we examined
Local haemorrhage induced by Bothrops jararaca venom: relationship to neurogenic inflammation.
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We investigated morphological alterations induced by s.c. injection of 2.5 microg of Bothrops jararaca venom in rats. Intense disorganisation of collagen fibres was observed 1 min after the venom injection, particularly at regions near vessels and nerves. Mast cells were degranulated, and
An investigation into the mechanism of capsaicin-induced oedema in rabbit skin.
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1. Oedema formation induced by intradermal capsaicin has been studied in rabbit skin. The effect of the anti-inflammatory steroid dexamethasone and also of a range of known inhibitors of oedema formation have been investigated in order to elucidate mechanisms involved in capsaicin-induced oedema
Stimulation of afferent nerve endings by intragastric capsaicin protects against ethanol-induced damage of gastric mucosa.
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Ablation of capsaicin-sensitive afferent neurons enhances experimentally induced ulceration in the rat gastric mucosa, which suggests that these neurons are involved in gastric mucosal protection. To provide direct evidence for such a function it was investigated whether stimulation of afferent
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