vasoactive intestinal peptide/hemoragie

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The effect of vasoactive intestinal peptide (VIP) on superoxide dismutase and catalase activities in renal tissues of rats exposed to hemorrhagic ischemia-reperfusion.

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The effect of vasoactive intestinal peptide (VIP) on the activities of superoxide dismutase and catalase was investigated in renal tissues of rats exposed to 30% hemorrhage followed by reperfusion. In addition to enzyme activities, renal tissues were also histologically evaluated. Thirty percent

Mast cell degranulation in hemorrhagic shock in rats and the effects of vasoactive intestinal peptide, aprotinin and H1 and H2-receptor blockers on degranulation.

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Various stressful stimuli cause mast cell degranulation. Hemorrhagic shock is one such stressful stimulus which may cause mast cell degranulation and histamine release. Histamine may be involved in the pathophysiology of hemorrhage. It was reported that there are large amounts of histamine in the

The effect of vasoactive intestinal peptide (VIP) and naloxone combination on survival rates in rats exposed to severe hemorrhage.

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In this experiment, the effects of different doses of vasoactive intestinal peptide (VIP) and naloxone (NLX) combinations on survival rates were investigated in rats exposed to 40% hemorrhage. A combination of 25 ng.kg-1 VIP+5 mg.kg-1 NLX showed the best results on survival. The important prospect

Effect of vasoactive intestinal peptide and naloxone combination on urinary N-acetyl-beta-D-glucosaminidase level and kidney histology of rats exposed to severe hemorrhage.

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Renal hypoperfusion which occurs in hemorrhagic shock creates an environment in which cellular injury and organ dysfunction can occur during the episode of shock as well as reoxygenation and reperfusion. At the same time, mast cell degranulation which is observed during hemorrhage may have an

Neuropeptide Y and vasoactive intestinal peptide in experimental subarachnoid hemorrhage: immunocytochemistry, radioimmunoassay and pharmacology.

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The involvement of noradrenaline (NA), neuropeptide Y, (NPY), 5-hydroxytryptamine (5-HT), acetylcholine (ACh) and vasoactive intestinal polypeptide (VIP) has been examined in the late phase of spasm after an experimental subarachnoid hemorrhage (SAH) in a rat model. Immunocytochemistry and

The effect of vasoactive intestinal peptide (VIP) and inhibition of nitric oxide on renal tissue injury of rats exposed to hemorrhagic ischemia and retransfusion: a possible interaction mechanism among mast cells and tissue histamine.

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Perivascular neuropeptides (NPY, VIP, CGRP and SP) in human brain vessels after subarachnoid haemorrhage.

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INTRODUCTION--Cerebral blood vessels are innervated by sympathetic nerve fibres storing neuropeptide Y (NPY), parasympathetic nerves storing acetylcholine, vasoactive intestinal peptide (VIP) and sensory afferent fibres containing calcitonin gene-related peptide (CGRP), substance P (SP) and

Evidence that noradrenergic activity does not mediate the inhibition of luteinizing hormone secretion caused by vasoactive intestinal peptide.

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We have recently shown that intracerebroventricular (i.c.v.) infusion of vasoactive intestinal peptide (VIP) in ovariectomized (OVX) rats causes a pronounced inhibition of pulsatile luteinizing hormone (LH) secretion. Since there is increasing evidence for an interaction between VIP- and

Chronic parasympathetic sectioning decreases regional cerebral blood flow during hemorrhagic hypotension and increases infarct size after middle cerebral artery occlusion in spontaneously hypertensive rats.

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Regional cerebral blood flow (rCBF) during controlled hemorrhagic hypotension (140-20 mm Hg) was assessed 10-14 days after chronic unilateral sectioning of parasympathetic and/or sensory fibers innervating pial vessels in spontaneously hypertensive rats (SHR). rCBF was measured in the cortical

Alterations in perivascular dilatory neuropeptides (CGRP, SP, VIP) in the external jugular vein and in the cerebrospinal fluid following subarachnoid haemorrhage in man.

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A possible involvement of perivascular vasodilatory neuropeptides in subarachnoid haemorrhage (SAH) has been evaluated in man by measuring the levels of calcitonin gene related peptide (CGRP)-, substance P (SP)- and vasoactive intestinal peptide (VIP)-like immunoreactivity (LI) in the cranial venous

Vasoactive intestinal peptide in cerebrospinal fluid.

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Immunoreactive vasoactive intestinal peptide (VIP) was measured in lumbar and ventricular cerebrospinal fluid (CSF) from patients with various neurological disorders and in 2 hour aliquots of cisternal fluid removed continuously from rhesus monkeys. Although most of the VIP in concentrated pools of

Vasoactive intestinal peptide in the regulation of renin secretion.

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We have previously shown that vasoactive intestinal peptide (VIP) is a renin-stimulating factor both in vivo and in vitro. In the present investigation we sought to determine whether VIP exerted this effect by a neural or humoral mechanism. To test for a neural effect, the renal nerves were

[Effects of vasoactive intestinal peptide on Toll-like receptor (TLR) 2 mRNA and TLR4 mRNA expression on acute lung injury induced by lipopolysaccharide in rat].

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OBJECTIVE Vasoactive intestinal peptide (VIP) is a neuro-peptide that can modulate immunity. Previous studies indicated that VIP can attenuate the deleterious consequences of severe sepsis and septic shock by regulating production of inflammatory cytokines in immune activated cells. The signaling

Hepatic inactivation of vasoactive intestinal peptide in man and dog.

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IN AN EFFORT TO DOCUMENT THE ROLE OF THE LIVER IN THE CATABOLISM OF VASOACTIVE INTESTINAL PEPTIDE, SEVERAL DIFFERENT TYPES OF EXPERIMENTS WERE CARRIED OUT, INCLUDING: 1) simultaneous measurement of portal and systemic immunoreactive vasoactive intestinal peptide, both in the basal state and

[Protective effects of vasoactive intestinal peptide on intestinal lesions induced by endotoxic shock in rat].

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OBJECTIVE Vasoactive intestinal peptide (VIP) is a neuro-peptide that can modulate immunity in several aspects. Previous reports showed that VIP attenuates the deleterious consequences of severe infection and septic shock by regulating production of inflammatory cytokines in immune activated cells.

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