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Human recombinant platelet phospholipase A2 exacerbates poly-L-arginine induced rat paw edema.
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In this study by using the human recombinant non-pancreatic-secreted platelet PLA2 (r-hnps-PLA2) and rabbit polyclonal antibodies directed against either the human (group II) or the porcine enzyme (group I), we have shown a possible involvement of platelet PLA2 in poly-L-arginine (25 kDa)-induced
Alleviation of brain edema by L-arginine following experimental subarachnoid hemorrhage in a rat model.
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Decreased levels of nitric oxide play a role in the development of cerebral ischemia secondary to subarachnoid hemorrhage (SAH). The protective effect of L-arginine on brain edema following SAH was investigated in this study. Rats were divided randomly into a sham-operated, a SAH+saline group and a
Effect of electroacupuncture on arginine vasopressin-induced endolymphatic hydrops.
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[An experimental study of arginine vasopressin on acute ischemic brain edema in gerbils (1)].
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The purpose of this experiments is to study the role of arginine vasopressin (AVP) in acute ischemic brain edema of mongolian gerbils. The results showed that the contents of AVP in ischemic cortex, hypothalamus and striatum increased remarkably in 15-120 minutes after ischemia, while the contents
[Using NO-synthase inhibitors derived from L-arginine for preventing acute experimental lung edema development in mice].
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The preventive and curative action of NO-synthase inhibitors derived from L-arginine was investigated on the model of toxic lung edema induced by phosgene (LCt50 - 84) in mice. The most pronounced decrease in the phosgene-induced lung edema was observed for aminoguanidine, NG-nitro-L-arginine
NC1900, an arginine vasopressin analogue, fails to reduce brain edema and improve neurobehavioral deficits in an intracerebral hemorrhagic stroke mice model.
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OBJECTIVE
There is mounting evidence suggesting that arginine vasopressin via its V1a receptor interaction is involved in the regulation of the brain water channel, aquaporin-4 (AQP4). The role of AQP4 in brain edema resolution has been thoroughly investigated in knock-out animal studies, which
Arginine-Vasopressin Receptor Blocker Conivaptan Reduces Brain Edema and Blood-Brain Barrier Disruption after Experimental Stroke in Mice.
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BACKGROUND
Stroke is a major cause of morbidity and mortality. Stroke is complicated by brain edema and blood-brain barrier (BBB) disruption, and is often accompanied by increased release of arginine-vasopressin (AVP). AVP acts through V1a and V2 receptors to trigger hyponatremia, vasospasm, and
Blockade of nitric oxide formation by N omega-nitro-L-arginine mitigates ischemic brain edema and subsequent cerebral infarction in rats.
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In order to investigate whether or not nitric oxide (NO) formation underlies the cellular mechanisms of ischemic brain damage, we examined the effects of N omega-nitro-L-arginine (L-NNA), a NO synthase inhibitor, on ischemic brain edema and subsequent infarction in rats with middle cerebral artery
OPC-21268, an orally effective, nonpeptide arginine vasopressin V1 receptor antagonist reduces vasogenic brain edema.
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We examined the effect of orally administered OPC-21268, a nonpeptide Arginine Vasopressin V1 receptor antagonist, on cold induced vasogenic brain edema in rat. Cold brain injury was induced by applying a copper rode cooled with liquid nitrogen for one minute. To mimic clinical use, one hour after
Effect of arginine vasopressin on the cortex edema in the ischemic stroke of Mongolian gerbils.
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Brain edema formation is one of the most important mechanisms of ischemia-evoked cerebral edema. It has been demonstrated that arginine vasopressin (AVP) receptors are involved in the pathophysiology of secondary brain damage after focal cerebral ischemia. In a well-characterized animal model of
Arginine vasopressin-aquaporin-2 pathway-mediated dehydration effects of electroacupuncture in guinea pig model of AVP-induced endolymphatic hydrops.
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OBJECTIVE
To investigate the effects of electroacupuncture (EA) on endolymphatic hydrops (EH) and the regulation of arginine vasopressin (AVP)-aquaporin-2 (AQP2) pathway in guinea pigs.
METHODS
EH was induced in male guinea pigs by an intraperitoneal injection of AVP. For the treatment, EA was
Arginine-Restricted Therapy Resistant Bilateral Macular Edema Associated with Gyrate Atrophy.
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Introduction. Gyrate atrophy is a rare genetical metabolic disorder affecting vision. Here, we report a 9-year-old boy with gyrate atrophy associated with bilateral macular edema at the time of diagnosis and the effect of long term metabolic control on macular edema. Case Presentation. A 9-year-old
Cyclical edema in a patient with hypothalamic disorders and chronic glomerulonephritis: arginine vasopressin-dependent atrial natriuretic hormone release.
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A 28-year-old woman had hypothalamic disorders (amenorrhea, obesity, psychiatric abnormalities, polydipsia and fever) and chronic glomerulonephritis. She also suffered from general edema associated with cyclical oliguria and polyuria. Her body weight and plasma osmolality increased during the
Effect of dipyrone, L-NAME and L-arginine on endotoxin-induced rat paw edema.
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Paw edema was induced in male Wistar rats (200-250 g) by intraplantar (ipl) administration of 2.5 micrograms endotoxin (Etx). Etx, like carrageenin, produced two distinct edema formation phases, an early phase (75 min) followed by a late phase (7 h). We showed that the edema formation in the early
Mechanism of action of arginine vasopressin on acute ischemic brain edema.
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The purpose of this experiment is to study the role of arginine vasopressin (AVP) in acute cerebral ischemic edema in Mongolian gerbils. The results show that intracerebroventricular injection (ICV) of AVP exacerbates acute ischemic brain edema, while ICV of AVP antiserum significantly decreases the
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