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arachidonic acid/кровотечение
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The role of the central arachidonic acid-thromboxane A2 cascade in cardiovascular regulation during hemorrhagic shock in rats.
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The aim of the current study was to elucidate the underlying central mechanism(s) of the cardiovascular effects evoked by centrally injected melittin and arachidonic acid (AA) in hemorrhaged hypotensive condition, specifically, from central AA release from the cell membrane under the influence of
A study on cisternal CSF levels of arachidonic acid metabolites after aneurysmal subarachnoid hemorrhage.
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Arachidonic acid (AA) metabolites may play an important role in the pathogenesis of cerebral vasospasm which complicate subarachnoid hemorrhage. Authors have studied levels of 4 major AA metabolites in lumbar CSF samples and in CSF collected from perianeurismatic cisterns of 40 patients admitted
Influence of blood volume on cerebrospinal fluid levels of arachidonic acid metabolites after subarachnoid hemorrhage: experimental study on the pathogenesis of cerebral vasospasm.
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Based on accumulating data indicating the important role of arachidonic acid metabolites in the pathogenesis of cerebral vasospasm, we examined the influence of alterations in blood volume on the cerebrospinal fluid (CSF) level of the subarachnoid hemorrhage (SAH). Three separate injections of
Treatment of hemorrhagic stroke with arachidonic acid.
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Eighty-seven year old man, previously healthy, active and independent, was admitted to a hospital unconscious with hemorrhagic stroke. Treatment with arachidonic acid was initiated two weeks after his admission. After one year, despite his age, large hemorrhagic area and a history of ischemic heart
The effects of low-fat diets rich in arachidonic acid on the composition of plasma fatty acids and bleeding time in Australian aborigines.
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In the present study we measured the bleeding times in fourteen Aborigines (10 diabetic, 4 non-diabetic) before and after 2 weeks on a diet of tropical seafood (rich in both arachidonic acid and the omega 3 PUFA), followed by 3 weeks on a diet in which kangaroo and freshwater fish (linoleic and
The relationship between menstrual blood loss and prostaglandin production in the human: evidence for increased availability of arachidonic acid in women suffering from menorrhagia.
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In this study we have obtained endometrium and myometrium from women whose menstrual blood loss had been measured objectively. Samples of tissue were snap frozen in liquid nitrogen for the estimation of PG content and tissue was homogenized and incubated with and without added arachidonic acid. PGE,
Arachidonic acid metabolism following aneurysm rupture. Evaluation of cerebrospinal fluid and serum concentration of 6-keto-prostaglandin F1 alpha and thromboxane B2 in patients with subarachnoid hemorrhage.
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Experimental investigations have suggested an important role of arachidonic acid metabolites in the genesis of cerebral vasospasm following subarachnoid hemorrhage. In this clinical study the cerebrospinal fluid (CSF) and serum levels of the two main arachidonic acid metabolites prostacyclin and
Arachidonic acid metabolism and pathophysiologic aspects of subarachnoid hemorrhage in rats.
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We studied the ex vivo production of prostaglandin D2, prostaglandin E2, 6-ketoprostaglandin F1 alpha, and leukotriene C4 in the brain tissue of rats subjected to experimental subarachnoid hemorrhage. The ex vivo method allows the study of arachidonic acid metabolites released from brain slices at
Beneficial effect of arachidonic acid during hemorrhagic shock in the dog.
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Arachidonic acid (AA), precursor of the bisenoic prostaglandins was infused at a rate of 120 mug/kg per min into the vena cava of dogs subjected to hemorrhagic shock to assess the effects of stimulation of the prostaglandin (PG) synthetase system on the shock state. Hemorrhagic shock was induced by
Cardiovascular effects of centrally administered arachidonic acid in haemorrhage-induced hypotensive rats: investigation of a peripheral mechanism.
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1. The aims of the present study were to determine the cardiovascular effects of arachidonic acid (AA) and to investigate the peripheral mechanisms mediating these effects in haemorrhage-induced hypotensive rats. 2. Acute haemorrhage was induced by withdrawing a total volume of 2.2 mL blood/100 g
Influence of experimental subarachnoid hemorrhage on nicotine-induced contraction of the rat basilar artery in relation to arachidonic acid metabolites signaling pathway.
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BACKGROUND
Smoking is one of the most important risk factors for cerebral circulatory disorders. The purpose of this study was to investigate the influence of experimental subarachnoid hemorrhage (SAH) on nicotine-induced contraction (arachidonic acid metabolites) in the basilar arteries of
Effect of nimodipine on arachidonic acid metabolites after subarachnoid hemorrhage.
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Arachidonic acid metabolites are under investigation as possible vasoactive agents involved in the pathogenesis of cerebral vasospasm after subarachnoid hemorrhage. Prostaglandins, as well as other vasoactive compounds, activate contractile proteins through utilization of extracellular bound Ca++ to
Arachidonic acid causes hidden blood loss-like red blood cell damage through oxidative stress reactions.
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BACKGROUND
Hidden blood loss (HBL) often occurs in the prosthetic replacement for joint, but the mechanism is still not clear.
METHODS
This study tried to establish an animal model of HBL by injecting arachidonic acid (AA) into the Sprague-Dawley rats. Different concentrations of AA were injected
Traumatic brain injury causes platelet adenosine diphosphate and arachidonic acid receptor inhibition independent of hemorrhagic shock in humans and rats.
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BACKGROUND
Coagulopathy in traumatic brain injury (CTBI) is a well-established phenomenon, but its mechanism is poorly understood. Various studies implicate protein C activation related to the global insult of hemorrhagic shock or brain tissue factor release with resultant platelet dysfunction and
Activation of peroxisome proliferator-activated receptor-γ by a 12/15-lipoxygenase product of arachidonic acid: a possible neuroprotective effect in the brain after experimental intracerebral hemorrhage.
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OBJECTIVE In this study, the authors investigated the involvement of 15( S)-hydroxyeicosatetraenoic acid (15(S)-HETE) in the regulation of peroxisome proliferator-activated receptor-γ (PPARγ) after intracerebral hemorrhage (ICH) and its effects on hemorrhage-induced inflammatory response and
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