prostaglandin/accident vascular cerebral

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Terutroban, a thromboxane/prostaglandin endoperoxide receptor antagonist, increases survival in stroke-prone rats by preventing systemic inflammation and endothelial dysfunction: comparison with aspirin and rosuvastatin.

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This study investigated the efficacy of terutroban, a specific thromboxane/prostaglandin endoperoxide receptor antagonist, on stroke incidence in spontaneously hypertensive stroke-prone rats (SHRSP). The effects of terutroban were compared with those of aspirin, another antiplatelet agent, and

Effect of acetylsalicylic acid on urinary excretion of prostaglandin E in stroke patients.

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In 12 of 76 stroke patients complicated by the syndrome of inappropriate secretion of antidiuretic hormone (SIADH), a significant increase in urinary prostaglandin E (PGE) (p less than 0.005), and a significant positive relationship between the plasma arginine vasopressin (AVR) level and urinary PGE

Effect of high potassium diets on the vascular and renal prostaglandin system in stroke-prone spontaneously hypertensive rats.

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High potassium (K) diets are known to have a protective effect on the endothelium and the kidney against hypertensive injury independent of blood pressure change. Vasodepressor prostaglandins (PGs) have been shown to be cytoprotective in various tissues. This study investigated the effect of high K

[Change in prostaglandin levels and ATPase activity of cardiac membrane fractions during the formation of cerebral hematomas in animals with a hereditary predisposition to stroke].

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The formation of subarachnoidal, intragastric, and intracerebral hepatomas provoked by stress in rats hereditarily predisposed to strokes was found to be accompanied by myocardial overstrain and changes in cardiac prostaglandin formations, as well as by a decrease in the activity of ion-transporting

Protective effect of cicletanine on hypertension-induced decreases in the renal kallikrein-kinin and prostaglandin systems in stroke-prone spontaneously hypertensive rats.

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We investigated the effect of two oral (p.o.) doses of cicletanine (5 and 30 mg/kg/day) for 4 weeks on urinary excretion (UKE), renal concentration (RKC) of kallikrein, and prostaglandin E2 (PGE2) and 6-keto-PGF1 alpha urinary excretion of stroke-prone (SP) spontaneously hypertensive rats (SHR) and

Cerebrospinal fluid prostaglandin F2 alpha in stroke patients: no relationship to the degree of neurological deficit.

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The concentration of prostaglandin F2 alpha (PGF2 alpha) was measured in cerebrospinal fluid (CSF) of 50 patients with recent stroke divided into three groups in respect to the time (up to 24 h) that expired between cerebrovascular insult and CSF sampling. 10 of the additionally studied persons were

Cryptogenic stroke in the setting of intravaginal prostaglandin therapy for elective abortion.

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Vaginal prostaglandin pessaries are considered safe and effective method of abortion within the first two trimesters of pregnancy. We present a case of a young woman, with no known risk factors for cerebrovascular events, who developed a cryptogenic stroke following administration of intravaginal

Prostaglandin E1-Mediated Collateral Recruitment Is Delayed in a Neonatal Rat Stroke Model.

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While arterial reflow after a stroke represents an important challenge for better outcomes, it is also very important that sudden recanalization does not produce local oxidative and nitrogen species, deleterious for the brain and more particularly the immature brain. Our objective was to determine

Altered growth response to prostaglandin E2 and its receptor signaling in mesangial cells from stroke-prone spontaneously hypertensive rats.

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OBJECTIVE Prostaglandin (PG) E2, a major arachidonic acid metabolite in the kidney, acts on four receptor subtypes (EP1, EP2, EP3 and EP4). One of major causes of end-stage renal failure is hypertensive renal disease, in which enhanced renal PGE2 production has been shown. In this study, to explore

Therapeutic effects of lipo-prostaglandin E1 on angiogenesis and neurogenesis after ischemic stroke in rats.

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Previous studies have demonstrated that prostaglandin E1 (PGE1) has a neuroprotective effect on cerebral ischemia. However, it remains unknown whether PGE1 promotes angiogenesis and neurogenesis after ischemic stroke. In this study, adult male Sprague-Dawley rats were subjected to permanently distal

Metabolic alterations in the endogenous formation of 6 keto-prostaglandin F1 alpha, thromboxane B2 and prostaglandin E2 in the brain-stem of stroke-resistant spontaneously hypertensive rats.

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Endogenous biosynthetic capacities for prostaglandin (PG)E2, thromboxane (TX)B2 (a stable degradation product of TXA2) and 6 keto-PGF1 alpha (a stable degradation product of PGI2) in the brain-stem fractions of stroke-resistant spontaneously hypertensive rats (SHRSR) and control Wistar-Kyoto rats

Measurement of prostaglandin E2 in cerebrospinal fluid in patients suffering from stroke.

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In 16 patients suffering from cerebrovascular events, prostaglandin (PG) E2 was measured in their cerebrospinal fluid and correlated with their clinical status and evolution. Prostaglandin E2 ranged from 200-3000 pg (picogram)/ml of cerebrospinal fluid. A positive correlation was found between PG E2

[The role of prostaglandin E2 in stroke-reperfusion injury].

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Although augmented prostaglandin E2 (PGE2) accumulation has been demonstrated at the lesion sites of rodent ischemia models, the role of postischemic PGE2 in neuronal survival has remained obscure. We recently identified the microsomal prostaglandin E synthase-1 (mPGES-1), an inducible terminal

The antiproteinuric action of enalapril in stroke-prone spontaneously hypertensive rats is unrelated to alterations in urinary prostaglandins.

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We examined whether the renal protective effect of the angiotensin I converting enzyme inhibitor enalapril in stroke-prone spontaneously hypertensive rats (SHRSP) is dose-related and associated with alterations in the urinary excretion of prostaglandin (PG) E2 and 6-keto-PGF1 alpha, a stable

Rosiglitazone and 15-deoxy-Delta12,14-prostaglandin J2 cause potent neuroprotection after experimental stroke through noncompletely overlapping mechanisms.

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Stroke triggers an inflammatory cascade which contributes to a delayed cerebral damage, thus implying that antiinflammatory strategies might be useful in the treatment of acute ischaemic stroke. Since two unrelated peroxisome proliferator-activated receptor-gamma (PPARgamma) agonists, the

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