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

Abstract

(Bito, 1972a,b). Thus CSF, in contrast to plasma (Samuelsson, 1972), might be expected to contain measurable levels of PG. Several studies (White et al., 1971;Denton et al., 1972;Pelofsky et al., 1972;Yamamoto et al., 1972;Nakano et al., 1973;Greenberg et al., 1974;La Torre et al., 1974) have shown that some of them such as PG F2 alpha are potent vasoconstrictor agents on cerebral arteries, while PG of the E type are vasodilators. Cerebrovascular events are followed by the liberation of different vasoactive agents (Wurtman and Zervas, 1974;Lavyne et al., 1975). In our study we found a positive correlation between PG E2 levels in CSF and the severity of a stroke. Patients and methodsSixteen patients suffering from suspected cerebral vascular events were admitted to Ichilov Hospital at random for clinical investigation. The clinical characteristics of the patients and findings of the investigations are summarised in There were seven men and nine women. Eight patients suffered from hypertension, five from diabetes mellitus, three of these had both hypertension and diabetes. Two patients had a history of myocardial infarction.The investigations included clinical examination, laboratory examination with measurement of coagulation factors, ECG, chest and skull radiographs, EEG, and isotopic brain scan in the first week and one month from the event. Four vessels angiography was done in 13 patients. Lumbar puncture was performed during the first 72 hours after admission for routine studies and PG E2 determination. Cerebrospinal fluid without any extraction was used for determination of PGE concentration by radioimmunoassay (Bauminger et al., 1973). No drugs with known anti-PG activities were added to the treatment. The patients were treated only with Hartmann (Ringer lactate) solution and glucose 5%. Manitol and diuretics were used when necessary.The patients were classified into two groups: (a) mild to moderate cerebrovascular accidentpatients who suffered from paresis which improved during one month (five patients), and (b) moderate to severe cerebrovascular accident-patients who developed changes of consciousness and paralysis that did not improve enough during the first month (11 patients of whom five died).The patients were followed up after the cerebrovascular event for nine to 12 months.

Transporter-mediated Prostaglandin E2 Elimination across the Rat Blood-brain Barrier and Its Attenuation by the Activation of N-methyl-D-aspartate Receptors

“…3) On the other hand, the level of PGE 2 in the brain is reported to be increased in various CNS diseases such as neural inflammation, seizure, and Alzheimer's disease and, thus, the neural excitatory signals and neurotoxicity are induced by the excess PGE 2 in the brain. 2,4) Therefore, it is conceivable that PGE 2 in the brain is related to the pathogenesis and progression of neural excitation and toxicity in patients with CNS diseases.…”

Brain Prostaglandins E₂ and F_2α following Neonatal Asphyxia in the Guinea Pig

“…Several of the prostaglandins are potent vasoactive sub stances, capable of either dilating or con stricting vessels [4,6,8,15,20,21,25,26]. Levels of prostaglandins increase in the cere brospinal fluid following a variety of insults to the adult brain such as stroke, hemorrhage, and trauma [3,7,13], and it has been sug gested that the increased levels of vasocon strictor prostaglandins in the brain may lead to cerebral artery constriction, thereby re stricting blood flow and enhancing the extent of brain damage in these conditions.…”

Inhibitory effect of vicenin-2 and scolymoside on secretory group IIA phospholipase A2

“…Because the average weight of used mouse is 27 g, and the average blood volume is 2 mL, the amount of VCN and SCL (11.9 or 23.8 μg per mouse) injected yielded a maximum concentration of 10 or 20 μM in the peripheral blood. VCN and SCL suppress the activation of ERK1/2 and cPLA 2 α induced by LPS Lipid mediators such as prostaglandin E2 (PGE2) play a central role during vascular inflammatory processes and PGE2 is one of the central inflammatory markers and key mediators of inflammation induced by bacterial infection (Carasso et al 1977;Gao et al 2009). PGE2 is produced from phospholipids by a cascade of enzymatic reactions involving phospholipase A 2 (PLA 2 ) and sPLA 2 -IIA is the most abundant isoform of secreted PLA 2 (Six & Dennis 2000;Kudo & Murakami 2002).…”

“…The activation of vascular endothelial is triggered by pro-inflammatory cytokines (Mehta & Malik 2006) and the transcription and protein expression of sPLA 2 -IIA is highly regulated by the inflammatory cytokines including LPS in a variety of cells including macrophages (Alaoui-El-Azher et al 2002), fibroblasts (Kuwata et al 2007), endothelial cells (Flynn & Hoff 1995) and astrocytes (Oka & Arita 1991). Lipid mediators such as prostaglandin E2 (PGE2) are key players in vascular inflammatory processes, which are mediated by (Carasso et al 1977;Gao et al 2009). PGE2 is produced from phospholipids by a cascade of enzymatic reactions involving PLA 2 , and sPLA 2 -IIA is the most abundant isoform of sPLA 2 (Six & Dennis 2000;Kudo & Murakami 2002).…”