Effect of a prostacyclin derivative (OP-41483) and a hyperosmotic agent (glycerol) on brain edema and metabolism in cerebral ischemia.

Katayama, Yasuo; Kashiwagi, Fumihiko; Memezawa, Hajime; Terashi, Akiro

doi:10.1253/jcj.56.1239

Cited by 5 publications

(1 citation statement)

References 14 publications

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“…PGI 2 can also play an important role in brain edema in cerebral ischemia (Katayama et al, 1992). While changes in the brain water content can correlate with ischemic size, it is also well accepted that focal ischemia, particularly if it is followed by reperfusion, leads to damage of the blood-brain barrier and allows water and macromolecules to pass from the vessels into the tissue (Toung et al, 2002).…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective properties of prostaglandin I2 IP receptor in focal cerebral ischemia

et al. 2010

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We and others have identified that inhibition of cyclooxygenase might not be the optimal approach to limiting brain damage after stroke. Now we are investigating the unique properties of the various prostaglandin receptors to determine whether blocking those that mediate toxicity or stimulating those that reduce toxicity will improve neurological outcomes. Here, we determined the respective contribution of the prostaglandin I2 (PGI2) receptor in transient middle cerebral artery (MCA) occlusion (tMCAO) and permanent MCAO (pMCAO) preclinical stroke models by using male wildtype (WT) and IP receptor knockout (IP−/−) C57Bl/6 mice. In addition, we investigated the putative preventive and therapeutic effects of the IP receptor agonist beraprost. The infarct volumes and neurological deficit scores (NDS) were significantly greater in IP−/− than in WT mice after both tMCAO and pMCAO. Interestingly, beraprost pretreatment (50 or 100 μg/kg p.o.) 30 min before tMCAO and post-treatment (100 μg/kg p.o.) at 2 or 4.5 h of reperfusion significantly reduced the neurological deficit score and infarct volume in WT mice. Post-treatment with beraprost (100 μg/kg p.o.) 4.5 h after pMCAO also significantly decreased neurological deficits and infarct volume in WT mice. Together, these novel findings suggest for the first time that PGI2 IP receptor activation can attenuate anatomical and functional damage following ischemic stroke.

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Section: Discussionmentioning

confidence: 99%