adenosine-5--(n-ethylcarboxamide) has been researched along with Ischemic-Attack--Transient* in 2 studies
2 other study(ies) available for adenosine-5--(n-ethylcarboxamide) and Ischemic-Attack--Transient
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Neuroprotective effect of paeoniflorin on cerebral ischemic rat by activating adenosine A1 receptor in a manner different from its classical agonists.
The effects of paeoniflorin (PF), a compound isolated from Paeony radix, on neurological impairment and histologically measured infarction volume following transient and permanent focal ischemia were examined in Sprague-Dawley rats. In transient ischemia model, rats were subjected to a 1.5-h occlusion of the middle cerebral artery (MCA). The administration of PF (2.5 and 5 mg kg(-1), s.c.) produced a dose-dependent decrease in both neurological impairment and the histologically measured infarction volume. Similar results were also obtained when PF (2.5, 5, and 10 mg kg(-1), s.c.) was given in permanent ischemia model. The neuroprotective effect of PF (10 mg kg(-1), s.c.) was abolished by pretreatment of DPCPX (0.25 mg kg(-1), s.c.), a selective adenosine A1 receptor (A1R) antagonist. PF (10, 40, and 160 mg kg(-1), i.v.) had no effect on mean arterial pressure (MAP) and heart rates (HR) in the conscious rat. Additionally, PF (10(-3) mol l(-1)) had no effect on noradrenaline- (NA-) or high K+ concentration-induced contractions of isolated rabbit primary artery. In competitive binding experiments, PF did not compete with the binding of [3H]DPCPX, but displaced the binding of [3H]NECA to the membrane preparation of rat cerebral cortex. This binding manner was distinguished from the classical A1R agonists. The results demonstrated that activation of A1R might be involved in PF-induced neuroprotection in cerebral ischemia in rat. However, PF had no 'well-known' cardiovascular side effects of classical A1R agonists. The results suggest that PF might have the potential therapeutic value as an anti-stroke drug. Topics: Adenosine-5'-(N-ethylcarboxamide); Animals; Benzoates; Binding, Competitive; Bridged-Ring Compounds; Cerebral Cortex; Disease Models, Animal; Dose-Response Relationship, Drug; Glucosides; Infarction, Middle Cerebral Artery; Inhibitory Concentration 50; Ischemic Attack, Transient; Male; Monoterpenes; Neuroprotective Agents; Paeonia; Plant Roots; Rats; Rats, Sprague-Dawley; Receptor, Adenosine A1; Time Factors; Xanthines | 2005 |
Adenosine receptor agonists inhibit the release of gamma-aminobutyric acid (GABA) from the ischemic rat cerebral cortex.
The effects of CPA (a selective A1 receptor agonist), NECA (a mixed A1 and A2 receptor agonist), and CGS 21680 (a selective A2 receptor agonist) on the ischemia-evoked release of gamma-aminobutyric acid (GABA) from rat cerebral cortex was investigated with the cortical cup technique. Cerebral ischemia (20 min) was elicited by four vessel occlusion. In control animals, superfusate GABA increased from a basal level of 206 +/- 26 nM (mean +/- S.E.M., n = 18) to 10,748 +/- 3,876 nM during the reperfusion period. Pretreatment with adenosine receptor agonists failed to affect basal levels of GABA release. However, CPA (10(-10) M), NECA (10(-9) M), and CGS 21680 (10(-8) M) significantly suppressed the ischemia-evoked release of GABA. The ability to block the ischemia-evoked release of GABA was not evident when the adenosine receptor agonists were administered at higher concentrations. Thus, the selective activation of either A1 or high-affinity A2a adenosine receptors results in an inhibition of ischemia-evoked GABA release. Topics: Adenosine; Adenosine-5'-(N-ethylcarboxamide); Analysis of Variance; Animals; Cerebral Cortex; Dose-Response Relationship, Drug; Electroencephalography; gamma-Aminobutyric Acid; Ischemic Attack, Transient; Kinetics; Male; Phenethylamines; Rats; Rats, Inbred Strains; Receptors, Purinergic; Time Factors | 1992 |