cinanserin and Ischemic-Attack--Transient

cinanserin has been researched along with Ischemic-Attack--Transient* in 2 studies

Other Studies

2 other study(ies) available for cinanserin and Ischemic-Attack--Transient

ArticleYear
Blockade of 5-HT2 receptors protects against impairment of working memory following transient forebrain ischemia in the rat.
    Neuroscience letters, 1991, Aug-19, Volume: 129, Issue:2

    The effects of the 5-HT2 receptor antagonists pirenperone, cinanserin and ritanserin on impairment of working memory in an animal model of cerebral ischemia were investigated, using a three-panel runway task. A 5-min period of ischemia caused a significant increase in the number of errors (attempts to pass through two incorrect panels of the 3 panel gates at 4 choice points). Pirenperone at 0.32 and 1.0 mg/kg, cinanserin 10 mg/kg and ritanserin 3.2 mg/kg administered i.p. immediately after blood flow reperfusion significantly reduced the increase in errors expected to occur 24 h after the 5 min of ischemia. These results suggest that the blockade of 5-HT2 receptors prevents the impairment of working memory following transient forebrain ischemia.

    Topics: Animals; Cinanserin; Ischemic Attack, Transient; Male; Memory; Piperidines; Rats; Rats, Inbred Strains; Ritanserin; Serotonin Antagonists

1991
Mechanism of cerebral arterial contraction induced by blood constituents.
    Journal of neurosurgery, 1980, Volume: 53, Issue:3

    In helically cut stips of cerebral, coronary, mesenteric, and renal arteries from dogs, a test solution containing hemoglobin (Hb) and soluble constituents, obtained by exposure of blood clot to distilled water, produced a dose-related contraction. The contraction of cerebral arteries was greater than that of the other arteries. Methemoglobin (metHb) caused only a slight contraction. The contractile response of cerebral arteries to the Hb-containing test solution was attenuated by aspirin (10(-5) to 2 X 10(-4) M), polypholretin phosphate (PPP, 3 X 10(-5) gm/ml), a prostaglandin (PG) antagonist, and cinanserin (10(-7) M), a serotonin antagonist. Combined treatment with these antagonists suppressed the response to the test solution, but only slightly attenuated contractions induced by K+. Phentolamine was ineffective. Contractions of measenteric arterial strips induced by the test solution were potentiated by aspirin, but were attenuated by PPP and cinanserin. Serum also produced contractions of cerebral and mesenteric arteries, which were attenuated by treatment with cinanserin or PPP. Contractile responses to Hb-containing solution and serum obtained from dogs pretreated with reserpine were weaker than those to the solutions obtained from control dogs. It may be concluded that the Hb-containing test solution releases vasoconstricting PG's from the cerebral arterial wall but vasodilating PG's from mesenteric arteries. The test solution appears to contain vasconstricting PG's and serotonin. Serum-induced contractions appear to be mediated mainly by serotonin.

    Topics: Animals; Aspirin; Cerebrovascular Circulation; Cinanserin; Dogs; Female; Hemoglobins; Ischemic Attack, Transient; Male; Phentolamine; Polyphloretin Phosphate; Prostaglandins; Serotonin; Subarachnoid Hemorrhage; Vasoconstriction

1980