The effect of ritanserin, a 5-HT2 receptor antagonist, on ischemic cerebral blood flow and infarct volume in rat middle cerebral artery occlusion

Kiyoshi Takagi, Myron Ginsberg, Mordecai Y T Globus, Raul Busto, W. Dalton Dietrich

Research output: Contribution to journalArticle

18 Citations (Scopus)

Abstract

Background and Purpose: In a previous study from our laboratory, ritanserin, a specific 5-HT2 serotonin receptor antagonist, reduced ischemic damage in the setting of transient global ischemia. In this study, we examined the effect of ritanserin on ischemic cerebral blood flow, systemic blood pressure, and infarct volume in the model of permanent focal ischemia with brain temperature controlled at 35.0°C to 36.0°C. Methods: Thirty- seven male Sprague-Dawley rats were used. The right middle cerebral artery was permanently occluded. Ritanserin (8 mg/kg) or vehicle was continuously administered intravenously for 90 minutes starting 10 minutes after middle cerebral artery occlusion. Cerebral blood flow was monitored by laser Doppler flowmetry in the ischemic cortex before and for 2 hours after arterial occlusion. Brains were perfusion-fixed 3 days later, and infarct volumes were measured. Results: Mean arterial blood pressure was not affected by treatment. In the vehicle and ritanserin groups, mean ischemic cerebral blood flow (percent of preischemic values) was 34.6 ± 14.7% (mean ± SD) and 26.6 ± 15.0%, respectively. Hemispheric infarct volumes were 119.3 ± 49.4 mm3 and 136.6 ± 49.6 mm3, respectively. No significant differences were recognized. Conclusions: Intravenous administration of ritanserin did not affect mean arterial blood pressure or cerebral blood flow in the ischemic region during the acute phase of ischemia. No protective effect of ritanserin was apparent in the setting of permanent focal ischemia when treatment was begun shortly after the onset of ischemia.

Original languageEnglish
Pages (from-to)481-486
Number of pages6
JournalStroke
Volume25
Issue number2
StatePublished - Feb 1 1994

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Cerebrovascular Circulation
Ritanserin
Serotonin 5-HT2 Receptor Antagonists
Middle Cerebral Artery Infarction
Arterial Pressure
Ischemia
Laser-Doppler Flowmetry
Middle Cerebral Artery
Brain Ischemia
Intravenous Administration
Sprague Dawley Rats
Perfusion
Blood Pressure
Temperature
Brain
Therapeutics

Keywords

  • cerebral ischemia, focal
  • rats
  • ritanserin
  • serotonin

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Neuroscience(all)

Cite this

The effect of ritanserin, a 5-HT2 receptor antagonist, on ischemic cerebral blood flow and infarct volume in rat middle cerebral artery occlusion. / Takagi, Kiyoshi; Ginsberg, Myron; Globus, Mordecai Y T; Busto, Raul; Dalton Dietrich, W.

In: Stroke, Vol. 25, No. 2, 01.02.1994, p. 481-486.

Research output: Contribution to journalArticle

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abstract = "Background and Purpose: In a previous study from our laboratory, ritanserin, a specific 5-HT2 serotonin receptor antagonist, reduced ischemic damage in the setting of transient global ischemia. In this study, we examined the effect of ritanserin on ischemic cerebral blood flow, systemic blood pressure, and infarct volume in the model of permanent focal ischemia with brain temperature controlled at 35.0°C to 36.0°C. Methods: Thirty- seven male Sprague-Dawley rats were used. The right middle cerebral artery was permanently occluded. Ritanserin (8 mg/kg) or vehicle was continuously administered intravenously for 90 minutes starting 10 minutes after middle cerebral artery occlusion. Cerebral blood flow was monitored by laser Doppler flowmetry in the ischemic cortex before and for 2 hours after arterial occlusion. Brains were perfusion-fixed 3 days later, and infarct volumes were measured. Results: Mean arterial blood pressure was not affected by treatment. In the vehicle and ritanserin groups, mean ischemic cerebral blood flow (percent of preischemic values) was 34.6 ± 14.7{\%} (mean ± SD) and 26.6 ± 15.0{\%}, respectively. Hemispheric infarct volumes were 119.3 ± 49.4 mm3 and 136.6 ± 49.6 mm3, respectively. No significant differences were recognized. Conclusions: Intravenous administration of ritanserin did not affect mean arterial blood pressure or cerebral blood flow in the ischemic region during the acute phase of ischemia. No protective effect of ritanserin was apparent in the setting of permanent focal ischemia when treatment was begun shortly after the onset of ischemia.",
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N2 - Background and Purpose: In a previous study from our laboratory, ritanserin, a specific 5-HT2 serotonin receptor antagonist, reduced ischemic damage in the setting of transient global ischemia. In this study, we examined the effect of ritanserin on ischemic cerebral blood flow, systemic blood pressure, and infarct volume in the model of permanent focal ischemia with brain temperature controlled at 35.0°C to 36.0°C. Methods: Thirty- seven male Sprague-Dawley rats were used. The right middle cerebral artery was permanently occluded. Ritanserin (8 mg/kg) or vehicle was continuously administered intravenously for 90 minutes starting 10 minutes after middle cerebral artery occlusion. Cerebral blood flow was monitored by laser Doppler flowmetry in the ischemic cortex before and for 2 hours after arterial occlusion. Brains were perfusion-fixed 3 days later, and infarct volumes were measured. Results: Mean arterial blood pressure was not affected by treatment. In the vehicle and ritanserin groups, mean ischemic cerebral blood flow (percent of preischemic values) was 34.6 ± 14.7% (mean ± SD) and 26.6 ± 15.0%, respectively. Hemispheric infarct volumes were 119.3 ± 49.4 mm3 and 136.6 ± 49.6 mm3, respectively. No significant differences were recognized. Conclusions: Intravenous administration of ritanserin did not affect mean arterial blood pressure or cerebral blood flow in the ischemic region during the acute phase of ischemia. No protective effect of ritanserin was apparent in the setting of permanent focal ischemia when treatment was begun shortly after the onset of ischemia.

AB - Background and Purpose: In a previous study from our laboratory, ritanserin, a specific 5-HT2 serotonin receptor antagonist, reduced ischemic damage in the setting of transient global ischemia. In this study, we examined the effect of ritanserin on ischemic cerebral blood flow, systemic blood pressure, and infarct volume in the model of permanent focal ischemia with brain temperature controlled at 35.0°C to 36.0°C. Methods: Thirty- seven male Sprague-Dawley rats were used. The right middle cerebral artery was permanently occluded. Ritanserin (8 mg/kg) or vehicle was continuously administered intravenously for 90 minutes starting 10 minutes after middle cerebral artery occlusion. Cerebral blood flow was monitored by laser Doppler flowmetry in the ischemic cortex before and for 2 hours after arterial occlusion. Brains were perfusion-fixed 3 days later, and infarct volumes were measured. Results: Mean arterial blood pressure was not affected by treatment. In the vehicle and ritanserin groups, mean ischemic cerebral blood flow (percent of preischemic values) was 34.6 ± 14.7% (mean ± SD) and 26.6 ± 15.0%, respectively. Hemispheric infarct volumes were 119.3 ± 49.4 mm3 and 136.6 ± 49.6 mm3, respectively. No significant differences were recognized. Conclusions: Intravenous administration of ritanserin did not affect mean arterial blood pressure or cerebral blood flow in the ischemic region during the acute phase of ischemia. No protective effect of ritanserin was apparent in the setting of permanent focal ischemia when treatment was begun shortly after the onset of ischemia.

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