Serotonin release into plasma during common carotid artery thrombosis in rats.

Background and PurposeIn a previous study from our laboratory, ritanserin, a specific 5-HT 2 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.

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“…We interpret these negative 69 have recently demonstrated a 5-fold increase in plasma serotonin levels after common carotid artery thrombosis.…”

Section: Discussionsupporting

confidence: 55%

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

Takagi

Ginsberg

Globus

et al. 1994

Stroke

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“…The two latter sources of increased serotonin may be of particular importance in the setting of acute thrombus formation by activated platelets, which has been recently demonstrated to be associated with release of serotonin into the plasma. 33 The rapid decrease of dialysate serotonin levels during reperfusion is consistent with reinstatement of active reuptake mechanisms on termination of the ischemic insult and with clearance of serotonin into the cerebrospinal fluid and systemic circulation. The mechanisms underlying the marked decreases in extracellular 5-HIAA during ischemia are also not clearly understood.…”

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confidence: 59%

Ischemia-induced extracellular release of serotonin plays a role in CA1 neuronal cell death in rats.

Globus

Wester

Busto

et al. 1992

Stroke

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Background and Purpose: Serotonin, via 5-HT 2 receptors, exerts an excitatory effect on CA1 neurons and may play a role in ischemia-induced excitotoxic damage. To evaluate the role of serotonin in ischemia, both neurochemical and histopathological studies were performed.Methods: Neurochemical studies included rats that were subjected to 12.5 or 20 minutes of normothermic ischemia by two-vessel occlusion plus hypotension, and extracellular serotonin levels were measured in the hippocampus (12.5 minutes' ischemia, n=5) or striatum (20 minutes' ischemia, n = 13) by microdialysis. In the histopathological study the effect of 8 mg/kg ritanserin, a 5-HT 2 antagonist, administered continuously from 30 minutes prior to ischemia until 1 hour of recirculation was evaluated in five rats subjected to 10 minutes of ischemia. After 3 days, the numbers of normal-appearing neurons in the CA1 subregions were counted.Results: Ischemia of 12.5 minutes' duration induced a fourfold increase in serotonin in the hippocampus (mean±SEM baseline, 1.86±0.25 pmol/ml perfusate; during ischemia, 8.14±0.89 pmol/ml; p<0.05 by analysis of variance). Twenty minutes of ischemia induced a 25-fold increase in serotonin in the dorsolateral striatum (baseline, 0.98±0.15 pmol/ml; ischemia, 24.4±5.93 pmol/ml; p<0.001). The histopathological study demonstrated severe ischemic damage in all CA1 subregions of nontreated animals (medial, 34±16 normal-appearing neurons, middle, 52.2±22.9 neurons; lateral, 56.6+21.8 neurons). Treatment with ritanserin significantly attenuated ischemic damage (medial, 117.6±6.5 neurons; middle, 131.4±4.9 neurons; lateral, 130±7.5 neurons; p<0.01 different from nontreated).Conclusions: Taken together, these results suggest that serotonin plays a detrimental role, mediated by 5-HT, receptors, in the development of ischemic damage. (Stroke 1992(Stroke ,23:1595(Stroke -1601 KEY WORDS • cerebral ischemia • ritanserin • serotonin • rats

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“…20 Pathological phenomena unique to thrombotic stroke have been observed: thrombogenically activated blood leads to the formation of blood-borne factors, which causes detrimental effects on blood-brain barrier and on ische- mic brain. [21][22][23] Therefore, this photochemically induced MCA occlusion model would facilitate greater understanding of the pathophysiology of thrombotic stroke. The mechanisms of ultraviolet laser induced-vascular dilatation are attributed to rapidly expanding vapor bubble formed intraluminally in smooth muscle at high energy density 24 or photolytic release of nitric oxide at low energy density.…”

Section: Yao Et Al Thrombotic Stroke and Reperfusion Model 2719mentioning

confidence: 99%

Photothrombotic Middle Cerebral Artery Occlusion and Reperfusion Laser System in Spontaneously Hypertensive Rats

Yao

Sugimori

Fukuda

et al. 2003

Stroke

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Background and Purpose-To establish a less invasive and reproducible focal ischemia model in the rat, we adopted a 2-laser system (ie, photothrombosis and YAG laser-induced reperfusion). Methods-The distal middle cerebral artery (MCA) of spontaneously hypertensive rats was occluded by 568-nm krypton laser and intravenous infusion of the photosensitizing dye rose bengal and was recanalized by 355-nm ultraviolet laser irradiation. Cerebral blood flow was determined by laser-Doppler flowmetry at the penumbral cortex. Infarct volume was determined at 3 days after distal MCA occlusion. Results-Brain temperature determined with infrared thermography was maintained within an acceptable range of approximately 1°C upper shift of the center of brain temperature distribution during krypton or YAG laser irradiation. The average of the values (23 experiments; nϭ163) of coefficient of variation of infarct volume was 21Ϯ6%, indicating high reproducibility of this model. After distal MCA occlusion, cerebral blood flow was decreased to 32Ϯ16% of the control values and was increased to 98Ϯ21% after YAG laser-induced reperfusion. Infarct volume in these rats was 61Ϯ18 mm 3 (coefficient of variationϭ30%; nϭ6). Conclusions-We have characterized a highly reproducible focal ischemia model utilizing a 2-laser system, one to induce thrombotic MCA occlusion and the other to facilitate reperfusion.

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Serotonin release into plasma during common carotid artery thrombosis in rats.

Cited by 41 publications

References 43 publications

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

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

Ischemia-induced extracellular release of serotonin plays a role in CA1 neuronal cell death in rats.

Photothrombotic Middle Cerebral Artery Occlusion and Reperfusion Laser System in Spontaneously Hypertensive Rats

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