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Showing 3 results for Vakili

Abedin Vakili, Toctam Sadough, Mahdi Zahedikhorasani,
Volume 11, Issue 1 (Spring 2007)
Abstract

Introduction: Several studies have indicated that late treatment of aminoguanidine (AG) reduces cerebral ischemic injuries in animal models. However, the effects of early treatment of AG on cerebral ischemic damage are not well understood. This study was designed to evaluate effect of early treatment of AG on cortex and striatum injuries as well as neurological dysfunctions in transient model of focal cerebral ischemia. Methods: Rats (n=30) were assigned to control or AG treated groups (75 or 150 mg/kg, i.p.,). Ischemia was induced by 60 min middle cerebral artery occlusion, followed by 24h reperfusion. Saline (control) or AG were administered at the onset of the ischemia. Twenty-four hours after the end of ischemia, neurological dysfunction scores were determined and then the infarct volumes of cortex and striatum were measured. Results: Administration of AG (75 and 150 mg/kg) at the beginning of ischemia, significantly reduced cortical and striatal infarct volumes by 47%, 69% and 42%, 36%, respectively (p<0.001). Moreover, AG only at dose 150 mg/kg significantly improves neurological dysfunction (p<0.01). Conclusion: Results of this study indicated that administration of AG in early phase of focal cerebral ischemia reduced cortical and striatal infarct volumes and improve neurological deficits in rat model of transient focal cerebral ischemia.
Abedin Vakili, Gholam Abbas Dehghani,
Volume 12, Issue 2 (Summer 2008)
Abstract

Introduction: Anesthetic agents, blood pressure, arterial pH and blood gases have found to influence on the pathophysiology of experimental stroke. Despite, there are very few comparative studies about effects of anesthetic agents in animal model of cerebral ischemia. Therefore, in this study, we investigated the effects of chloral hydrate and pentobarbital anesthesia, as comparative study, on infarct size and motor neurological dysfunctions and physiological parameters in a transient model of focal cerebral ischemia. Method: Twenty-four male Sprague-Dawley rats were divided into chloral hydrate (400 mg/kg ip, n=10) and pentobarbital sodium (60 mg/kg ip, n=14) anesthesia groups. Temporary focal cerebral ischemia was induced by 90 min middle cerebral artery occlusion (MCAO), followed by 23 h reperfusion. Physiologic parameters were measured before and after ischemia. Cortical, striatal infarct volumes and motor dysfunction were determined 24 h after MCAO. Results: Cortical and striatal infarct volume in pentobarbital sodium anesthetized rats were 84±8 and 26±2 mm3 that significantly lower from chloral hydrate group (208±10, 62±2 mm3 respectively, P<0.001). Moreover, neurological motor dysfunction significantly was lower in pentobarbital sodium anesthetized in comparison with chloral hydrate group (P<0.01). Physiologic values were similar between anesthetic groups except mean arterial pressure was significantly greater in the pentobarbital group in comparison with chloral hydrate group (P<0.05). Conclusion: Finding of this study indicated that brain injuries and motor neurological deficits in rat anesthetized with chloral hydrate are higher than from pentobarbital sodium groups in temporary model of focal cerebral ischemia. Thus, the effects of anesthetic agents must be considered in experimental cerebral ischemic studies.
Abedin Vakili, Somaye Mojarrad,
Volume 12, Issue 4 (Winter 2009)
Abstract

Pervious studies have shown that pentoxifylline (PTX) has beneficial effects in reduction of stroke and brain trauma injuries in experimental animals. However, there is very little and controversial information about the effect of PTX on brain edema in cerebral ischemia. Therefore, the aim of this study was to determine the effects of different doses of PTX on brain edema and neurological motor dysfunction in a rat model of transient focal cerebral ischemia. Methods: Transient focal cerebral ischemia was induced in Wistar rats by 60 min middle cerebral artery occlusion, followed by 23 h reperfusion. PTX was injected at doses of 15, 30 and 60 mg/kg ip at the beginning of ischemia. Twenty-four h after ischemia, neurological motor dysfunction and the percentage of brain water content (edema) were determined. Results: Administration of PTX at the dose of 60 mg/kg significantly reduced brain water content (P<0.001) and neurological motor dysfunction (P<0.01) in comparison with the control group, while 15 and 30 mg/kg of PTX had no significant effect on any of the parameters. Conclusion: The findings of this study indicate that PTX only at the dose of 60 mg/kg exerts anti-edematous effects and improves neurological motor dysfunction in the acute phase of transient focal cerebral ischemia in rat.

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