Transient Bilateral Common Carotid Occlusion Research Articles

Vanillic acid attenuates cerebral hyperemia, blood-brain barrier disruption and anxiety-like behaviors in rats following transient bilateral common carotid occlusion and reperfusion.

Transient bilateral common carotid artery occlusion (tBCCAO), followed by reperfusion, is a model of transient global hypoperfusion. In the present study we aimed to investigate the probable effects of Vanillic acid (VA) on some physiological parameters including cerebral hyperemia, blood-brain barrier (BBB) disruption, anxiety behaviors and neurological deficits induced by bilateral occlusion of the common carotid arteries and reperfusion (BCCAO/R) in rats. Rats were randomly divided into four groups; Sham, BCCAO/R, VA and VA+ BCCAO/R. Chronic cerebral hypoperfusion was induced after 2weeks of pretreatment by VA. Subsequently, sensorimotor scores, elevated plus maze tests, cerebral hyperemia, and BBB disruption were evaluated 72h after 30min of BCCAO. Pretreatment of rats by VA improved sensory motor signs, anxiolytic behavior in BCCAO/R rats compared with untreated rats (p < 0.05). Further, VA attenuated reactive hyperemia and BBB disruption in BCCAO/R rats compared with untreated rats (p < 0.01). To our knowledge, this study is the first to reveal VA could attenuate reactive hyperemia and improve BBB disruption following BCCAO/R, and could improve neurological scores and anxiety like behaviors in this model of cerebral hypoperfusion. These results suggest that VA could be a promising pretreatment agent in cerebral hypoperfusion.

Vanillic acid attenuates effects of transient bilateral common carotid occlusion and reperfusion in rats

Cerebral hypoperfusion induced by transient bilateral common carotid arteries occlusion (tBCCAO), is associated with deleterious alterations in several physiological parameters of the animals. This study aims to investigate the effects of vanillic acid (VA) on memory impairment, locomotion and exploratory deficits, as well as histological and hippocampal long-term potentiation (LTP) injuries induced by tBCCAO procedure followed by reperfusion (BCCAO/R) in rats. Adult male Wistar rats (250–300g) were divided randomly into four groups: Sham-Operated group “Sham”; Vehicle+BCCAO/R group “BCCAO/R”; Vehicle+ Vanillic acid group “VA”; VA (100mg/kg) +BCCAO/R group “VA +BCCAO/R”. Cerebral hypoperfusion was induced after 14days of pretreatment with VA and/or normal saline. To induce the animal model of hypoperfusion, bilateral common carotid arteries were occluded for 30min, followed by 72h of reperfusion. Subsequently, behavioral, histopathological and electrophysiological parameters were evaluated after BCCAO/R. Data showed that pretreatment of VA markedly improved locomotion in tBCCAO rats compared with the untreated BCCAO/R rats (p<0.05). Moreover, pretreatment of VA significantly ameliorated memory impairment in “VA+BCCAO/R” group compared with the “BCCAO/R” group (P<0.01). The field excitatory postsynaptic potential (fEPSP) amplitude and slope were significantly decreased in “BCCAO/R” group compared with Sham group (P<0.001). Data indicate that fEPSP amplitude and slope were increased in “VA+BCCAO/R” group compared with the “BCCAO/R” group (P<0.001). Furthermore, histopathological observation in VA pretreated tBCCAO rats showing markedly attenuated of cell death (P<0.01) and arrangement of CA1 neurons as compared with the untreated BCCAO/R rats. Our data confirm the protective role of VA against transient cerebral ischemia and reperfusion in rats. Moreover, it proposes that VA has a beneficial role in cerebrovascular insufficiency states.