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1- Department of Physiology, School of Medicine, AJA University of Medical Sciences, Tehran, Iran.
2- Neurogenic Inflammation Research Center, Mashhad University of Medical Sciences, Mashhad, Iran.
3- Department of Physiology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
Abstract:  
Introduction: The central mechanism responsible for cardiovascular response to lipopolysaccharide (LPS) - induced hypotension is not completely determined and it is suggested numerous brain areas such as dorsal periaqueductal gray (dPAG) are involved. In this study the cardiovascular effect of the dPAG during LPS-induced hypotension was evaluated.
Methods: Twenty male Wistar rats divided into four groups including 1) Control (Saline microinjected into dPAG), 2) Lidocaine 2%, 3) LPS (intravenously injected), and 4) Lidocaine + LPS were used. Catheterization of the femoral artery and vein was performed for the recording of blood pressure and LPS injection, respectively. Saline and lidocaine were microinjected into the dPAG nucleus then, LPS injection was done. Cardiovascular responses throughout of experiments were recorded and changes (∆) of systolic blood pressure (SBP), mean arterial pressure (MAP) and heart rate (HR) were calculated over time and was compared with those control and LPS groups, using repeated measures ANOVA.
Results: LPS significantly reduced ∆SBP and ∆MAP (P<0.05) and did not change the ∆HR than the control group. Lidocaine did not significantly affect basic ∆SBP, ∆MAP and ∆HR compared to the control. Injection of lidocaine before LPS significantly attenuated reduction of ∆SBP and ∆MAP evoked by LPS (P<0.05).
Conclusion: Our data showed that blockade of the dPAG by lidocaine significantly ameliorates the hypotension induced by LPS. It confirms involvement of the dPAG in cardiovascular regulation during LPS-induced hypotension.
Type of Study: Original | Subject: Behavioral Neuroscience
Received: 2020/08/16 | Accepted: 2020/08/25

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