Effect of Electrical Vagus Nerve Stimulation on Cerebral Blood Flow and Neurological Outcome in Asphyxial Cardiac Arrest Model of Rats.

Neurocrit Care

Department of Emergency Medicine, Seoul National University Bundang Hospital, 82, Gumi-ro 173 Beon-gil, Bundang-gu, Seongnam-si, Gyeonggi-do, 13620, Republic of Korea.

Published: June 2019

Background: Vagus nerve stimulation (VNS) during post-resuscitation may increase recovery of cerebral blood flow (CBF) and reduce neurological injury.

Objective: This study was designed to investigate the effect of electrical VNS on neurological outcomes following cardiac arrest (CA).

Methods: Male Sprague-Dawley rats (n = 48) were subjected to the asphyxial CA model and blindly allocated to the VN isolation (CA + VN isolation) or VNS group (CA + VNS group). Cardiopulmonary resuscitation was initiated 450 s after pulseless electrical arrest, and the left cervical vagus nerve was electrically stimulated (0.05 mA, 1 Hz) for 3 h in the CA + VNS group. The neurological deficit score (NDS) and overall performance category (OPC) were assessed at 24 h after resuscitation, and histological injury of the hippocampus was evaluated. Independent experiments were performed to evaluate the effect of VNS on global cortical CBF after resuscitation using laser speckle Doppler imaging through a thinned skull window from pre-arrest to 6 h after resuscitation.

Results: The baseline characteristics were not significantly different between the two groups. The NDS was significantly higher, and the OPC was substantially lower in the CA + VNS group (p = 0.022 and p = 0.049, respectively) supported by decrease in histological injury of the hippocampal CA1 region. CBF in the early period of post-return of spontaneous circulation (ROSC) was significantly higher in the CA + VNS group (p < 0.05 at post-ROSC 2 h and 4 h), and 4-hydroxynonenal was significantly lower in the CA + VNS group (p = 0.026).

Conclusions: VNS improved cerebral perfusion and neurological outcomes at 24 h after ROSC in an asphyxial CA model of rats.

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Source
http://dx.doi.org/10.1007/s12028-018-0640-7DOI Listing

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