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Autonomic reactions and peri-interventional alterations in body weight as potential supplementary outcome parameters for thromboembolic stroke in rats

DOI: 10.1186/2040-7378-4-7

Keywords: Thromboembolic stroke, Autonomic changes, Heart rate, Mean arterial pressure, Body weight

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Abstract:

Forty-eight rats underwent thromboembolic middle cerebral artery occlusion (MCAO) while recording heart rate (HR) and mean arterial pressure (MAP). After assessing early functional impairment (Menzies score), animals were assigned to control procedure or potentially neuroprotective treatment with normobaric (NBO) or hyperbaric oxygen (HBO). Four or 24 hours after ischemia onset, functional impairment was re-assessed and FITC-albumin administered intravenously obtaining leakage-related blood–brain barrier (BBB) impairment. Body weight was documented prior to MCAO and 4 or 24 hours after ischemia onset.During MCAO, HR was found to increase significantly while MAP decreased. The amount of changes in HR was positively correlated with early functional impairment (P?=?0.001): Severely affected animals provided an increase of 15.2 compared to 0.8 beats/minute in rats with low impairment (P?=?0.048). Regarding body weight, a decrease of 9.4% within 24 hours after MCAO occurred, but treatment-specific alterations showed no significant correlations with respective functional or BBB impairment.Future studies should routinely include autonomic parameters to allow inter-group comparisons and better understanding of autonomic reactions due to experimental stroke. Prospectively, autonomic consequences might represent a useful outcome parameter enhancing the methodological spectrum of preclinical stroke studies.Stroke is an ongoing health issue with high socioeconomic relevance [1], contributing to 10-12% of deaths in Western countries [2] and accounting for approximately 4% of health-care costs [3]. In focal cerebral ischemia, only tissue plasminogen activator as recanalizing strategy has shown beneficial effects in pharmacological clinical trials (e.g., [4]). On the contrary, numerous potentially neuroprotective drugs have failed to reproduce their impressive preclinical results in randomized clinical trials [5-7], e.g., NXY-059 [8]. This situation might be caused by the complex

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