Abstract

BackgroundHypothermic circulatory arrest (HCA) in aortic arch surgery has a significant risk of neurological injury despite the newest protective techniques and strategies. Nitric oxide (NO) could exert a protective role, reduce infarct area and increase cerebral perfusion. This study aims to investigate the possible neuroprotective effects of NO administered in the oxygenator of selective antegrade cerebral perfusion (SCP) during HCA.MethodsThirty male SD adult rats (450–550 g) underwent cardiopulmonary bypass (CPB), cooling to 22°C body core temperature followed by 30 min of HCA. Rats were randomized to receive SCP or SCP added with NO (20 ppm) administered through the oxygenator (SCP-NO). All animals underwent CPB-assisted rewarming to a target temperature of 35°C in 60 min. At the end of the experiment, rats were sacrificed, and brain collected. Immunofluorescence analysis was performed in blind conditions.ResultsNeuroinflammation assessed by allograft inflammatory factor 1 or ionized calcium-binding adapter molecule 1 expression, a microglia activation marker was lower in SCP-NO compared to SCP (4.11 ± 0.59 vs. 6.02 ± 0.18%; p < 0.05). Oxidative stress measured by 8oxodG, was reduced in SCP-NO (0.37 ± 0.01 vs. 1.03 ± 0.16%; p < 0.05). Brain hypoxic area extent, analyzed by thiols oxidation was attenuated in SCP-NO (1.85 ± 0.10 vs. 2.74 ± 0.19%; p < 0.05). Furthermore, the apoptotic marker caspases 3 was significantly reduced in SCP-NO (10.64 ± 0.37 vs. 12.61 ± 0.88%; p < 0.05).ConclusionsNitric oxide administration in the oxygenator during SCP and HCA improves neuroprotection by decreasing neuroinflammation, optimizing oxygen delivery by reducing oxidative stress and hypoxic areas, finally decreasing apoptosis.

Highlights

  • Hypothermic circulatory arrest (HCA) is required during aortic arch surgery [1]

  • To analyze the degree of oxidative stress and apoptosis, we evaluate the expression of 8oxo-2′-deoxyguanosine (8oxodG) (ABCAM, UK) and caspases 3 (Cell Signaling, USA) [21,22,23]

  • Ionized calcium binding adapter molecule 1 (Iba1) expression is specific for microglia cells and macrophages and indicates an inflammatory activation, and its amount correlates with the degree of neuroinflammation

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Summary

Introduction

Hypothermic circulatory arrest (HCA) is required during aortic arch surgery [1]. Since the 1990’s, selective brain perfusion (SCP) techniques have become increasingly common [2, 3]. Despite these advancements, neurological damage of different severity develops in 5–20% of patients, mainly in urgent interventions for aortic dissection [4]. Neurological damage comprises permanent neurological dysfunction (PND) and temporary neurological dysfunction (TND). These two types of damage differ for etiopathogenesis, histological and clinical manifestation. Hypothermic circulatory arrest (HCA) in aortic arch surgery has a significant risk of neurological injury despite the newest protective techniques and strategies. This study aims to investigate the possible neuroprotective effects of NO administered in the oxygenator of selective antegrade cerebral perfusion (SCP) during HCA

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