Comparative effects of dexmedetomidine and propofol on brain and lung damage in experimental acute ischemic stroke

Giselle C Sousa,Denise Battaglini,Chiara Robba,Mariana A Antunes,Pedro L Silva,Cynthia S Samary,Marcos Vinicius Fernandes,Paolo Pelosi,Patricia R M Rocco,Fernanda F Cruz,Christina Takyia,Carla M Da Silva

doi:10.1038/s41598-021-02608-1

Abstract

Acute ischemic stroke is associated with pulmonary complications, and often dexmedetomidine and propofol are used to decrease cerebral metabolic rate. However, it is unknown the immunomodulatory actions of dexmedetomidine and propofol on brain and lungs during acute ischemic stroke. The effects of dexmedetomidine and propofol were compared on perilesional brain tissue and lung damage after acute ischemic stroke in rats. Further, the mean amount of both sedatives was directly evaluated on alveolar macrophages and lung endothelial cells primarily extracted 24-h after acute ischemic stroke. In twenty-five Wistar rats, ischemic stroke was induced and after 24-h treated with sodium thiopental (STROKE), dexmedetomidine and propofol. Dexmedetomidine, compared to STROKE, reduced diffuse alveolar damage score [median(interquartile range); 12(7.8–15.3) vs. 19.5(18–24), p = 0.007)], bronchoconstriction index [2.28(2.08–2.36) vs. 2.64(2.53–2.77), p = 0.006], and TNF-α expression (p = 0.0003), while propofol increased VCAM-1 expression compared to STROKE (p = 0.0004). In perilesional brain tissue, dexmedetomidine, compared to STROKE, decreased TNF-α (p = 0.010), while propofol increased VCAM-1 compared to STROKE (p = 0.024). In alveolar macrophages and endothelial cells, dexmedetomidine decreased IL-6 and IL-1β compared to STROKE (p = 0.002, and p = 0.040, respectively), and reduced IL-1β compared to propofol (p = 0.014). Dexmedetomidine, but not propofol, induced brain and lung protection in experimental acute ischemic stroke.

Highlights

Acute ischemic stroke is associated with pulmonary complications, and often dexmedetomidine and propofol are used to decrease cerebral metabolic rate
To the best of our knowledge, it is unknown whether the aforementioned immunomodulation in central nervous system (CNS) proffered by dexmedetomidine and propofol during acute ischemic stroke is further extended to the lung
We investigated if both anesthetics would act directly on alveolar macrophages and lung endothelial cells primarily extracted 24-h after acute ischemic stroke

Summary

Introduction

Acute ischemic stroke is associated with pulmonary complications, and often dexmedetomidine and propofol are used to decrease cerebral metabolic rate It is unknown the immunomodulatory actions of dexmedetomidine and propofol on brain and lungs during acute ischemic stroke. The effects of dexmedetomidine and propofol were compared on perilesional brain tissue and lung damage after acute ischemic stroke in rats. Dexmedetomidine (α2-adrenergic agonist) and propofol (non-barbiturate sedative) are commonly used in the clinical management of patients with acute ischemic stroke who require admission to a neurocritical care w ard[1] Both decrease cerebral metabolic rate and present anti-inflammatory, antioxidant and anti-apoptotic properties[2,3]. We hypothesized that 24 h after acute ischemic stroke, dexmedetomidine and propofol might promote brain and lung protection with direct effects on pulmonary macrophages and endothelial cells. We investigated if both anesthetics would act directly on alveolar macrophages and lung endothelial cells primarily extracted 24-h after acute ischemic stroke

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