Impaired microcirculation after subarachnoid hemorrhage in an in vivo animal model

Kuo-Chuan Wang,Jui-Chang Tsai,Sung-Chun Tang,Wei-Chou Lin,Dar-Ming Lai,Yong-Kwang Tu,Sung-Tsang Hsieh,Jing-Er Lee,Chih-Peng Lin

doi:10.1038/s41598-018-31709-7

Abstract

The influence of aneurysmal subarachnoid hemorrhage (SAH) on brain microcirculation has not yet been systematically investigated. We established an animal model to examine (1) the brain surface microcirculation (2) the influences of cerebrospinal fluid (CSF) from aneurysmal SAH on the brain surface microcirculation. A rat SAH model was induced by injection of autologous arterial blood into the cisterna magnum, and the brain surface microcirculation was evaluated by a capillary videoscope with craniotomy at the fronto-parietal region. CSF from SAH rats and SAH patients was applied on the brain surface of naïve rats to assess the resulting microcirculatory changes. In the SAH rats, diffuse constriction of cortical arterioles within 24 hours of SAH was observed. Similar patterns of microcirculation impairment were induced on normal rat brain surfaces via application of CSF from SAH rats and SAH patients. Furthermore, the proportion of subjects with arteriolar vasoconstriction was significantly higher in the group of SAH patients with delayed ischemic neurological deficits (DIND) than in those without DIND (p < 0.001). This study demonstrated impaired microcirculation on brain surface arterioles in a rat model of SAH. CSF from SAH rats and patients was responsible for impairment of brain surface microcirculation.

Highlights

Conventional wisdom holds that vasospasm of major cerebral vessels following aneurysmal subarachnoid hemorrhage (SAH) is responsible for detrimental neurological outcomes
To investigate whether the findings related to rCSF from SAH rats could be extended to human SAH, we further examined the effects of hCSF from SAH patients on the brain cortical microcirculation in naïve rats. hCSF from SAH patients induced vasoconstriction of the rat brain cortical microcirculation after hCSF superfusion for 2 hours (Fig. 6B,C) (Video) including the sa (37.5 ± 23.1%, range: 23 to 100%) and the ta (60.1 ± 28.4%, range: 35 to 100%). hCSF from controls and artificial cerebrospinal fluid (CSF) did not induce any significant changes in microcirculation (Fig. 8A)
This study investigated the effect of SAH on brain microcirculation and its clinical significance by establishing a platform to examine brain surface microcirculation

Summary

Introduction

Conventional wisdom holds that vasospasm of major cerebral vessels following aneurysmal subarachnoid hemorrhage (SAH) is responsible for detrimental neurological outcomes Despite this prevailing hypothesis, a growing number of reports have suggested the existence of alternative mechanisms of neurological deficits[1,2]; for example, ischemic brain injury could develop within the normal range of cerebral perfusion pressure[3,4]. We aimed to examine the effect of SAH on brain surface microcirculation in a rat model of SAH, and assessed: (1) pathological alterations of microcirculation vasculature, and (2) physiological changes in cerebral regional blood flow and tissue oxygenation. We further extended this experimental system in order to www.nature.com/scientificreports/.

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