Postresuscitation Cerebral Vasospasm and Capillary Failure After Experimental Asphyxial Cardiac Arrest

Background Disrupted cerebral blood flow is suggested to contribute to secondary brain injury after cardiac arrest (CA). This study aimed to investigate cerebral microcirculation after return of spontaneous circulation (ROSC) following asphyxial CA. We hypothesized that contraction of pericytes after ROSC compromises cerebral capillary blood flow. Methods Transgenic C57BL/6NRj mice (n=19) of both sexes were studied. Mice were expressing tdTomato as a fluorescent reporter under the control of the platelet‐derived growth factor receptor β promoter to label pericytes. Chronic cranial windows were implanted 3 weeks before the experiment. Four minutes of asphyxial CA was followed by cardiopulmonary resuscitation. Two‐photon microscopy assessed cerebral hemodynamics in the same cohort of mice at both 3 and 24 hours after ROSC. Results Of 13 mice in the CA group, 9 achieved ROSC; 6 and 5 mice survived to 3 and 24 hours after ROSC, respectively. Arterial blood pressure was similar between groups 3 and 24 hours after ROSC. At 3 hours after ROSC, pial arteries and penetrating arterioles were constricted in the CA group compared with sham (arteriole diameter, 12.2 μm [95% CI, 10.9–13.4] versus 15.6 μm [95% CI, 13.8–17.5] in CA and sham; P =0.003). Similarly, first‐ and second‐ to third‐order capillaries showed reduced diameters 3 hours after ROSC (first‐order diameter, 3.9 μm [95% CI, 3.5–4.2] versus 5.3 μm [95% CI, 4.8–5.9] in CA and sham; P =0.002). The vasoconstriction was associated with slower red blood cell velocities throughout the capillary network (for second‐ to third‐order capillaries upstream from venule; 0.78 mm/s [95% CI, 0.46–1.09] versus 2.14 mm/s [95% CI, 1.73–2.55]; P <0.001) and increased capillary flow stalling. Artery‐to‐vein mean transit time was increased and relative transit‐time heterogeneity was decreased 3 hours after ROSC. By 24 hours after ROSC, vessel diameters, blood flow velocity, transit time, and capillary stalling were not different compared with sham. Conclusions Cerebrovascular vasospasm 3 hours after ROSC was associated with impaired cerebral microcirculation and increased capillary flow stalling.

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Journal
Journal of the American Heart Association
Published
2026-06-09
DOI
https://doi.org/10.1161/jaha.125.047582
Primary Topic
Cardiac Arrest and Resuscitation
Type
article
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article

Postresuscitation Cerebral Vasospasm and Capillary Failure After Experimental Asphyxial Cardiac Arrest

Christian Staehr, Asger Granfeldt, Cecilie Munch Johannsen, Eugenio Gutiérrez‐Jiménez et al.
Journal of the American Heart Association
Cardiac Arrest and Resuscitation
article

Postresuscitation Cerebral Vasospasm and Capillary Failure After Experimental Asphyxial Cardiac Arrest

Christian Staehr, Asger Granfeldt, Cecilie Munch Johannsen, Eugenio Gutiérrez‐Jiménez, Victoria Hinkley
article en

Abstract

Background Disrupted cerebral blood flow is suggested to contribute to secondary brain injury after cardiac arrest (CA). This study aimed to investigate cerebral microcirculation after return of spontaneous circulation (ROSC) following asphyxial CA. We hypothesized that contraction of pericytes after ROSC compromises cerebral capillary blood flow. Methods Transgenic C57BL/6NRj mice (n=19) of both sexes were studied. Mice were expressing tdTomato as a fluorescent reporter under the control of the platelet‐derived growth factor receptor β promoter to label pericytes. Chronic cranial windows were implanted 3 weeks before the experiment. Four minutes of asphyxial CA was followed by cardiopulmonary resuscitation. Two‐photon microscopy assessed cerebral hemodynamics in the same cohort of mice at both 3 and 24 hours after ROSC. Results Of 13 mice in the CA group, 9 achieved ROSC; 6 and 5 mice survived to 3 and 24 hours after ROSC, respectively. Arterial blood pressure was similar between groups 3 and 24 hours after ROSC. At 3 hours after ROSC, pial arteries and penetrating arterioles were constricted in the CA group compared with sham (arteriole diameter, 12.2 μm [95% CI, 10.9–13.4] versus 15.6 μm [95% CI, 13.8–17.5] in CA and sham; P =0.003). Similarly, first‐ and second‐ to third‐order capillaries showed reduced diameters 3 hours after ROSC (first‐order diameter, 3.9 μm [95% CI, 3.5–4.2] versus 5.3 μm [95% CI, 4.8–5.9] in CA and sham; P =0.002). The vasoconstriction was associated with slower red blood cell velocities throughout the capillary network (for second‐ to third‐order capillaries upstream from venule; 0.78 mm/s [95% CI, 0.46–1.09] versus 2.14 mm/s [95% CI, 1.73–2.55]; P <0.001) and increased capillary flow stalling. Artery‐to‐vein mean transit time was increased and relative transit‐time heterogeneity was decreased 3 hours after ROSC. By 24 hours after ROSC, vessel diameters, blood flow velocity, transit time, and capillary stalling were not different compared with sham. Conclusions Cerebrovascular vasospasm 3 hours after ROSC was associated with impaired cerebral microcirculation and increased capillary flow stalling.

Journal of the American Heart Association
The University of Queensland (AU), University of the Sunshine Coast (AU), Aarhus University (DK), Aarhus University Hospital (DK)
Good health and well-being
Openalex Percentile: Top 6%
Cardiac Arrest and Resuscitation
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