Introduction: Cerebral ischemia causes multiple organ dysfunction. The lungs are among the most affected organs; pneumonia leading to respiratory failure greatly reduces life expectancy following stroke. Nevertheless, the consequences of ischemic stroke on lung function including end-expiratory lung volume and respiratory mechanics have not been characterized.

Methods: Global cerebral ischemia was produced by bilateral common carotid artery occlusion (2VO, n=7), focal brain ischemia was achieved by unilateral middle cerebral artery occlusion (MCAO, n=5), and sham operated group served as control group (C, n=6). Three days later, rats were anesthetized and mechanically ventilated. End-expiratory lung volume (EELV) was measured by whole body plethysmography. Airway resistance (Raw), tissue damping (G) and elastance (H) were determined by forced oscillations. Measurements were performed under end-expiratory pressure (PEEP) of 0, 3, and 6 cmH2O.

Results: EELV was unaltered in the 2VO and MCAO groups compared to Group C. Respiratory mechanics exhibited no significant change in the 2VO rats, and Raw was not affected by MCAO or 2VO. Conversely, MCAO caused significant elevations in G at PEEP 3 (1132±167 vs.717±82 cmH2O/l, MCAO vs. C, p<0.001) and H (3613±185 vs. 2760±531 cmH2O/l, MCAO vs. C, p<0.05), with differences remaining at other PEEP levels.

Discussion: Neither global ischemia by 2VO nor focal ischemia by MCAO affects the static lung volumes, and 2VO has no effect on respiratory mechanics. However, marked deteriorations in the respiratory mechanics develop after MCAO, which impair primarily the tissue viscoelastic properties without affecting airway function.

Funding: OTKA-NKFIH K138032, EU H2020-HCEMM (No. 739593)