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Disordered Breathing In An Aged Model of Ischemic Stroke
Author(s) -
Mulkey Daniel,
Patrizz Anthony,
Chen Xinnian,
Kolb Adam,
McCullough Louise
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.660.10
Subject(s) - medicine , stroke (engine) , respiratory system , anesthesia , hypercapnia , hypoventilation , hypoxia (environmental) , central chemoreceptors , cardiology , ventilation (architecture) , breathing , chemistry , mechanical engineering , organic chemistry , oxygen , engineering
Respiratory dysfunction is a common complication of stroke associated with increased mortality. Stroke‐disorder breathing typically presents as Cheyne‐Stokes respiration which is thought to result from hyper‐activation of central chemoreceptors. We test this hypothesis by characterizing the CO2 ventilatory response before and after ischemic stroke. Further, since neurons in the retrotrapezoid nucleus are important chemoreceptors and their activity is regulated by KCNQ channels, we also test whether KCNQ channels can be targeted for the treatment of stroke related breathing problems. We used aged mice for these experiments because stroke mainly affects the elderly. Stroke was induced by middle cerebral artery occlusion (MCAO) and breathing was measured by plethysmography. Sham animals are subjected to the same surgery but with no occlusion. All MCAO‐treated mice exhibited hypoventilation with increased apneas (both frequency and duration) that were often preceded by short bursts of respiratory activity. Stroked mice also showed decreased respiratory stability as evidenced by a drop in approximate entropy. However, the ventilatory response to CO2 as similar between stroke and sham and systemic injection of retigabine further suppressed basal respiratory activity in MCAO/sham mice. These results show that MCAO‐treated mice exhibit a phenotype reminiscent of periodic breathing in stroke patients and they suggest that increased chemoreceptor gain is not the underlying cause of stroke‐disorder breathing.