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Ventilatory impairment in a rat model of central dysmyelination
Author(s) -
Johnson Rebecca Ann,
Duncan Ian D.,
Mitchell Gordon S.
Publication year - 2009
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.23.1_supplement.784.10
Subject(s) - hypercapnia , ventilation (architecture) , medicine , respiratory system , plethysmograph , cardiology , respiratory minute volume , anesthesia , mechanical engineering , engineering
Although respiratory complications are the major cause of morbidity/mortality in advanced myelin disorders (i.e. MS), little is known concerning mechanisms whereby lack of myelin impairs ventilation, or how patients compensate for such changes (i.e. plasticity). To establish a model for future studies concerning mechanisms of ventilatory impairment/compensation, we tested the hypothesis that respiratory function progressively declines with advancing disease in a genetic model of CNS dysmyelination, the Long Evans shaker rat ( les ). Ventilatory measurements were made via whole‐body plethysmography in les and wild‐type rats at baseline and during hypercapnia (7%CO 2 ). In young (P59) rats, there were no differences in breathing between les and wild‐type groups in either condition (p>0.05). However, by P150, significant decreases between groups were observed in mean inspiratory flow (Vt/Ti), breathing frequency and minute ventilation during baseline (40%, 47% and 37%, respectively) and hypercapnia (40%, 44% and 50%, respectively) (all p<0.05). Thus, ventilatory capacity is maintained in young, dysmyelinated rats, but ventilatory impairment develops as les rats age. This study provides the foundation for mechanistic studies of respiratory insufficiency and therapeutic interventions in myelin disorders. Support: NIH NS057778 , UW ICTR via NIH CTSA 1UL1RR025011, NMSS TR3761