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Respiratory neural output during hypercapnia in a rat model of central dysmyelination
Author(s) -
BakerHerman Tracy Lee,
Mitchell Gordon S.,
Duncan Ian D.,
Johnson Rebecca A.
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.784.9
Subject(s) - hypercapnia , respiratory system , ventilation (architecture) , respiratory burst , phrenic nerve , anesthesia , medicine , control of respiration , cardiology , chemistry , endocrinology , physics , immunology , thermodynamics
Respiratory complications contribute to morbidity/mortality in advanced myelin disorders, but little is known concerning mechanisms whereby dysmyelination impairs breathing. Preliminary studies using a genetic model of CNS dysmyelination, the Long Evans shaker rat ( les ), suggest that ventilation is impaired with advancing disease. We tested the hypothesis that respiratory impairment is associated with abnormal inspiratory neural output in les rats. Surprisingly, les rats (P185, n = 3) had higher phrenic burst frequencies than wild‐type controls in baseline (45 vs 33 bursts/min, respectively) and hypercapnia (52 vs 41 bursts/min, respectively; both p<0.05). Although percent increase in phrenic burst amplitude from baseline during hypercapnia was increased in les rats, this apparent difference was due to a tendency for decreased baseline amplitudes (0.6 vs 1.8 volts, respectively; p>0.05). Since peak voltages during hypercapnia (2.7 vs 3.6 volts, respectively; p>0.05) were similar in les and wild‐type rats, it appears that the capacity to increase phrenic burst amplitude is preserved. However, abnormalities were observed in the pattern of phrenic activity during a burst, including exaggerated synchronized activity and a decrementing discharge pattern, which may suggest a degree of dyscoordination in sculpting the phrenic burst. Support: NIH HL69064, NMSS TR3761, UW ICTR ‐ NIH CTSA 1UL1RR025011