AJP - Regulatory, Integrative and Comparative Physiology, Vol 271, Issue 1 91-100, Copyright © 1996 by American Physiological Society
Respiration and medullary blood flow during sinusoidal hypoxia in the peripherally chemodenervated cat
Q. P. Yu, J. E. Melton, J. A. Neubauer and N. H. Edelman
Department of Medicine, University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School, New Brunswick 08903-0019, USA.
The hypothesis that hypoxic respiratory depression is mediated by changes
in medullary blood flow (MBF) was assessed in 18 anesthetized, paralyzed,
vagotomized, peripherally chemodenervated, ventilated cats exposed to
sinusoidal hypoxic hypoxia. In nine cats, the dynamic response of the
central respiratory controller to hypoxia was studied by varying the cycle
time of sinusoidal hypoxia (cycle time = 2.5, 4, 6, 10, and 15 min). Peak
phrenic neurogram amplitude (PNA) followed sinusoidal oscillations in the
hypoxic input [arterial O2 saturation (SaO2)] at all cycle times. The
relationship between PNA and SaO2 was expressed as the transfer function of
the system and was approximated as a first-order differential equation with
a time constant of 78 +/- 1 s, a value consistent with a previous
measurement of the time constant of the change in respiration following a
change in brain blood flow. In a separate study, MBF was continuously
measured during sinusoidal hypoxia (cycle time = 6 min; n = 9) with a
laser-Doppler flow probe to directly assess the role of MBF in production
of hypoxic respiratory depression. PNA and MBF followed SaO2 oscillations
during sinusoidal hypoxia. Infusion of sodium nitroprusside (20
micrograms.kg-1.min-1 iv) increased MBF by 30-40% and abolished MBF
oscillations during subsequent sinusoidal hypoxia but had no effect on PNA
oscillations. We conclude that the increase in brain blood flow seen during
sinusoidal hypoxia is not the primary cause of the accompanying central
hypoxic respiratory depression.
