Journal of Applied Physiology, Vol 72, Issue 4 1522-1528, Copyright © 1992 by American Physiological Society
Triangularis sterni and phrenic nerve responses to progressive brain hypoxia
L. O. Chae, 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.
Activity of the respiratory muscles that are not normally active during
eupnea (genioglossal and abdominal) has been shown to be more vulnerable to
hypoxic depression than inspiratory diaphragmatic activity. We hypothesized
that respiratory muscles that are active at eupnea would be equally
vulnerable to isocapnic progressive brain hypoxia (PBH). Phrenic (PHR) and
triangularis sterni nerve (TSN) activity were recorded in anesthetized
peripherally chemodenervated vagotomized ventilated cats. Hypercapnia
[arterial PCO2 (PaCO2) = 57 +/- 3 (SE) Torr] produced parallel increases in
peak PHR and TSN activity. PBH [0.5% CO-40% O2-59.5% N2, arterial O2
content (CaO2) reduced from 13.1 +/- 1.0 to 3.7 +/- 0.3 vol%] resulted in
parallel decreases of peak PHR and TSN activity to neural apnea. PBH was
continued until PHR gasping ensued (CaO2 = 2.9 +/- 0.2 vol%); TSN activity
remained silent during gasping. After 6-12 min of recovery (95% O2-5% CO2;
CaO2 = 7.8 +/- 0.8 vol%; PaCO2 = 55 +/- 2 Torr), peak PHR activity was
increased to 110 +/- 18% (% of activity at 9% CO2) whereas peak TSN
activity was augmented to 269 +/- 89%. The greater augmentation of TSN
activity during the recovery period could not be explained solely by
hypercapnia. In conclusion, we found that 1) TSN expiratory and PHR
inspiratory activities are equally vulnerable to hypoxic depression and 2)
recovery from severe hypoxia is characterized by a profound augmentation of
TSN expiratory activity.
