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School of Medicine, Case Western Reserve University, Cleveland, Ohio 44106-4938
Received 2 January 1996; accepted in final form 29 May 1996.
LaManna, J. C., M. A. Haxhiu, K. L. Kutina-Nelson, S. Pundik, B. Erokwu, E. R. Yeh, W. D. Lust, and N. S. Cherniack.
Decreased energy metabolism in brain stem during central
respiratory depression in response to hypoxia. J. Appl. Physiol. 81(4): 1772-1777, 1996.
Metabolic changes in the brain stem were measured at the time when oxygen deprivation-induced respiratory depression occurred. Eucapnic ventilation with 8% oxygen in vagotomized urethan-anesthetized rats
resulted in cessation of respiratory drive, monitored by recording
diaphragm electromyographic activity, on average within 11 min (range
5-27 min), presumably via central depressant mechanisms. At that
time, the brain stems were frozen in situ for metabolic analyses. By
using 20-µm lyophilized sections from frozen-fixed brain
stem, microregional analyses of ATP, phosphocreatine, lactate, and
intracellular pH were made from 1)
the ventral portion of the nucleus gigantocellularis and the
parapyramidal nucleus; 2) the
compact and ventral portions of the nucleus ambiguus;
3) midline neurons;
4) nucleus tractus solitarii; and
5) the spinal trigeminal nucleus. At
the time of respiratory depression, lactate was elevated threefold in
all regions. Both ATP and phosphocreatine were decreased to 50 and 25%
of control, respectively. Intracellular pH was more acidic by
0.2-0.4 unit in these regions but was relatively preserved in the
chemosensitive regions near the ventral and dorsal medullary surfaces.
These results show that hypoxia-induced respiratory depression was
accompanied by metabolic changes within brain stem regions involved in
respiratory and cardiovascular control. Thus it appears that there was
significant energy deficiency in the brain stem after hypoxia-induced
respiratory depression had occurred.
ventral medulla oblongata; intracellular pH; adenosine
5
-triphosphate; phosphocreatine; lactate
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