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Tissue oxygen (PO2), K+ (aKe), pH (pHe) and Ca2+ ([Ca2+]e) were measured in the region of the ventral respiratory group (VRG) in the in vitro brainstem-spinal cord preparation of neonatal rats. During tissue anoxia, elicited by superfusion of N2-gassed solutions, an initial increase in the frequency of respiratory activity, lasting between 2 and 12 min, turned into a frequency depression. During anoxia periods of up to 60 min, respiratory activity persisted in solutions containing CO2/bicarbonate, whereas a complete blockade was observed after 15-25 min in N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid- (Hepes)-buffered salines. After such anoxic apnea, respiratory rhythmicity could be reactivated by superfusion of hypoxic, CO2/bicarbonate-buffered solutions. In both types of hypoxic solutions, aKe increased by maximally 1.5 mM, whereas an initial increase of pHe by up to 0.05 pH units turned, after 2-4 min, into an acidification which could exceed 0.5 pH units. In contrast, [Ca2+]e remained unaffected by anoxia. Addition of 2-5 mM cyanide (CN-) to oxygenated Hepes-buffered saline evoked an increase in PO2 in the VRG from 100 to more than 300 mmHg. The effects of CN- on respiratory activity, aKe and pHe were almost identical to those during anoxia. In oxygenated, CO2/bicarbonate-free solutions of different pH, however, an increase in pHe in the VRG led to a decrease in respiratory frequency, whereas a fall of pHe produced a frequency acceleration. A rise of aKe in the VRG by more than 2 mM as induced by superfusion of a 7 mM K+ solution led to a sustained increase of respiratory frequency. The results indicate that blockade of aerobic metabolism does not severely perturb K+ and Ca2+ homeostasis and that the biphasic response to anoxia is not directly related to the observed changes in PO2, aKe, pHe, or [Ca2+]e. In the respiratory network of neonatal mammals, CO2 might provide a stimulus for long-term maintenance of respiratory activity under oxygen depletion.

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Respiratory (C3-C5) activity and extracellular K+, pH and Ca2+ (aKe, pHe, [Ca]e, respectively) in the ventral respiratory group (VRG) were measured in vitro. In brainstem-spinal cord preparations from 0- to 1-day-old rats, lowering of bath glucose content from 30 to 10 mM for 1 h did not affect aKe or rhythmic activity. In preparations from 2- to 3-day-old animals, however, an aKe rise by about 1 mM and disturbance of rhythm occurred after a delay of 50 min. Glucose-free saline resulted, after about 30 min, in reversible blockade of respiratory rhythm and an aKe rise by more than 8 mM, whereas pHe remained unaffected. Exposure to anoxia for 30 min after 1 h of pre-incubation in 10 mM glucose led to a progressive rise of aKe, and a fall of [Ca]e. The concomitant suppression of rhythm was irreversible in preparations from 2- to 3-day-old animals. Similar effects on aKe and [Ca]e and irreversible blockade of rhythm were revealed during anoxia in glucose-free solution, or by addition of 2-5 mM iodoacetate to oxygenated or hypoxic solutions. Iodoacetate led to a slow increase of pHe by more than 0.2 pH units, which was accelerated by anoxia. Our findings show that normal respiratory network functions in the en bloc medulla, in particular from rats older than 1 day, depend on high bath glucose levels, necessary for effective utilization of anaerobic metabolism.

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