Anoxic disturbance of the isolated respiratory network of neonatal rats

Völker, Antje; Ballanyi, Klaus; Richter, Diethelm W.

doi:10.1007/bf00241960

Cited by 46 publications

(31 citation statements)

References 47 publications

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“…The functional relevance of anaerobic metabolism was studied by exposure to anoxia after lowering the glucose concentration or during addition of iodoacetate, a blocker of anaerobic glycolysis [23,33]. In superfusates containing 30 mM glucose, experimentally induced anoxia of the entire en bloc preparation does not severely impair ion homeostasis, and respiratory activity persists for more than 1 h at a reduced frequency [2,5,24,31]. The results show that glucose levels of 10 mM are not sufficient to provide long-term maintenance of respiratory network function or protection from anoxic insults.…”

Section: Introductionmentioning

confidence: 99%

Functional relevance of anaerobic metabolism in the isolated respiratory network of newborn rats

1996

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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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Section: Introductionmentioning

confidence: 99%

Functional relevance of anaerobic metabolism in the isolated respiratory network of newborn rats

1996

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“…An increase in central respiratory activity also occurs in in vitro preparations in which chemoreceptor afferents are deleted (2,3). Hence, activation of medullary chemosensory neurons (4) or direct stimulation of respiratory neurons (2) contributes to the increased respiratory response to hypoxia.…”

Section: Introductionmentioning

confidence: 99%

Role of nitric oxide in hypoxia-induced hyperventilation and hypothermia: participation of the locus coeruleus

Fabris

Anselmo-Franci

Branco

1999

Braz J Med Biol Res

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Hypoxia elicits hyperventilation and hypothermia, but the mechanisms involved are not well understood. The nitric oxide (NO) pathway is involved in hypoxia-induced hypothermia and hyperventilation, and works as a neuromodulator in the central nervous system, including the locus coeruleus (LC), which is a noradrenergic nucleus in the pons. The LC plays a role in a number of stress-induced responses, but its participation in the control of breathing and thermoregulation is unclear. Thus, in the present study, we tested the hypothesis that LC plays a role in the hypoxia-induced hypothermia and hyperventilation, and that NO is involved in these responses. Electrolytic lesions were performed bilaterally within the LC in awake unrestrained adult male Wistar rats weighing 250-350 g. Body temperature and pulmonary ventilation (V E ) were measured. The rats were divided into 3 groups: control (N = 16), sham operated (N = 7) and LC lesioned (N = 19), and each group received a saline or an N G -nitro-L-arginine methyl ester (L-NAME, 250 µg/µl) intracerebroventricular (icv) injection. No significant difference was observed between control and sham-operated rats. Hypoxia (7% inspired O 2 ) caused hyperventilation and hypothermia in both control (from 541.62 ± 35.02 to 1816.18 ± 170.7 and 36.3 ± 0.12 to 34.4 ± 0.09, respectively) and LC-lesioned rats (LCLR) (from 694.65 ± 63.17 to 2670.29 ± 471.33 and 36 ± 0.12 to 35.3 ± 0.12, respectively), but the increase in V E was higher (P<0.05) and hypothermia was reduced (P<0.05) in LCLR. L-NAME caused no significant change in V E or in body temperature under normoxia, but abolished both the hypoxia-induced hyperventilation and hypothermia. Hypoxia-induced hyperventilation was reduced in LCLR treated with L-NAME. L-NAME also abolished the hypoxia-induced hypothermia in LCLR. The present data indicate that hypoxia-induced hyperventilation and hypothermia may be related to the LC, and that NO is involved in these responses.

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“…Other phenomena can be elicited by repeated bouts of hypoxia, including progressive augmentation, where the ventilatory response to each successive bouts increases, and longterm facilitation (LTF), where ventilation is often elevated for up to several hours on return to normoxia (21, 24, 30). These time-dependent phenomena may have profound effects on the stability of the respiratory system; consequently, the neuronal mechanisms responsible have been the focus of considerable interest.Time-dependent ventilatory responses to hypoxia have largely been attributed to central mechanisms (5,27,29), triggered by the barrage of afferent input from the carotid bodies and/or through the direct effect of hypoxia on central neuronal circuits (3,28,33). However, some have argued that time-dependent changes in carotid body output may have a more direct role (24).…”

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confidence: 99%

“…Time-dependent ventilatory responses to hypoxia have largely been attributed to central mechanisms (5,27,29), triggered by the barrage of afferent input from the carotid bodies and/or through the direct effect of hypoxia on central neuronal circuits (3,28,33). However, some have argued that time-dependent changes in carotid body output may have a more direct role (24).…”

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Time-dependent modulation of carotid body afferent activity during and after intermittent hypoxia

Cummings¹,

Wilson²

2005

American Journal of Physiology-Regulatory, Integrative and Comp

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-The ventilatory response to several minutes of hypoxia consists of various time-dependent phenomena, some of which occur during hypoxia (e.g., short-term depression), whereas others appear on return to normoxia (e.g., posthypoxic frequency decline). Additional phenomena can be elicited by acute, intermittent hypoxia (e.g., progressive augmentation, long-term facilitation). Current data suggest that these phenomena originate centrally. We tested the hypothesis that carotid body afferent activity undergoes time-dependent modulation, consistent with a direct role in these ventilatory phenomena. Using an in vitro rat carotid body preparation, we found that 1) afferent activity declined during the first 5 min of severe (40 Torr PO 2), moderate (60 Torr PO2), or mild (80 Torr PO 2) hypoxia; 2) after return to normoxia (100 Torr PO2) and after several minutes of moderate or severe hypoxia, afferent activity was transiently reduced compared with prehypoxic levels; and 3) with successive 5-min bouts of mild, moderate, or severe hypoxia, afferent activity during bouts increased progressively. We call these phenomena sensory hypoxic decline, sensory posthypoxic decline, and sensory progressive augmentation, respectively. These phenomena were stimulus specific: similar phenomena were not seen with 5-min bouts of normoxic hypercapnia (100 Torr PO 2 and 50 -60 Torr PCO2) or hypoxic hypocapnia (60 Torr PO2 and 30 Torr PCO2). However, bouts of either normoxic hypercapnia or hypocapnic hypoxia resulted in sensory long-term facilitation. We suggest time-dependent carotid body activity acts in parallel with central mechanisms to shape the dynamics of ventilatory responses to respiratory chemostimuli. control of breathing; blood gases; peripheral chemoreceptor; response; dynamics THE MAGNITUDE AND DYNAMICS (or "time dependence") of the ventilatory response of adult mammals to hypoxia depends on the magnitude, length, and history of hypoxic exposure. Thus, for a single isolated bout of hypoxia, the acute response is characterized by a rapid increase in breathing frequency and tidal volume. During sustained hypoxia, the ventilatory response remains elevated relative to prehypoxic levels. However, both breathing frequency (short-term depression) and tidal volume (hypoxic ventilatory decline, HVD) decrease from their peak levels (24). After mammals return to normoxia, breathing frequency can fall below prehypoxic levels, a phenomenon referred to as posthypoxic frequency decline (PHFD) (4, 24). Other phenomena can be elicited by repeated bouts of hypoxia, including progressive augmentation, where the ventilatory response to each successive bouts increases, and longterm facilitation (LTF), where ventilation is often elevated for up to several hours on return to normoxia (21, 24, 30). These time-dependent phenomena may have profound effects on the stability of the respiratory system; consequently, the neuronal mechanisms responsible have been the focus of considerable interest.Time-dependent ventilatory responses to hypoxia have largely ...

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Anoxic disturbance of the isolated respiratory network of neonatal rats

Cited by 46 publications

References 47 publications

Functional relevance of anaerobic metabolism in the isolated respiratory network of newborn rats

Functional relevance of anaerobic metabolism in the isolated respiratory network of newborn rats

Role of nitric oxide in hypoxia-induced hyperventilation and hypothermia: participation of the locus coeruleus

Time-dependent modulation of carotid body afferent activity during and after intermittent hypoxia

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