Carbon dioxide sensitivity during hypoglycaemia‐induced, elevated metabolism in the anaesthetized rat

Bin-Jaliah, Ismaeel; Maskell, Peter; Kumar, Prem

doi:10.1113/jphysiol.2004.080085

Cited by 28 publications

(37 citation statements)

References 52 publications

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“…These results suggest that, in general, peripheral chemoreceptor activity does not participate in the fed/fasted variation of the central respiratory output. This is not necessarily consistent with previous notions that hypoglycemia stimulates chemoafferent activity, or that it increases _ V E and ventilatory responses to hypoxia or hypercapnia [32][33][34]. The carotid bodies are believed to be important sensors for hypoxia and hypoglycemia, whose action is based on an insulin-induced severe hypoglycemia [35].…”

Section: Fed/fasted Variation In Ventilatory and Metabolic Responses supporting

confidence: 74%

Effects of fasting on hypoxic ventilatory responses and the contribution of histamine H1 receptors in mice

et al. 2010

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We tested the hypothesis that fasting affects hypoxic ventilatory responses through metabolic changes via histamine H1 receptors. Wild-type (WT) and histamine H1 receptor knockout (H1RKO) mice were studied in fed and fasted states. In the fed WT, hypoxic-gas exposure elicited an increase and a subsequent decline in ventilation (hypoxic ventilatory decline or HVD). HVD was influenced by fasting in breathing pattern with metabolic rate. Fasting elicited hypoglycemia, a drop in R, and increases in free fatty acid and ketone bodies in the serum. In H1RKO, HVD was blunted in the fed state, but it appeared in the fasted state. There was a minimal drop in R following fasting and a low triglyceride concentration. Thus, fasting affects HVD through a change in energy mobilization from glucose to lipid metabolism. Histamine H1 receptors are involved in HVD during fed and fasted states, resulting in adaptation to the environmental conditions.

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Section: Fed/fasted Variation In Ventilatory and Metabolic Responses supporting

confidence: 74%

Effects of fasting on hypoxic ventilatory responses and the contribution of histamine H1 receptors in mice

et al. 2010

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“…Therefore, the dissection of direct effect of hypoglycemia as a chemostimulant is extremely difficult, if not impossible. And second, since the gluscosensing properties are evidenced in cultured chemoreceptor cells and CB slices (21,40,59) and not in freshly isolated intact CB and/or CB-CSN preparations (1,4,5,11), it would appear, as suggested by Kumar (33), that the observed capacity of chemoreceptor cells to sense glucose levels represents a phenotypic change occurring in culture conditions.…”

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confidence: 94%

“…In fact, several studies carried out in intact animals have claimed that the CB is indeed a glucose sensor, having a role on glucose homeostasis (2,32,51,54). Unfortunately, there is a nearly even number of studies performed both in intact animals and in intact isolated CB preparations denying the role of chemoreceptor cells as glucoreceptors (1,4,5,11,52). Without neglecting a role for the CB in glucose homeostasis, the concept on contention is the nature of the CB as a glucoreceptor.…”

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confidence: 94%

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Effects of low glucose on carotid body chemoreceptor cell activity studied in cultures of intact organs and in dissociated cells

Gallego-Martín

Fernandez-Martinez

Rigual

et al. 2012

American Journal of Physiology-Cell Physiology

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The participation of the carotid body (CB) in glucose homeostasis and evidence obtained in simplified cultured CB slices or dissociated cells have led to the proposal that CB chemoreceptor cells are glucoreceptors. However, data generated in intact, freshly excised organs deny CB chemoreceptor cells' glucosensing properties. The physiological significance of the contention has prompted the present study, performed in a newly developed preparation of the intact CB organ in culture that maintains chemoreceptor cells' microenvironment. Chemoreceptor cells of intact CBs in culture retained their capacity to store, synthesize, and secrete catecholamine in response to hypoxia for at least 6 days. Aglycemia did not elicit neurosecretion in dissociated chemoreceptor cells or in intact CB in culture, but potentiated hypoxia-elicited neurosecretion, exclusively, in 1-day-old intact CB cultures and dissociated chemoreceptor cells cultured for 24 h. In fura 2-loaded cells, aglycemia (but not 1 mM) caused a slow Ca(2+)-dependent and nifedipine-insensitive increase in fluorescence at 340- to 380-nm wavelength emission ratio and augmented the fluorescent signal elicited by hypoxia. Association of nifedipine and KBR7943 (a Na(+)/Ca(2+) exchanger inhibitor) completely abolished the aglycemic Ca(2+) response. We conclude that chemoreceptor cells are not sensitive to hypoglycemia. We hypothesize that cultured chemoreceptor cells become transiently more dependent on glycolysis. Consequently, aglycemia would partially inhibit the Na(+)/K(+) pump, causing an increase in intracellular Na(+) concentration, and a reversal of Na(+)/Ca(2+) exchanger. This would slowly increase intracellular Ca(2+) concentration and cause the potentiation of the hypoxic responses. We discuss the nature of the signals detected by chemoreceptor cells for the CB to achieve its glycemic homeostatic role.

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“…1B), quantitative analysis of both subsystems can determine how changes in both the controller and plant elements affect V E or Pa CO 2 (5,6,17,18,41,45,46,48); however, to what extent changes in central blood volume (CBV) influence these variables and thus, by consequence, the operating point (V E or Pa CO 2 response) of the respiratory control system remain unclear.…”

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confidence: 99%

Manipulation of central blood volume and implications for respiratory control function

Miyamoto

Bailey

Nakahara

et al. 2014

American Journal of Physiology-Heart and Circulatory Physiology

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The respiratory operating point (ventilatory or arterial PCO 2 response) is determined by the intersection point between the controller and plant subsystem elements within the respiratory control system. However, to what extent changes in central blood volume (CBV) influence these two elements and the corresponding implications for the respiratory operating point remain unclear. To examine this, 17 apparently healthy male participants were exposed to water immersion (WI) or lower body negative pressure (LBNP) challenges to manipulate CBV and determine the corresponding changes. The respiratory controller was characterized by determining the linear relationship between end-tidal PCO 2 (PETCO 2 ) and minute ventilation (V E) [V E ϭ S ϫ (PET CO 2 Ϫ B)], whereas the plant was determined by the hyperbolic relationship between V E and PETCO 2 (PETCO 2 ϭ A/V E ϩ C). Changes in V E at the operating point were not observed under either WI or LBNP conditions despite altered PET CO 2 (P Ͻ 0.01), indicating a moving respiratory operating point. An increase (WI) and a decrease (LBNP) in CBV were shown to reset the controller element (PETCO 2 intercept B) rightward and leftward, respectively (P Ͻ 0.05), without any change in S, whereas the plant curve remained unaltered at the operating point. Collectively, these findings indicate that modification of the controller element rather than the plant element is the major factor that contributes toward an alteration of the respiratory operating point during CBV shifts. system analysis; respiratory control; central blood volume; head-out water immersion; lower body negative pressure THE RESPIRATORY SYSTEM is an important chemoreflex-feedback control system that maintains arterial PCO 2 (Pa CO 2 ), O 2 , and pH remarkably constant via ventilatory regulation. It can be divided into two subsystems (Fig. 1A): a controller (controlling element) and a plant (controlled element) (5,17,18,21,35,41,45,46).Recently, we have characterized these subsystem elements in an open-loop condition and constructed a respiratory equilibrium diagram to illustrate the mechanisms of respiratory control at rest and during exercise in endurance-trained and untrained subjects (46,48,52). Briefly, the controller element approximates a straight line where minute ventilation (V E) increases as a function of Pa CO 2 . The element can be broadly divided into chemoreflex and nonchemoreflex drives to breathe (39). The plant element approximates a hyperbola with a positive asymptote where Pa CO 2 decreases asymptotically as a function of V E (APPENDIX).Since respiration is determined from an intersection point between these two elements on the respiratory equilibrium diagram (Fig. 1B), quantitative analysis of both subsystems can determine how changes in both the controller and plant elements affect V E or Pa CO 2 (5,6,17,18,41,45,46,48); however, to what extent changes in central blood volume (CBV) influence these variables and thus, by consequence, the operating point (V E or Pa CO 2 response) of the respiratory co...

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Carbon dioxide sensitivity during hypoglycaemia‐induced, elevated metabolism in the anaesthetized rat

Cited by 28 publications

References 52 publications

Effects of fasting on hypoxic ventilatory responses and the contribution of histamine H1 receptors in mice

Effects of fasting on hypoxic ventilatory responses and the contribution of histamine H1 receptors in mice

Effects of low glucose on carotid body chemoreceptor cell activity studied in cultures of intact organs and in dissociated cells

Manipulation of central blood volume and implications for respiratory control function

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