Influence of Glucose on the Gasping Pattern of Young Animals Subjected to Acute Anoxia

Selle, W. A.

doi:10.1152/ajplegacy.1944.141.3.297

Cited by 22 publications

(4 citation statements)

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“…Himwich et al found that intraperitoneal glucose increased the survival of P8 rats from 16 to 30 min in undiluted nitrogen (33). Similar improvements in cardiovascular function and survival were subsequently reported by others in perinatal rodents (23,24,34,66,67).…”

Section: Discussionsupporting

confidence: 86%

Effects of antenatal dexamethasone and hyperglycemia on cardiovascular adaptation to asphyxia in preterm fetal sheep

Lear

Davidson

Dhillon

et al. 2020

American Journal of Physiology-Regulatory, Integrative and Comp

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Antenatal glucocorticoids improve outcomes among premature infants but are associated with hyperglycemia, which can exacerbate hypoxic-ischemic injury. It is still unclear how antenatal glucocorticoids or hyperglycemia modulate fetal cardiovascular adaptations to severe asphyxia. In this study, preterm fetal sheep received either saline or 12 mg i.m. maternal dexamethasone, followed 4 h later by complete umbilical cord occlusion (UCO) for 25 min. An additional cohort of fetuses received titrated glucose infusions followed 4 h later by UCO, to control for the possibility that hyperglycemia contributed to the cardiovascular effects of dexamethasone. Fetuses were studied for 7 d after UCO. Maternal dexamethasone was associated with fetal hyperglycemia (p<0.001), increased arterial pressure (p<0.001) and reduced femoral (p<0.005) and carotid (p<0.05) vascular conductance before UCO. UCO was associated with bradycardia, femoral vasoconstriction and transient hypertension. For the first 5 min of UCO, fetal blood pressure in the dexamethasone-asphyxia group was greater than saline-asphyxia (p<0.001). However, the relative increase in arterial pressure was not different from saline-asphyxia. Fetal heart rate and femoral vascular conductance fell to similar nadirs in both saline and dexamethasone-asphyxia groups. Dexamethasone did not affect the progressive decline in femoral vascular tone or arterial pressure during continuing UCO. By contrast, there were no effects of glucose infusions on the response to UCO. In summary, maternal dexamethasone but not fetal hyperglycemia increased fetal arterial pressure before and for the first 5 min of prolonged UCO but did not augment the cardiovascular adaptations to acute asphyxia.

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Section: Discussionsupporting

confidence: 86%

Effects of antenatal dexamethasone and hyperglycemia on cardiovascular adaptation to asphyxia in preterm fetal sheep

Lear

Davidson

Dhillon

et al. 2020

American Journal of Physiology-Regulatory, Integrative and Comp

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“…tials to generate high cerebral lactate concentrations. FurIn contrast, administration of glucose improves the "survival thermore, the final brain lactate concentration showed the response" of newborn rodents exposed to ischemic or anoxic same linear correlation with rei ischemia plasma glucose insults (9). A longer survival response was initially attributed to concentration for all four age groups.…”

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confidence: 86%

The Effect of Age on Glucose-Modulated Cerebral Agonal Glycolytic Rates Measured In Vivo by 1H NMR Spectroscopy

et al. 1991

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ABSTRACT. The purpose of this study was to investigate Abbreviations the effect of plasma glucose concentration on cerebral agonal glycolytic rates in piglets of different ages. Twenty-AGR, initial agonal glycolytic rate four piglets were divided into four different age groups [glu~ose],~,,,,, arterial blood plasma glucose concentration corresponding to 113, 121, 128, and 145 d postconception 'H NMR, proton nuclear magnetic resonance (normal gestation = 115 d). For each group the agonal k, first order rate constant for lactate accumulation Km, blood plasma glucose concentration at which the glycolytic rate was measured by monitoring the rate of glycolytic rate is half maximal cerebral lactate accumulation after total ischemia. Ische-[la~tate]~,,~, final postmortem brain lactate concentration mia was induced by cardiac arrest, and the rate of lactate MAP, mean arterial blood pressure formation was measured in vivo using proton nuclear mag-V, , , , maximum agonal glycolytic rate netic resonance spectroscopy. Before cardiac arrest, the blood plasma glucose concentration for individual piglets was adjusted to a specific value in the range 1-30 mM. The dependence of agonal glycolytic rate upon blood glucose concentration was analyzed for each age group, usingThe role of glucose status in immature animals exposed to the ~i~h~~l i~-~~~~~~ equation to evaluate v,,,, the max-hypoxic-ischemia insults is controversial (1). In adults, an eleimal rate of glucose utilization, and K~ the concentration vated blood glucose concentration during cerebral ischemia is of plasma glucose at which the half maximal rate of detrimental to the recovery of normal brain function and strucutilization occurs. V,,, for the two youngest age groups of ture. A detrimental role for elevated glucose is based on the piglets had significantly different ( p < 0.05) values presumption that there is excessive lactate production during pared with each other (1.38 f 0.17 and 1.92 f 0.64 pmol. hyperglycemic hypoxia-ischemia compared with when glucose is g -~, min-~, respectively) and with the two older groups of not elevated. Support for this comes from studies of juvenile animals (2.99 f 0.52 and 3.42 f 0.65 pmo1.g-' .min-', monkeys (2) and adult rats (3, 4) that were made hyperglycemic respectively). The Km values determined for the two young-before or during ischemia or anoxia and showed increased morphologic brain damage and poorer clinical recovery compared est age piglets. During combined anaerobic glycolysis, with glucose being converted to lactate and hypergl~cemia and severe ischemia, newborns will not be concurrent production of H+ (5, 7). Several clinical studies have levels lactate as as reported that adult stroke patients with elevated blood glucose 2-to 4-wk-old ~iglets. However, despite the differences in have a poorer prognosis than their normoglycemic counterparts glycolytic rates, all four age groups showed similar poten-(8). tials to generate high cerebral lactate concentrations. FurIn contrast, administration of glucose improves the "su...

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“…The number of gasps was counted from the stored image in reference to sharp deflections in the PZT-derived vibration signal. Gasps comprising double openings of the jaw (double or diphasic gasps) (Selle, 1944) were counted as two gasps in these experiments.…”

Section: Abrupt Ischemia Caused By Decapitationmentioning

confidence: 99%

Disruption of Kir6.2‐containing ATP‐sensitive potassium channels impairs maintenance of hypoxic gasping in mice

Miyake

Yamada

Kosaka

et al. 2007

Eur J of Neuroscience

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Hypoxic gasping emerges under severe hypoxia/ischemia in various species, exerting a life-protective role by assuring minimum ventilation even in loss of consciousness. However, the molecular basis of its generation and maintenance is not well understood. Here we found that mice lacking Kir6.2- but not Kir6.1-containing ATP-sensitive potassium (K(ATP)) channels [knockout (KO) mice] exhibited few gaSPS when subjected to abrupt ischemia by decapitation, whereas wild-type mice all exhibited more than 10 gaSPS. Under anesthesia, wild-type mice initially responded to severe hypoxic insult with augmented breathing (tachypnea) accompanied by sighs and subsequent depression of respiratory frequency. Gasping then emerged and persisted stably (persistent gasping); if the hypoxia continued, several gaSPS with distinct patterns appeared (terminal gasping) before cessation of breathing. KO mice showed similar hypoxic responses but both depression and the two types of gasping were of much shorter duration than in wild-type mice. Moreover, in the unanesthetized condition, the onset of terminal gasping in KO mice, which was always earlier than in wild-type mice, was unaltered by decreasing O(2) concentrations within the severe range (4.5-7.0%), whereas onset in wild-type mice became earlier in response to lowered O(2) concentrations. Thus, the mechanism responsible for regulating the hypoxic response in accordance with the severity of the hypoxia was dysfunctional in these KO mice, suggesting that Kir6.2-containing K(ATP) channels are critically involved in the maintenance rather than the generation of hypoxic gasping and depression of respiratory frequency.

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Influence of Glucose on the Gasping Pattern of Young Animals Subjected to Acute Anoxia

Cited by 22 publications

References 0 publications

Effects of antenatal dexamethasone and hyperglycemia on cardiovascular adaptation to asphyxia in preterm fetal sheep

Effects of antenatal dexamethasone and hyperglycemia on cardiovascular adaptation to asphyxia in preterm fetal sheep

The Effect of Age on Glucose-Modulated Cerebral Agonal Glycolytic Rates Measured In Vivo by 1H NMR Spectroscopy

Disruption of Kir6.2‐containing ATP‐sensitive potassium channels impairs maintenance of hypoxic gasping in mice

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