Respiratory and neuroendocrine responses of piglets to hypoxia during postnatal development

Moss, Immanuela R.; Runold, Michael; Dahlin, Ingrid; Fredholm, Bertil B.; Nyberg, Fred; Lagercrantz, Hugo

doi:10.1111/j.1748-1716.1987.tb08273.x

Cited by 28 publications

(21 citation statements)

References 29 publications

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“…The baseline levels of VT and RF, blood gases, ABP and HR recorded in the 3-day-old, Saffan-anaesthetized piglets of the present study were comparable to those recorded by others in conscious or lightly sedated piglets of a similar age (Darnall, 1985;Moss, Runold, Dahlin, Fredholm, Nyberg & Lagercrantz, 1987;Darnall et al 1991;Rosen, Schecter, Mellins & Haddad, 1993). The levels of P°and ABP were markedly lower than those expected in adult mammals, but well within the range expected in a newborn mammal.…”

Section: Responses Evoked In Newborn Pigletsmentioning

confidence: 50%

Postnatal development of the pattern of respiratory and cardiovascular response to systemic hypoxia in the piglet: the roles of adenosine.

Elnazir

Marshall

Kumar

1996

The Journal of Physiology

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1. In 3-day-old and 3-week-old spontaneously breathing piglets anaesthetized with Saffan, we have studied ventilatory and cardiovascular responses evoked by 5 min periods of hypoxia (breathing 10 and 6% 02). 2. In 3-day-old piglets both 10 and 6% 02 evoked an increase followed by a secondary fall in ventilation, a gradual tachycardia and a renal vasoconstriction, with an increase in femoral blood flow that was attributable to femoral vasodilatation. Arterial blood pressure rose initially but fell towards control values by the 5th minute of hypoxia.3. The stable adenosine analogue 2-chloroadenosine (2-CA; 30 mg kg-' i.v.) evoked bradycardia and renal vasoconstriction, but had no effect on femoral vasculature. These responses were blocked by the adenosine receptor antagonist 8-phenyltheophylline (8-PT; 8 mg kg-1 i.v.). 8-PT also abolished the secondary fall in ventilation evoked by 10 and 6% 02 and the renal vasoconstriction evoked by 10 % 02, but had no effect on the tachycardia, or on the femoral vascular response. 4. By contrast, in 3-week-old piglets both 10 and 6% 02 evoked a sustained increase in ventilation, tachycardia and a rise in arterial pressure with renal vasoconstriction, but no change in renal blood flow and substantial femoral vasodilatation with an increase in femoral blood flow. 2-CA evoked bradycardia and renal vasoconstriction, as in 3-day-old piglets, but also evoked pronounced femoral vasodilatation. 8-PT blocked these responses and the hypoxia-induced femoral vasodilatation, but had no significant effect on other components of the hypoxia-induced response. 5. We propose that there is postnatal development of the ventilatory and cardiovascular responses evoked by systemic hypoxia and of the role of locally released adenosine in these responses: at 3 days, adenosine released within the central nervous system and within the kidney is a major contributor to the secondary fall in ventilation and renal vasoconstriction, respectively, whereas at 3 weeks, adenosine makes little contribution to the ventilatory response, or renal vasoconstriction, but is largely responsible for hypoxia-induced vasodilatation in skeletal muscle.

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Section: Responses Evoked In Newborn Pigletsmentioning

confidence: 50%

Postnatal development of the pattern of respiratory and cardiovascular response to systemic hypoxia in the piglet: the roles of adenosine.

Elnazir

Marshall

Kumar

1996

The Journal of Physiology

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“…There may be other neurochemicals, such as adenosine, opioids, and prostaglandins, that play a role in the ventilatory response to hypoxia during development (11,37). Adenosine is an inhibitory amino acid that has been shown to depress respiration in early life.…”

Section: Discussionmentioning

confidence: 99%

Brainstem Amino Acid Neurotransmitters and Ventilatory Response to Hypoxia in Piglets

et al. 2008

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ABSTRACT:The ventilatory response to hypoxia is influenced by the balance between inhibitory (GABA, glycine, and taurine) and excitatory (glutamate and aspartate) brainstem amino acid (AA) neurotransmitters. To assess the effects of AA in the nucleus tractus solitarius (NTS) on the ventilatory response to hypoxia at 1 and 2 wk of age, inhibitory and excitatory AA were sampled by microdialysis in unanesthetized and chronically instrumented piglets. Microdialysis samples from the NTS area were collected at 5-min intervals and minute ventilation (V E ), arterial blood pressure (ABP), and arterial blood gases (ABG) were measured while the animals were in quiet sleep. A biphasic ventilatory response to hypoxia was observed in wk 1 and 2, but the decrease in V E at 10 and 15 min was more marked in wk 1. This was associated with an increase in inhibitory AA during hypoxia in wk 1. Excitatory AA levels were elevated during hypoxia in wk 1 and 2. Changes in ABP, pH, and ABG during hypoxia were not different between weeks. These data suggest that the larger depression in the ventilatory response to hypoxia observed in younger piglets is mediated by predominance of the inhibitory AA neurotransmitters, GABA, glycine, and taurine, in the NTS. T he difference in ventilatory response to hypoxia between neonatal and adult subjects is well documented (1-3). The ventilatory response to hypoxia during the neonatal period is characterized by an increase in ventilation (1-2 min) followed by a decrease in minute ventilation (V E ) to values below or close to baseline levels. In contrast, a more sustained ventilatory response to hypoxia is described in adults (4). The initial increase in ventilation is mediated by the peripheral chemoreceptors, whereas subsequent changes are centrally mediated (5,6).The change from the neonatal to the adult ventilatory response is thought to occur during early postnatal life in most species (7,8). Previous studies have demonstrated that this change in the ventilatory response occurs within the first 1-2 wk of life in piglets (9 -11).Several mechanisms may be responsible for the ventilatory depression observed during hypoxia soon after birth. These include deterioration in lung mechanics (12), changes in metabolism (13), and a predominance of inhibitory over excitatory neurotransmitters in the CNS (14). Previous studies from our laboratory have demonstrated a role for amino acids (AA) in the hypoxic ventilatory response in newborn animals (5,(15)(16)(17). The balance between excitatory AA, such as glutamate and aspartate, and inhibitory AA, such as GABA and glycine, may influence the ventilatory response to hypoxia in the neonatal and postnatal periods. In newborn animals, it has been suggested that the increase in the release of the CNS inhibitory amino acid neurotransmitter GABA may be responsible for the hypoxic ventilatory depression (9,16,18). However, it is also possible that the biphasic response in ventilation during hypoxia may be due to a reduction in the release of central excitatory AA neur...

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“…Although catecholamines have been shown to affect respiration via peripheral chemosensory mechanisms [18], the presence of dopamine and norepinephrine cell bodies in the brainstem suggests a central respiratory control mechanism involving these neurotransmitters [19]. McCrimmon and Lalley [20] showed that clonidine, an · 2 -adrenergic agonist, decreased phrenic nerve activity in chloralose-anesthetized cats, in which the peripheral ventilatory input was removed by sectioning the vagus, aortic and carotid sinus nerves.…”

Section: Discussionmentioning

confidence: 99%

Effect of Norepinephrine on Fetal Breathing in Sheep

Weintraub

Alvaro²,

Baier³

et al. 1997

Neonatology

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We tested the hypothesis that the surge of norepinephrine at birth is associated with the establishment of continuous breathing. Therefore, we studied whether the administration of norepinephrine could enhance fetal breathing during administration of oxygen, or 100% O₂ plus cord occlusion, and if phenoxybenzamine would reverse these changes. Fetal sheep were instrumented in late gestation to measure electrocortical activity and diaphragmatic electromyography. These parameters and blood gases were measured before and during in utero administration of nitrogen, 100% O₂, 100% O₂ plus umbilical cord occlusion, and subsequently during umbilical reperfusion and recovery. Nine fetuses (14 experiments) received continuous norepinephrine (0.13 µg/kg/min) throughout the experiment while 9 other fetuses (18 experiments) underwent the same treatment without the hormonal infusion. We found that norepinephrine inhibited the breathing induced by 100% O₂ plus cord occlusion, despite a significant increase in the duration of low-voltage electrocortical activity; phenoxybenzamine reverted these changes. The findings suggest that the surge of norepinephrine at birth is probably not the primary mechanism for establishment of continuous breathing.

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Respiratory and neuroendocrine responses of piglets to hypoxia during postnatal development

Cited by 28 publications

References 29 publications

Postnatal development of the pattern of respiratory and cardiovascular response to systemic hypoxia in the piglet: the roles of adenosine.

Postnatal development of the pattern of respiratory and cardiovascular response to systemic hypoxia in the piglet: the roles of adenosine.

Brainstem Amino Acid Neurotransmitters and Ventilatory Response to Hypoxia in Piglets

Effect of Norepinephrine on Fetal Breathing in Sheep

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