Sympathoadrenal responses to acute and chronic hypoxia in the rat.

Johnson, Tim; Young, James B.; Landsberg, Lewis

doi:10.1172/jci110876

Cited by 103 publications

(57 citation statements)

References 32 publications

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“…The first set of studies involved the determination of plasma catecholamine concentrations and cardiac sympathetic neuron activity by measurement of NE turnover in the neurons using [3H]-NE as the tracer substance. The methods used were modifications of techniques previously established in developing and adult rats by Landsberg and others (20)(21)(22)(23)(24) The pups were then placed in a wood chipbedded, covered clear plastic chamber with the air temperature maintained at 29°C by a convective heat source. The pups were studied for up to 120 min under normoxic conditions receiving room air or under hypoxic conditions receiving a gas mixture with an Fio2 of 0.09, Fico2 of 0.025, balanced with nitrogen, administered into the chamber at a flow rate of 2 literslmin.…”

Section: Methodsmentioning

confidence: 99%

Neonatal Sympathoadrenal Response to Acute Hypoxia: Impairment after Experimental Intrauterine Growth Retardation

Shaul

1989

Pediatr Res

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ABSTRACT. Svm~athoadrenal svstem function mav be Abbreviations altered following i;trauterine growth retardation (IUGR). We tested the hypothesis that the growth-retarded newborn rat pup has increased basal sympathoadrenal activity under normoxic conditions and a blunted sympathoadrenal response to acute hypoxia. IUGR was established by uterine artery ligation on d 18 of gestation in Sprague-Dawley rats. Growth-retarded pups were chosen as those whose birth wt was more than 2 x S D below the mean birth wt of control pups delivered to sham-operated dams. At 24 + 12 h of age cardiac sympathetic neuronal activity (CSNA) was determined by 3H-norepinephrine tracer and a-methyltyrosine techniques. Adrenal medullary catecholamine synthesis (CAT SYN) was measured by '4C-tyrosine precursor methods, and adrenal catecholamine release (CAT REL) was determined using a-methyl-tyrosine. IUGR and control pups were studied over a 120-min period of normoxia or hypoxia (Fioz = 0.09). Under normoxic conditions, the IUGR pups had increased CSNA and increased adrenal CAT SYN and CAT REL compared to controls. Adrenal CAT REL in normoxic IUGR pups was selective for epinephrine. In response to acute hypoxia, control pups had increased CSNA and increased adrenal CAT SYN and CAT REL compared to normoxic controls, with the proportion of norepinephrine and epinephrine released mimicking the ratio of the two amines in the adrenal. In contrast, in hypoxic IUGR pups CSNA and adrenal CAT SYN did not increase, and norepinephrine alone was released from the adrenal medulla. It is speculated that IUGR in the rat may lead to an acceleration of cardiac sympathetic innervation and premature establishment of neural regulation of adrenomedullary function, resulting in impaired sympathoadrenal responses to acute stresses such as hypoxia. Compromised sympathoadrenal system function in the IUGR fetus or newborn may contribute to the pathogenesis of the perinatal morbidities and the increased perinatal mortality known to occur in this high risk population. (Pediatr Res 25:466-472, 1989)

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Section: Methodsmentioning

confidence: 99%

Neonatal Sympathoadrenal Response to Acute Hypoxia: Impairment after Experimental Intrauterine Growth Retardation

Shaul

1989

Pediatr Res

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“…We speculate that chronic hypoxia alters CA pathways, increasing the susceptibility of these infants to later stressors. Adrenomedullary release of CA are important mediators of two common stressors that compromise the neonatal transition to extrauterine life: hypoxia and hypoglycemia (1)(2)(3)(4)(5). In the absence of the adrenal medulla, the fetus and newborn show maladaptive responses resulting in increased morbidity and mortality (6-8).…”

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Neonatal Stress: Effects of Hypoglycemia and Hypoxia on Adrenal Tyrosine Hydroxylase Gene Expression

DeCristofaro

LaGamma

1994

Pediatr Res

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Catecholamines (CA) are released from and resynthesized in the adrenal medulla in response to stress. In the mature animal, stimulus-secretion-synthesis coupling occurs through transsynaptic (neuronal) activity. In contrast, in the immature animal, before functional adrenal innervation, certain stressors (hypoglycemia and glycopenia) do not result in CA release. Additionally, it is not known whether release and biosynthesis remain coupled in the neonate as they are in the adult. Therefore, to evaluate whether neonatal stressors can induce CA biosynthesis at the genomic level "directly7' before function adrenal innervation, we studied the expression of the tyrosine hydroxylase (TH) gene, the rate-limiting enzyme in CA biosynthesis. Newborn rat pups were made either hypoxic, hypoglycemic, or cellularly glycopenic (2-deoxyglucose). Neither hypoxic stress nor insulin-induced hypoglycemic stress altered steady state levels of TH mRNA in the neonate. However, cellular glycopenia resulted in a significant 2-fold rise in TH mRNA levels ( p < 0.05). As expected, each of these stressors increased TH mRNA levels in the mature adult rat. Thus, neonatal hypoxia and hypoglycemia appear to require intact neurogenic impulse activity, whereas cellular glycopenia may "directly" induce TH RNA, perhaps through hormonal mechanisms. This developmental model allows for the analysis of mechanisms governing adrenal CA release separate from those governing biosynthesis at the level of TH RNA. Acute neonatal hypoxic stress results in adrenal CA release without increasing TH RNA. Intrauterine growth retardation from chronic prenatal hypoxemia results in neonatal CA depletion and decreased CA responsiveness. We speculate that chronic hypoxia alters CA pathways, increasing the susceptibility of these infants to later stressors. (Pediatr Res 36: 71F723, 1994) Abbreviations TH, tyrosine hydroxylase 2-DG, 2-deoxyglucose CA, catecholamine Adrenomedullary release of CA are important mediators of two common stressors that compromise the neonatal transition to extrauterine life: hypoxia and hypoglycemia (1-5). In the absence of the adrenal medulla, the fetus and newborn show maladaptive responses resulting in increased morbidity and mortality (6-8). Because functional innervation of the rat adrenal medulla occurs after the first postnatal week of life (9-ll), a developmental window exists whereby the direct effects of stressors can be examined, independent of neuronal impulse activity.Hypoxia, insulin-induced hypoglycemia, and 2-DGinduced glycopenia act transsynaptically to release adrenal C A in the adult (12-15). On the other hand, in the neonatal rat during the first week of life, hypoglycemic

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“…Excitatory effects on the sympathoadrenal function of acute hypoxia (NAHAS et al, 1954;BAUGH et al, 1959;FOWLER et al, 1961;BECKER and KREUZER, 1968;STEINSLAND et al, 1970;JOHNSON et al, 1983;ROSE et al, 1983) or hypercapnia and acidosis (TENNY, 1956;MILLAR,1960;LIGOU and NAHAS, 1960;NAHAS et al, 1960;MORRIS and MILLAR,1962;CANTU et a!., 1966;O'BRODovICH et a!.,1982;ROSE et al, 1983) have been established in both humans and experimental animals. However, in most studies, the adrenaline level in systemic blood was accepted as an index of the adrenomedullary activity.…”

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confidence: 99%

Hypoxia and hypercapnia increase the sympathoadrenal medullary functions in anesthetized, artificially ventilated rats.

et al. 1989

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Graded hypoxia (FETo2 14-6%) and hypercapnia (FETC2 6-10%), which were applied for 45 s and 2 min, respectively, to urethane anesthetized and artificially ventilated rats produced an increase in adrenal sympathetic efferent nerve activity in parallel with increases in adrenaline and noradrenaline secretion measured in the adrenal venous effluent. Percentage increases in adrenaline and noradrenaline were almost equal. In rats whose carotid sinus nerves (CSN) were bilaterally cut, hypoxia did not produce any effect on adrenal sympathetic nerve activity or catecholamine secretion. In contrast, excitatory adrenal nerve and catecholamine secretory responses to hypercapnia remained unchanged in CSN denervated rats. After severing a splanchnic nerve whose branches innervated the adrenal gland, while maintaining the resting level of catecholamine secretion by low-frequency stimulation of the peripheral end of the splanchnic nerve, hypoxia did not produce any increase in catecholamine secretion. Hypercapnia (FETCo2 8 and 10%), however, induced catecholamine secretion from denervated adrenal medulla, although the magnitude of the response was significantly lower than that in animals with adrenal nerve intact. It is concluded that hypoxia stimulates the adrenal medulla via the carotid chemoreceptor reflex whereas hypercapnia acts mainly via mechanisms besides carotid chemoreceptors such as central chemoreceptors with some direct stimulatory effect on the adrenal medulla. The functional significance of these dual mechanisms of sympathoadrenal excitation during hypoxia and hypercapnia is discussed.

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Sympathoadrenal responses to acute and chronic hypoxia in the rat.

Cited by 103 publications

References 32 publications

Neonatal Sympathoadrenal Response to Acute Hypoxia: Impairment after Experimental Intrauterine Growth Retardation

Neonatal Sympathoadrenal Response to Acute Hypoxia: Impairment after Experimental Intrauterine Growth Retardation

Neonatal Stress: Effects of Hypoglycemia and Hypoxia on Adrenal Tyrosine Hydroxylase Gene Expression

Hypoxia and hypercapnia increase the sympathoadrenal medullary functions in anesthetized, artificially ventilated rats.

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