Influence of Acute Hypoxia on Sympathectomized and Adrenalectomized Dogs

Nahas, Gabriel G.; Mather, George W.; Wargo, Jennifer; Adams, W. L.

doi:10.1152/ajplegacy.1954.177.1.13

Cited by 49 publications

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“…Experiments reported elsewhere (25) demonstrating a more pronounced effect of ganglionic blockade on NE turnover in hypoxic animals than control animals were consistent with a primary increase in sympathetic nerve impulse traffic accounting for the acceleration of NE turnover in hypoxia. Thus, 10.5% oxygen increased SNS activity in rat heart by day 3 of exposure and this effect persisted through day 14. Table I.…”

Section: Resultsmentioning

confidence: 80%

“…In human subjects acutely exposed to hypoxia, for example, both increased (2,3) or unchanged (4) catecholamine levels in plasma or urine have been observed. In animals, evidence for and against sympathoadrenal activation in acute hypoxia has similarly been presented (5)(6)(7)(8)(9)(10). Chronic hypoxia in man is associated with increased SNS activity (11,12), although many relevant studies were conducted at high altitude and are, therefore, complicated by cold exposure and physical exertion.…”

Section: Introductionmentioning

confidence: 99%

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Sympathoadrenal responses to acute and chronic hypoxia in the rat.

1983

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A B S T R A C T The sympathoadrenal responses to acute and chronic hypoxic exposure at 10.5 and 7.5% oxygen were determined in the rat. Cardiac norepinephrine (NE) turnover was used to assess sympathetic nervous system (SNS) activity, and urinary excretion of epinephrine (E) was measured as an index of adrenal medullary activity. The responses of the adrenal medulla and SNS were distinct and dependent upon the degree and duration of hypoxic exposure. Chronic hypoxia at 10.5% oxygen increased cardiac NE turnover by 130% after 3, 7, and 14 d of hypoxic exposure. Urinary excretion of NE was similarly increased over this time interval, while urinary E excretion was marginally elevated. In contrast, acute exposure to moderate hypoxia at 10.5% oxygen was not associated with an increase in SNS activity; in fact, decreased SNS activity was suggested by diminished cardiac NE turnover and urinary NE excretion over the first 12 h of hypoxic exposure, and by a rebound increase in NE turnover after reexposure to normal oxygen tension. Adrenal medullary activity, on the other hand, increased substantially during acute exposure to moderate hypoxia (2-fold increase in urinary E excretion) and severe hypoxia (>10-fold). In distinction to the lack of effect of acute hypoxic exposure (10.5% oxygen), the SNS was markedly stimulated during the first day of hypoxia exposure at 7.5% oxygen, an increase that was sustained throughout at least 7 d at 7.5% oxygen. These results demonstrate that chronic exposure to moderate and severe hypoxia increases the activity of the SNS and adrenal medulla, the effect being

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Section: Resultsmentioning

confidence: 80%

Section: Introductionmentioning

confidence: 99%

Sympathoadrenal responses to acute and chronic hypoxia in the rat.

1983

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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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“…In this respect, there is evidence for a direct effect of hypoxia on adrenal catecholamine release (especially when the sympathetic nervous system is compromised) in the foetal calf (Comline & Silver, 1966), the dog (Nahas et al, 1954;Hammill et al, 1979), the piglet (Lee et al, 1980) and the rat (Johnson et al, 1983). In addition, hypercapnia and acidosis also stimulate adrenal catecholamine release and when they occur together stimulation of the gland is even greater, whether or not there is accompanying hypoxia (Morris & Millar, 1962;Nahas et al, 1967).…”

Section: Discussionmentioning

confidence: 99%

Effect of artificial respiratory volume on the cardiovascular responses to an α₁‐ and an α₂‐adrenoceptor agonist in the air‐ventilated pithed rat

MacLean¹

1988

British J Pharmacology

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1 The effect of varying artificial respiratory volume (at a fixed rate of 54 min-) on cardiac output, its distribution and tissue blood flows were determined with tracer microspheres in control pithed rats or during pressor responses to either the a1-adrenoceptor agonist phenylephrine or the a2-agonist xylazine. Phenylephrine was investigated in the presence of propranolol (3 mg kg 1). The rats were pithed under halothane anaesthesia. 2 A respiratory volume of 15 ml kg-produced modest hypercapnia (Paco2 = 47 mmHg), hypoxia (Pao2 = 60 mmHg) and acidosis (pH = 7.35) relative to control animals respired at 20 ml kg1 (Paco2 = 32 mmHg; Pao2 = 77 mmHg; pH = 7.47). In rats respired at 15 ml kg 1, total peripheral resistance was lower, and cardiac output greater (due to increased stroke volume), than in the controls. Lowering respiratory volume reduced distribution of cardiac output to the kidneys, increased it to the large intestine and also increased blood flow through the gastrointestinal tract, skin and spleen. A respiratory volume of 30 ml kg-1 gave mild hypocapnia (Paco2 = 19 mmHg), hyperoxia (Pao2 = 101 mmHg) and alkalosis (pH = 7.59) compared to 20 ml kg'-but had no effect on cardiac output distribution or organ blood flow although heart rate was 29% greater at 30 ml kg-'. 3 Xylazine (500 pg bolus followed by lOOI gmin1 infusion) at all three respiratory volumes gave well-sustained mean pressor responses of 62-64 mmHg by increasing both total peripheral resistance and cardiac output (resulting from increased stroke volume). It increased the proportion of cardiac output passing to the liver, reduced that going to the spleen and gastrointestinal tract and increased cardiac, renal and hepatosplanchnic blood flows. 4 The secondary, relatively sustained, pressor effect of phenylephrine (5 pg bolus followed by 0.4 pg min1 infusion, i.v.) varied at the 3 respiratory volumes with mean values from 32 to 53 mmHg. This response was due to both increased total peripheral resistance and cardiac output (resulting from greater stroke volumes and/or heart rates). Phenylephrine increased the proportion of cardiac output passing to the gastrointestinal tract, heart, kidneys and hepatosplanchnic bed and increased cardiac, hepatosplanchnic, renal and gastrointestinal blood flows. 5 Respiratory volume had no effect on the cardiovascular effects of xylazine. However, respiratory volume modified the effects of phenylephrine on heart rate and changed the relative contributions of stroke volume and heart rate to the increased cardiac output. It also influenced the effects of phenylephrine on cardiac output distribution to the liver, epididimides and hepatosplanchnic bed and on blood flow through skeletal muscle and the large intestine. 6 Changes in respiratory volume of air ventilated pithed rats thus influence cardiac output, its distribution and regional blood flows. Such changes can also differently influence the responses of various vascular beds to phenylephrine whilst having no effect on their responses to xylazine.

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Influence of Acute Hypoxia on Sympathectomized and Adrenalectomized Dogs

Cited by 49 publications

References 0 publications

Sympathoadrenal responses to acute and chronic hypoxia in the rat.

Sympathoadrenal responses to acute and chronic hypoxia in the rat.

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

Effect of artificial respiratory volume on the cardiovascular responses to an α₁‐ and an α₂‐adrenoceptor agonist in the air‐ventilated pithed rat

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Influence of Acute Hypoxia on Sympathectomized and Adrenalectomized Dogs

Cited by 49 publications

References 0 publications

Sympathoadrenal responses to acute and chronic hypoxia in the rat.

Sympathoadrenal responses to acute and chronic hypoxia in the rat.

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

Effect of artificial respiratory volume on the cardiovascular responses to an α1‐ and an α2‐adrenoceptor agonist in the air‐ventilated pithed rat

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Effect of artificial respiratory volume on the cardiovascular responses to an α₁‐ and an α₂‐adrenoceptor agonist in the air‐ventilated pithed rat