The Adrenal Gland and the Cardiovascular Changes in Acute Anoxic Anoxia in Dogs

Baugh, Christopher W.; Cornett, Rachel; Hatcher, John M.

doi:10.1161/01.res.7.4.513

Cited by 26 publications

(12 citation statements)

References 17 publications

(6 reference statements)

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“…First, such concentrations have been assayed during hypoxemia by a number of investigators in previous studies and have been found to be elevated. This increase in adrenergic activity appears to be responsible for the augmentation of heart rate, contractility, and cardiac output in those investigations (3,4,22,23,24,25). Second, other investigators have described recently a poor correlation between circulating catecholamine concentrations and changes in contractility (8).…”

Section: Resultsmentioning

confidence: 79%

Augmentation of Cardiac Output with Intravenous Catecholamines in Unanesthetized Hypoxemic Newborn Lambs

et al. 1987

Pediatr Res

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Section: Resultsmentioning

confidence: 79%

Augmentation of Cardiac Output with Intravenous Catecholamines in Unanesthetized Hypoxemic Newborn Lambs

et al. 1987

Pediatr Res

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“…Thus, two different mechanisms of adrenal medullary excitation by hypoxia or hypercapnia may potentiate the final catecholamine secretory effect during asphyxia. These different mechanisms responsible for adrenomedullary excitation are apparently meaningful as a biological evolutionary adaptation developed to secure vital bodily reactions (BAUGH et al, 1959;LEE and DOWNING, 1983). SEIDLER and SLOTKIN (1986) have recently shown that the normal adrenomedullary response to hypoxia correlates with the survival rate of neonatal mammals.…”

Section: Discussionmentioning

confidence: 99%

“…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.…”

mentioning

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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“…On the other hand, Nahas, poxemia, but cardiac output measurements were not Mather, Wargo, and Adams (9) and Baugh, Cornett, made. The roles of catecholamines and beta-adrenergic and Hatcher (10) found that the cardiac output rise receptors in the regulation of cardiac output during was abolished by adrenalectomy. The reason for the hypoxemia have been studied with conflicting results.…”

Section: Methodsmentioning

confidence: 99%

Effects of Splenectomy and Beta-Adrenoceptor Blockade on Cardiac Output Response to Acute Hypoxemia

Liang¹,

Huckabee²

1973

J. Clin. Invest.

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A B S T R A C T Acute hypoxemia produced by the inhalation of 8% and 5% oxygen increased cardiac output in intact anesthetized dogs by 38% and 62%, respectively. Although practolol, a cardioselective betaadrenergic blocking agent, reduced the increase in cardiac output in dogs subjected to severe hypoxemia (5% 02 breathing) from 62% to 43%, it only slightly reduced the cardiac output rise in dogs subjected to moderate hypoxemia (8% 02 breathing). Splenectomy, on the other hand, abolished the increase in cardiac output produced by moderate hypoxemia except for a small initial rise, but it reduced the increase in cardiac output during severe hypoxemia only to 37%. The entire increase, except for a small initial rise, disappeared only when splenectomized dogs were pretreated with practolol. Sham operation did not affect the cardiac output response to hypoxemia. It is concluded that an intact spleen is required for a significant portion of the increased cardiac output that occurs during both moderate and severe hypoxemia and that catecholamines do not participate in the regulation of cardiac output unless severe hypoxemia occurs.

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The Adrenal Gland and the Cardiovascular Changes in Acute Anoxic Anoxia in Dogs

Cited by 26 publications

References 17 publications

Augmentation of Cardiac Output with Intravenous Catecholamines in Unanesthetized Hypoxemic Newborn Lambs

Augmentation of Cardiac Output with Intravenous Catecholamines in Unanesthetized Hypoxemic Newborn Lambs

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

Effects of Splenectomy and Beta-Adrenoceptor Blockade on Cardiac Output Response to Acute Hypoxemia

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