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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Late-gestation fetal sheep respond to slow hemorrhage with increases in plasma concentrations of adrenocorticotropic hormone (ACTH), hydrocortisone, arginine vasopressin (AVP), and plasma renin activity (PRA) that correlate to the acidemia and hypercapnia also produced by hemorrhage. This study was designed to investigate the role of peripheral chemoreceptors in the mediation of these responses. Chronically catheterized fetal sheep were left intact or were subjected to bilateral section of cervical vagosympathetic trunks and carotid sinus nerves. At least 5 days after surgical preparation (between 121 and 138 days of gestation) fetuses were bled at a rate of 11 ml/10 min for 2 h. Denervated fetuses were studied with or without simultaneous infusion of phenylephrine. Denervation exaggerated the decrease in mean arterial pressure and arterial pH and the increase in arterial PCO2 during hemorrhage. Infusion of phenylephrine in the denervated fetuses prevented the decrease in blood pressure and reduced the magnitudes of changes in blood gases. Fetal plasma ACTH, hydrocortisone, and PRA responses to the hemorrhage were exaggerated in the denervated fetuses (not infused with phenylephrine) compared with the intact fetuses. Phenylephrine infusion attenuated the ACTH response and inhibited the AVP response but did not alter the PRA response. We conclude that the sectioned fibers are important for the maintenance of blood pressure and blood gases during hemorrhage and that the PRA, AVP, and ACTH responses to slow hemorrhage are not mediated by peripheral chemoreceptors.
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PMID:Reflex control of fetal arterial pressure and hormonal responses to slow hemorrhage. 173 13

The control of aldosterone secretion may be altered during acute changes in arterial blood gases. We studied the blood gas, plasma electrolyte, renin (PRA), adrenocorticotropic hormone (ACTH), and aldosterone (ALDO) responses to acute hypercapnia (4 and 8% CO2), acute hypocapnic hypoxia (10% O2), acute severe normocapnic hypoxia (7% O2-4% CO2), and acute hypercapnic hypoxia (7% O2-8% CO2) in conscious, cannulated Long-Evans rats. Normoxia resulted in normal levels of PRA (6.9 +/- 2.0 ng.ml-1.h-1), ACTH (96 +/- 32 pg/ml), and ALDO (10 +/- 3 ng/dl). Hypercapnia had no effect on PRA but did lead to an increase in ACTH (to 298 +/- 69 pg/ml) and ALDO (to 33 +/- 7 ng/dl) during 8% CO2 exposure. Normocapnic hypoxia resulted in a significant increase in ACTH (to 196 +/- 14 pg/ml) and ALDO (to 30 +/- 3 ng/dl). Hypercapnic hypoxia resulted in the greatest increases in PRA (to 30 +/- 2 ng.ml-1.h-1), ACTH (to 397 +/- 114 pg/ml), and ALDO (to 41 +/- 5 ng/dl). We conclude that in conscious rats 1) hypercapnia (less than 80 Torr) had no significant effect on PRA, 2) isocapnic, severe hypoxia (Po2 approximately 34 Torr) increased ACTH, and 3) the combination of hypercapnia and hypoxia was a very potent stimulus to PRA, ACTH, and ALDO. The ALDO responses to increases in endogenous ACTH and angiotensin II appear to be normal in conscious rats during acute hypoxia and/or hypercapnia.
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PMID:Renin, ACTH, and aldosterone during acute hypercapnia and hypoxia in conscious rats. 283 42

Previous studies have demonstrated that fetal adrenocorticotropic hormone (ACTH) and arginine vasopressin (AVP) are increased during periods of acidemia produced by infusion of acid intravenously or by acidemia secondary to hypovolemia. The purpose of this study was to quantify ACTH and AVP responses to hypercapnic acidemia and to test the role of the peripheral chemoreceptors in the control of these responses. Chronically catheterized fetal sheep were subjected to carotid sinus denervation and bilateral vagotomy or were studied intact. At least 5 days after surgery, fetuses were exposed to a 60-min period of normocapnia or hypercapnia, delivered via a polyethylene bag containing 5-8% CO2 in 21% O2 fitted over the head of the pregnant ewe. Hypercapnia significantly increased fetal arterial PCO2 to 55.2 +/- 1.8 and 55.9 +/- 2.2 mmHg and decreased arterial pH to 7.257 +/- 0.011 and 7.281 +/- 0.010 in intact and denervated fetuses, respectively. Fetal mean arterial blood pressure was decreased slightly in the denervated fetuses during hypercapnia. Fetal plasma AVP was increased in both groups equally, and plasma ACTH and cortisol were increased in the denervated fetuses only. Fetal heart rate was increased significantly in intact but not denervated fetuses. We conclude that respiratory acidemia is a mild stimulus to AVP secretion and that this response is not attenuated by peripheral chemodenervation.
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PMID:The adrenocorticotropic hormone and arginine vasopressin responses to hypercapnia in fetal and maternal sheep. 838 63

In fish, the catecholamine hormones adrenaline and noradrenaline are released into the circulation, from chromaffin cells, during numerous 'stressful' situations. The physiological and biochemical actions of these hormones (the efferent adrenergic response) have been the focus of numerous investigations over the past several decades. However, until recently, few studies have examined aspects involved in controlling/modulating catecholamine storage and release in fish. This review provides a detailed account of the afferent limb of the adrenergic response in fish, from the biosynthesis of catecholamines to the exocytotic release of these hormones from the chromaffin cells. The emphasis is on three particular topics: (1) catecholamine biosynthesis and storage within the chromaffin cells including the different types of chromaffin cells and their varying arrangement amongst species; (2) situations eliciting the secretion of catecholamines (e.g. hypoxia, hypercapnia, chasing); (3) cholinergic and non-cholinergic (i.e. serotonin, adrenocorticotropic hormone, angiotensin, adenosine) control of catecholamine secretion. As such, this review will demonstrate that the control of catecholamine storage and release in fish chromaffin cells is a complex processes involving regulation via numerous hormones, neurotransmitters and second messenger systems.
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PMID:The adrenergic stress response in fish: control of catecholamine storage and release. 982 12

Acute hypercapnia was studied to assess its potential as a noninvasive and simple test for evoking neuroendocrine, cardiovascular and psychological responses to stress in man. A single breath of four concentrations of carbon dioxide (CO(2)), 5%, 25%, 35% and 50%, was administered to nine healthy volunteers in a randomized, single-blind fashion. Although no adverse effects occurred, most subjects were unable to take a full inspired vital capacity breath of 50% CO(2). In response to the remaining exposures, subjective and somatic symptoms of anxiety increased in a dose-dependent manner. Unlike 5% and 25% CO(2), 35% CO(2) stimulated significant adrenocorticotropic hormone and noradrenaline release at 2 min and cortisol and prolactin release at 15 min following inhalation. This same dose also provoked a significant bradycardia that was followed by an acute pressor response. No significant habituation of psychological, hypothalamic-pituitary-adrenal (HPA) or cardiovascular responses following 35% CO(2) was seen when this dose was repeated after 1 week. A single breath of 35% CO(2) safely and reliably produced sympathetic and HPA axis activation and should prove a useful addition to currently available laboratory tests of the human stress response.
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PMID:Acute carbon dioxide exposure in healthy adults: evaluation of a novel means of investigating the stress response. 1504 56