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

The marine dogfish (Squalus acanthias) and the seawater-adapted rainbow trout (Oncorhynchus mykiss) were exposed to acute environmental hypercapnia or hypoxia to evaluate (i) the dynamics of catecholamine release into the circulation and (ii) the impact of catecholamine release on gill ventilation and blood oxygen transport. This comparison was undertaken to test the hypothesis that the pattern and consequences of catecholamine release differ in the two species according to the presence or absence of a Root effect and a red blood cell (rbc) ss-adrenergic response. Hypercapnia and hypoxia elicited marked increases in plasma catecholamine levels in the trout but not in the dogfish. In the trout, catecholamine release occurred abruptly during hypoxia when arterial PO2 (PaO2) decreased below 2.7 kPa. In the dogfish, plasma catecholamine levels remained stable during hypoxia even when PaO2 fell below 2.0 kPa. Trout and dogfish displayed pronounced hyperventilatory responses during both hypercapnia and hypoxia. In trout, the hyperventilatory response consisted of an increase in ventilation amplitude (estimated by opercular cavity pressure changes) with no change in ventilation frequency (fv), whereas in the dogfish, both amplitude (estimated by spiracular cavity pressure changes) and fv increased significantly. The use of an extracorporeal circulation and frequent blood sampling demonstrated that plasma catecholamine levels and ventilation amplitude were not correlated during hypoxia in either species. During hypercapnia in trout, the bolus injection of a catecholamine cocktail (final nominal circulating levels 200 nmol l-1 adrenaline, 50 nmol l-1 noradrenaline) caused a rapid (within 2 min) 33 % reduction in ventilation amplitude that persisted for 3 min; fv was unaffected. This hypoventilatory response occurred concurrently with activation of rbc Na+/H+ exchange and an increase in arterial blood O2 content (CaO2) and O2 specifically bound to haemoglobin (O2/Hb). During hypoxia in trout, a similar injection of catecholamines activated rbc Na+/H+ exchange and increased O2/Hb yet was without effect on ventilation amplitude or fv. In dogfish during hypercapnia or hypoxia, injection of a catecholamine cocktail (final nominal circulating levels 125 nmol l-1 adrenaline, 125 nmol l-1 noradrenaline) caused slight but significant reductions in fv (3-4 min-1) without affecting ventilation amplitude. Catecholamine injections did not affect blood oxygen transport in dogfish. The results demonstrate significant differences in the nature of catecholamine release in dogfish and trout that may reflect, in part, the absence of a Root effect and rbc adrenergic Na+/H+ exchange in the elasmobranch. The present data do not support the hypothesis that circulating catecholamines play a major role in controlling breathing during hypoxia or hypercapnia.
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PMID:Consequences of catecholamine release on ventilation and blood oxygen transport during hypoxia and hypercapnia in an elasmobranch Squalus acanthias and a teleost Oncorhynchus mykiss 932 17

1. The placental vascular bed is normally fully dilated. Therefore, changes in vascular resistance elsewhere in the body can affect uteroplacental blood flow (UBF). For example, antihypertensive drugs, such as diazoxide, hydralazine and the angiotensin-converting enzyme inhibitor captopril, cause falls in arterial pressure and, hence, in UBF. 2. Angiotensin II (AngII), prostacyclin and nitric oxide (NO) all influence uteroplacental vascular tone. Angiotensin II in a pharmacological dose (62.5 micrograms/h) had a biphasic effect on UBF in the sheep. Initially, there was a rise in UBF as pressure rose; however, by 16-24 h, UBF had fallen. The AngII-induced fall in UBF caused severe foetal hypoxia and hypercapnia. 3. Prostacyclin may protect the uteroplacental circulation from vasoconstrictors such as AngII, as the vasoconstrictor effect of AngII in the uteroplacental circulation is enhanced following indomethacin. 4. Oestrogen-induced uterine artery vasodilation is nitrergic dependent. As well, nitrergic nerves alter the responsiveness of pregnant uterine arteries to noradrenaline. 5. Thus, both systemic and local factors are important in the control of UBF and in promoting foetal health and growth.
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PMID:Effects of drugs on uteroplacental blood flow and the health of the foetus. 936 71

In fishes, catecholamines increase red blood cell intracellular pH through stimulation of a sodium/proton (Na+/H+) antiporter. This response can counteract potential reductions in blood O2 carrying capacity (due to Bohr and Root effects) when plasma pH and intracellular pH decrease during hypoxia, hypercapnia, or following exhaustive exercise. Tuna physiology and behavior dictate exceptionally high rates of O2 delivery to the tissues often under adverse conditions, but especially during recovery from exhaustive exercise when plasma pH may be reduced by as much as 0.4 pH units. We hypothesize that blood O2 transport during periods of metabolic acidosis could be especially critical in tunas and the response of rbc to catecholamines elevated to an extreme. We therefore investigated the in vitro response of red blood cells from yellowfin tuna (Thunnus albacares) and skipjack tuna (Katsuwonus pelamis) to catecholamines. Tuna red blood cells had a typical response to catecholamines, indicated by a rapid decrease in plasma pH. Amiloride reduced the response, whereas 4,4'diisothiocyanatostilbene-2,2'-disulphonic acid enhanced both the decrease in plasma pH and the increase in intracellular pH. Changes in plasma [Na+], [Cl-], and [K+] were consistent with the hypothesis that tuna red blood cells have a Na+/H+ antiporter similar to that described for other teleost red blood cells. Red blood cells from both tuna species were more responsive to noradrenaline than adrenaline. At identical catecholamine concentrations, the decrease in plasma pH was greater in skipjack tuna blood, the more active of the two tuna species. Based on changes in plasma pH, the response of red blood cells to catecholamines from both tuna species was less than that of rainbow trout (Oncorhynchus mykiss) red blood cells, but greater than that of cod (Gadus morhua) red blood cells. Noradrenaline had no measurable influence on the O2 affinity of skipjack tuna blood and only slightly increased the O2 affinity of yellowfin tuna blood. Our results, therefore, do not support our original hypothesis. The catecholamine response of red blood cells from high-energy-demand teleosts (i.e., tunas) is not enhanced compared to other teleosts. There are data on changes in cardio-respiratory function in tunas caused by acute hypoxia and modest increases in activity, but there are no data on the changes in cardio-respiratory function in tunas accompanying the large increases in metabolic rate seen during recovery from exhaustive exercise. However, we conclude that during those instances where high rates of O2 delivery to the tissues are needed, tunas' ability to increase cardiac output, ventilation volume, blood O2 carrying capacity, and effective respiratory (i.e., gill) surface area are probably more important than are the responses of red blood cells to catecholamines. We also use our data to investigate the extent of the Haldane effect and its relationship to blood O2 and CO2 transport in yellowfin tuna. Yellowfin tuna blood shows a large Haldane effect; intracellular pH increases 0.20 units during oxygenation. The largest change in intracellular pH occurs between 40-100% O2 saturation, indicating that yellowfin tuna, like other teleosts, fully exploit the Haldane effect over the normal physiological range of blood O2 saturation.
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PMID:Responses of the red blood cells from two high-energy-demand teleosts, yellowfin tuna (Thunnus albacares) and skipjack tuna (Katsuwonus pelamis), to catecholamines. 974 21

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

The effect of normoxia, hypoxia and hypercapnia on the extracellular pH, partial pressure carbon dioxide (pCO2), partial pressure oxygen (pO2) and HCO3- levels after noradrenaline treatment of Rana balcanica erythrocytes, was investigated. Noradrenaline caused a significant reduction of the extracellular pH which may have been due to the activation of red blood cell Na+/H+ exchange. Significant falls in the partial extracellular pressure of CO2 and O2 were evident. The initial reduction in extracellular pCO2 and pO2 was followed by a rise reflecting the desensitization of the Na+/H+ exchange after 15 min of hormone stimulation. Both hypercapnia and hypoxia increased the magnitude of these changes in relation to normoxia, although the greatest changes were observed under hypercapnic conditions. The involvement of alpha 1 receptors in regulating the concentration of respiratory gases after catecholamine stimulation was demonstrated. It is suggested that these responses increased the effectiveness of gas transfer over the respiratory surfaces.
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PMID:Influence of noradrenaline on the respiratory status of Rana balcanica red cell suspension under normoxia, hypoxia and hypercapnia: alpha 1-receptor involvement. 1047 27

The objective of this study was to assess the blood pressure pattern in patients with nasal polyposis. Twenty-seven patients with nasal polyposis (18 males and 9 females), ranging in age from 15 to 72 years (mean 37.1 years) were eligible for inclusion in the study. All patients were hospitalized overnight before surgery. After the basal blood pressure measurements were taken, non-invasive ambulatory blood pressure monitoring was carried out. Oxygen saturation was measured via a finger probe and venous blood sampling was taken for catecholamine level during the full night. All measurements were repeated 4 months after nasal surgery. Mean values for nocturnal decline in blood pressure and heart rate before surgery were less marked than those measured after surgery. Mean decline values (+/- SD) were; 4.6 +/- 2.4 mmHg for systolic blood pressure, 5.8 +/- 3.8 mmHg for diastolic blood pressure, and 7.9 +/- 3.9 beats/min for heart rate before surgery, 9.3 +/- 2.8 mmHg, 8.5 +/- 4.1 mmHg and 10.4 +/- 4.3 beats/min after surgery (p < 0.01), respectively. Whereas mean and minimum SaO2 (%) significantly increased (p < 0.01), catecholamine levels decreased (p < 0.05 for adrenaline, p < 0.01 for noradrenaline) after surgery. A correlation was found between BMI and blood pressure as well as between duration of obstruction and blood pressure. Patients who snored had higher blood pressure values than those who did not. Our data show that in cases of nasal polyposis, hypoxia, hypercapnia, snoring, and sleep disorders may develop and persons with nasal polyposis and snoring have an increased risk of hypertension and loss of nocturnal decline in blood pressure.
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PMID:Loss of nocturnal decline of blood pressure in patients with nasal polyposis. 1059 94

Stretch of the rat mesenteric artery ring pretreated with noradrenaline evoked a myogenic response consisting of the fast and slow phases which were maximal at about 3.5 and 45.1 s after the stretch, resp. Hypercapnic acidosis inhibited both phases of the response. Role of Ca2+ in origin of the two phases is discussed.
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PMID:[Myogenic reactions of the rat isolated mesenteric artery: effect of acidosis and the primary vessel tone]. 1129 8

In recent years, immense progress has been made in understanding central chemosensitivity at the cellular and functional levels. Combining molecular biological techniques (early gene expression as an index of cell activation) with neurotransmitter immunohistochemistry, new information has been generated related to neurochemical coding in chemosensory cells. We found that CO(2) exposure leads to activation of discrete cell groups along the neuraxis, including subsets of cells belonging to monoaminergic cells, noradrenaline-, serotonin-, and histamine-containing neurons. In part, they may play a modulatory role in the respiratory response to hypercapnia that could be related to their behavioral state control function. Activation of monoaminergic neurons by an increase in CO(2)/H(+) could facilitate respiratory related motor discharge, particularly activity of upper airway dilating muscles. In addition, these neurons coordinate sympathetic and parasympathetic tone to visceral organs, and participate in adjustments of blood flow with the level of motor activity. Any deficit in CO(2) chemosensitivity of a network composed of inter-related monoaminergic nuclei might lead to disfacilitation of motor outputs and to failure of neuroendocrine and homeostatic responses to life-threatening challenges (e.g. asphyxia) during sleep.
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PMID:Monoaminergic neurons, chemosensation and arousal. 1173 54

The objective of the present study was to evaluate the respiratory effects of cannabinoids and their influence on cardiovascular homeostasis.In spontaneously breathing urethane-anaesthetised rats, intravenous injection of the two synthetic cannabinoid receptor agonists WIN55212-2 and CP55940 strongly and dose-dependently lowered mean arterial pressure, heart rate and the plasma noradrenaline concentration. The cardiovascular depressive effects were associated with a large decrease in respiratory rate, hypoxia, hypercapnia and blood acidosis. All depressor effects of WIN55212-2 were abolished by the selective CB(1) cannabinoid receptor antagonist SR141716A. The bradycardia elicited by WIN55212-2 was inhibited by the muscarinic acetylcholine receptor antagonist methylatropine. The natural agonist Delta(9)-tetrahydrocannabinol also elicited cardiovascular and respiratory depression. In contrast, WIN55212-3, an enantiomer of WIN55212-2 lacking affinity for cannabinoid receptors, had no effect. The cannabinoid-evoked decreases in blood pressure and heart rate were much more pronounced in spontaneously breathing than in artificially ventilated urethane-anaesthetised rats. In contrast, the plasma noradrenaline concentration was lowered equally in both preparations. Our results show that activation of CB(1) cannabinoid receptors not only induces cardiovascular depression, but also markedly impairs ventilation. The second major finding of the present study is that the respiratory depression evoked by cannabinoids largely amplifies the cardiovascular depression.
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PMID:Analysis of the respiratory effects of cannabinoids in rats. 1368 88

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


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