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

Graded hypoxia (FETO2 14-6%) and hypercapnia (FETCO2 6-10%), which were applied for 45s 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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PMID:Hypoxia and hypercapnia increase the sympathoadrenal medullary functions in anesthetized, artificially ventilated rats. 251 41

To evaluate the effects of succinylcholine on cardiac arrhythmias and serum levels of potassium and catecholamines, dogs with hypoxia alone and with hypoxia and hypercarbia were studied during anesthesia with halothane or enflurane. After the injection of succinylcholine (0.3 mg/kg), cardiac arrhythmias occurred in all halothane:hypoxia dogs and in 70% of dogs given halothane during hypoxia:hypercarbia. No dogs given enflurane anesthesia developed arrhythmias. Serum potassium levels increased significantly 3 and 5 min after succinylcholine in all groups. Serum epinephrine levels increased in the halothane-hypoxia:hypercarbia and enflurane:hypoxia groups and, after the injection of succinylcholine, epinephrine levels increased further in dogs in the halothane:control, halothane:hypoxia, halothane-hypoxia:hypercarbia, enflurane:hypoxia, and enflurane-hypoxia:hypercarbia groups. Norepinephrine levels increased with enflurane-hypoxia:hypercarbia and after the succinylcholine in the halothane:hypoxia, halothane-hypoxia:hypercarbia, and enflurane-hypoxia:hypercarbia groups. The results suggest that succinylcholine induces arrhythmias by sympathetic stimulation and that halothane sensitizes the myocardium to arrhythmias at the same levels of serum catecholamines and potassium in the presence of hypoxia or hypoxia:hypercarbia more than does enflurane.
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PMID:Mechanisms of succinylcholine-induced arrhythmias in hypoxic or hypoxic:hypercarbic dogs. 368

The effects of pargyline administration during three days on male rats for stress reaction caused by hypercapnia, taking into account the contents of noradrenaline in the left auricle, the right auricle, the ventricle, the spleen and the hypothalamus have been studied. The stress by CO2 only produces a significant depletion of noradrenaline at the hypothalamus level. The administration of pargyline (50 mg/kg/day) induces significant increases in the content of noradrenaline in all the tissues. The increases in noradrenaline content are greater when the pargyline is given before the stress.
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PMID:[Effect of pargyline on the response to CO2 stress]. 400 36

1. Two unstable high molecular weight toxins have been isolated from tentacles of Chironex fleckeri by exclusion chromatography. Both are cardiotoxic; the lower molecular weight fraction is also a potent haemolysin.2. Both toxins reduce the rate, amplitude of contraction and coronary flow in the isolated, perfused guinea-pig heart. Relative to the mouse lethal dose the haemolytic fraction is less potent in this preparation than the purely cardiotoxic fraction.3. Both toxins cause a rise in arterial pressure in anaesthetized rats and rabbits by a direct action on the vascular musculature. This is followed by hypotension, bradycardia and cardiac irregularity. An increase in respiratory rate is followed by apnoea of variable duration, which is associated with a rise in arterial pressure. Animals frequently show arterial pressure oscillations with periods of apnoea interspersed with hyperpnoea.4. The carotid occlusion reflex is depressed during hypotensive periods after both toxins, although (-)-noradrenaline can still elicit a marked pressor response. Bilateral cervical vagotomy has but little effect on the response to either toxin, save to prevent hyperpnoea, but radical denervation of sinoaortic afferents reduces the arterial pressure fall after the initial hypertensive response, suggesting that this fall is due to a combination of baroreceptor stimulation and a fall in cardiac output. Blood pressure oscillations are still seen, possibly due to central stimulation by hypercapnia.5. Interference with the efferent arm of the vasomotor reflex arc with hexamethonium, bretylium or phenoxybenzamine either abolishes or markedly reduces the blood pressure oscillations without affecting the initial hypertensive response.6. The cardiovascular effects of the two toxins are thought to be due to direct vasoconstriction, cardiotoxicity, baroreceptor stimulation and possibly depression of the vasomotor centre. The resultant disordering of the feed-back system regulating vasomotor tone leads to the characteristic arterial pressure oscillations.
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PMID:Cardiovascular effects of toxins isolated from the cnidarian Chironex fleckeri Southcott. 439 29

1. In anaesthetized pregnant rabbits near term, cardiac output and its distribution were measured by injection of isotope-labelled microspheres. Hypocapnia (mean arterial P(CO) (2) 18 mm Hg), induced by intermittent positive pressure hyperventilation, caused a 43% reduction in maternal placental blood flow, attributed mainly to vasoconstriction. Myometrial flow was not significantly changed.2. Moderate hypercapnia (mean arterial P(CO) (2) 46 mm Hg) caused no change in placental flow, compared with observations made while breathing air spontaneously (P(CO) (2) 31 mm Hg).3. Intravenous infusions of adrenaline or noradrenaline 1 mug/kg. min caused maternal placental vasoconstriction.4. During the especially warm summer of 1969, there was a mean 46% reduction in maternal placental blood flow in pregnant rabbits near term, breathing room air spontaneously with normal blood gas values and rectal temperatures. This was associated with an increase in the number of runts and dead foetuses.
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PMID:The effect of hyperventilation on maternal placental blood flow in pregnant rabbits. 456 82

1. Ventricular ectopic beats were recorded in eight of thirteen conscious horses following the intravenous administration of adrenaline in doses of 3 mug/kg. Following pre-treatment with either atropine sulphate (0.1 mg/kg) or propranolol hydrochloride (0.1 mg/kg), the same dose level of adrenaline failed to produce ventricular ectopic beats.2. Halothane anaesthesia sensitized the equine heart to the arrhythmogenic actions of adrenaline; the incidence and duration of ventricular arrhythmias being greater than in conscious animals. In comparison with the findings in conscious horses, ether anaesthesia appeared to protect the heart against adrenaline-induced arrhythmias.3. From a comparison of the arrhythmogenic, chronotropic and pressor actions of adrenaline, noradrenaline and isoprenaline during halothane anaesthesia, it was concluded that sensitization to the arrhythmogenic actions of catecholamines resulted primarily from the action of halothane on the ventricle. The results also indicated that the pressor responses to catecholamines during halothane anaesthesia probably played some part in the genesis of arrhythmias.4. No "spontaneous" ventricular arrhythmias were recorded in twenty-four horses anaesthetized with halothane or in sixteen animals under ether anaesthesia.5. The available evidence indicates that a moderate to fairly severe degree of hypercapnia produced little increase in sympathetic control of the myocardium during halothane anaesthesia; the absence of irregularities in ventricular rhythm during halothane anaesthesia were attributed to this factor.
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PMID:Influence of halothane and catecholamines on heart rate and rhythm in the horse. 542 92

One-day-old rats were exposed to a gas mixture of 15% CO2-21% O2-64% N2 for a 30-min period. Monoamine synthesis in whole brain was measured during, and at various intervals after, hypercapnia by estimating the accumulation of dihydroxyphenylalanine (DOPA) and 5-hydroxytryptophan (5-HTP) after inhibition of aromatic L-amino-acid decarboxylase with NSD 1015. Endogenous concentrations of tyrosine, dopamine (DA), noradrenaline (NA), tryptophan, 5-hydroxytryptamine (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) were measured at the same intervals. Exposure to CO2 induced an increased synthesis of catecholamines and 5-HT. Further, an increase in DA concentration was seen during hypercapnia, while NA and 5-HT were unchanged. After the CO2 exposure the increased in vivo synthesis rates of catecholamines and 5-HT were rapidly normalized, as was the endogenous DA concentration. A slight increase in 5-HT and 5-HIAA concentrations was seen immediately after CO2 exposure. These results indicate that in neonatal animals, hypercapnia induces changes in central monoamine neurons, primarily an increased synthesis. These alterations may be relevant to some physiological changes seen during CO2 exposure, such as the alteration in central respiratory performance.
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PMID:Monoamine synthesis and concentration in neonatal rat brain during hypercapnia and recovery. 612 54

To determine the importance of dopamine and noradrenaline as neurotransmitters during chemoreception in the cat carotid body we investigated the contents of both compounds as well as the activity of dopamine-beta-hydroxylase (DBH) under different arterial PO2 and PCO2 conditions. The superior cervical ganglion was used as a control organ. In the carotid body and the ganglion an inverse relationship exists between the catecholamine content and the DBH activity. The carotid body has a high catecholamine content with a low DBH activity whereas the superior cervical ganglion has a low catecholamine content and high DBH activity. Hypercapnia did not produce any significant change in the catecholamine content or in the DBH content of the carotid body. However, in comparison with hyperoxia, hypoxia produced a significant change (p less than 0.05) in the noradrenaline content without changing the DBH activity. The dopamine content under these conditions did not change significantly. The results may indicate that the high catecholamine content of the carotid body is the result of a high retention and/or low rate of degradation rather than of a high rate of synthesis.
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PMID:Dopamine-beta-hydroxylase activity of the cat carotid body under different arterial O2 and CO2 conditions. 641 72

In Wistar rats exposed during one hour to mixtures of oxygen and carbon dioxide producing hypoxia, hypercapnia, hyperoxia and hypocapnia, and so on, adrenaline contents of the suprarenals is reduced by high concentration of carbon dioxide (30%), with or without hypoxia. Noradrenaline contents is increased by carbon dioxide (15 to 30%). Hypercapnia is more potent than hypoxia as a suprarenal stimulus.
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PMID:[CO2 and the catecholamine content of the adrenal medulla of the rat]. 644 72

1. The effect of beta-adrenergic and dopaminergic agonists and antagonists on the chemoreceptor response to graded hypoxia and hypercapnia was tested in nineteen cats and ten rabbits anaesthetized either with chloralose-urethane or pentobarbitone sodium, paralysed with pancuronium bromide and artificially ventilated.2. The inhibitory action of dopamine was confirmed. The inhibition following intra-arterial bolus injection was blocked by haloperidol; dopamine then excited and this excitation was blocked with propranolol. Adrenaline or noradrenaline caused a transient inhibition followed by a marked excitation. The inhibition was blocked with haloperidol and the excitation blocked with propranolol or metoprolol. Isoprenaline excited without inhibition and this was blocked with propranolol or metoprolol.3. A novel finding was that the chemoreceptor response to hypoxia was markedly reduced or even abolished with propranolol or metoprolol. The response was enhanced with a constant infusion of isoprenaline, adrenaline or noradrenaline in proportion to the degree of hypoxia, an effect mimicked by raising CO(2). The chemoreceptor response to hypoxia was similarly enhanced by haloperidol and depressed by a constant infusion of dopamine in proportion to the degree of hypoxia.4. The effect of these drugs on the chemoreceptor response to hypercapnia was less constant. In the majority of tests the aminergic agonists and antagonists caused a parallel shift of the CO(2) response curves in the same direction as the O(2) response curves and by amounts proportional to the degree of hypoxia. In some tests these drugs caused a change in the slope of the CO(2) response curves but only if P(a, O2) was less than 60 mmHg.5. One interpretation of these results is that hypoxia exerts a presynaptic action, causing the release of noradrenaline and dopamine from Type I cells, and that these substances act upon aminergic receptors on the sensory fibre, causing a change in potential and discharge frequency proportional to the rates of dopamine and noradrenaline release.6. An additional or alternative interpretation is that O(2) and CO(2) (the latter most probably acting on intracellular pH) alter the sensitivity of the aminergic receptors to their agonists.
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PMID:Adrenergic mechanisms and chemoreception in the carotid body of the cat and rabbit. 680 33


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