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

Dopamine is present in the carotid body and has been postulated to be an inhibitory neurotransmitter. The purpose of this study was to determine the effects of dopamine on ventilation in man and to examine its mechanism of action. Dopamine (0.5-10 mug/kg per min) was infused in eight normal men at different levels of arterial chemoreceptor activity, produced by varying the inspired Po(2). During normoxia dopamine produced a small decrease in minute ventilation (Ve) and an increase in arterial Pco(2). When arterial chemoreceptors were stimulated by hypoxia, infusion of dopamine produced a marked initial depression of Ve followed by a sustained although less pronounced decrease in Ve. An increase in Pa(co) (2) and a decrease in Pao(2) were also observed. When arterial chemoreceptor activity was suppressed by hyperoxia, infusion of dopamine did not affect ventilation. Subjects also breathed a hypercarbic, hyperoxic gas mixture. The hypercarbia produces hyperventilation by stimulating central chemoreceptors, whereas the hyperoxia suppresses peripheral chemoreceptors. Dopamine did not alter ventilation while the subjects were breathing this gas mixture. These studies suggest that dopamine suppresses ventilation in man through an action on the arterial chemoreceptor reflex. These findings support the hypothesis that dopamine is an inhibitory neurotransmitter in the carotid body, and that release of dopamine may modulate the sensitivity of peripheral arterial chemoreceptors.
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PMID:Depression of ventilation by dopamine in man. Evidence for an effect on the chemoreceptor reflex. 64 Nov 49

To understand the role of carotid chemoreceptor activity in the ventilatory responses to sustained hypoxia (30 min) the following measurements were made in cats anesthetized with alpha-chloralose: (1) carotid chemoreceptor and ventilatory responses to isocapnic hypoxia and to hypercapnia during hyperoxia; (2) carotid chemoreceptor responses to isocapnic hypoxia after dopamine receptor blockade; and (3) ventilatory responses to hypoxia after bilateral section of carotid sinus nerves (CSN). Transition to hypoxia (PaO2 approximately equal to 52 Torr) from hyperoxia gradually increased carotid chemoreceptor activity by ten fold and ventilation by two fold without any detectable overshoot. Termination of isocapnic hypoxia with hyperoxia (PaO2 greater than 300 Torr) at 30 min promptly restored the carotid chemoreceptor activity to prehypoxic level. Ventilation also decreased promptly, but remained above the control value. Induction of hypercapnia (from 31.8 Torr to 43.9 Torr) during hyperoxia was followed by a prompt increase in the chemoreceptor activity by four fold which subsequently diminished, and by a gradual four fold increase in ventilation. Termination of hypercapnia after 30 min was followed by a prompt return of chemoreceptor activity and by a slow return of ventilation to near control levels. Dopamine receptor blockade increased carotid chemoreceptor responsiveness to acute hypoxia but did not alter the response pattern during sustained hypoxia. After bilateral CSN section, ventilation decreased during maintained hypoxia. Thus, a stimulatory peripheral and inhibitory central effects of hypoxia could produce a biphasic ventilatory response to short-term hypoxia in the anesthetized cat with intact CSN but did not manifest it. The results suggest that the chemosensory input not only promptly stimulates ventilation but also prevents the subsequent depressant effect of hypoxia on the brain-stem respiratory mechanisms and hence presumably a biphasic ventilatory response in the anesthetized cat.
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PMID:Carotid body chemoreceptor and ventilatory responses to sustained hypoxia and hypercapnia in the cat. 297 Jan 7

To investigate the effect of intravenous dopamine on the chemical regulation of ventilation, we studied the ventilatory responses to hypercapnic hypoxia during dopamine infusion. Intravenous dopamine (3 micrograms X kg-1 X min-1) was administered to six healthy human subjects. Two hypoxic challenges (PETO2 = 52.5 +/- 2.5 mm Hg, SaO2 = 88.8 +/- 2.2%; mean +/- SD) were administered at three CO2 levels (PETCO2 = 40.8 +/- 0.5, 45.6 +/- 0.2, 49.8 +/- 0.3 mm Hg) to each subject. The ventilatory responses were quantified by calculation of slopes and intercepts of the relationship between minute exhaled ventilation (VE) and arterial hemoglobin saturation (SaO2), and by the relationship between this slope (delta VE/delta SaO2) and carbon dioxide tension. Dopamine caused a 77% reduction in delta VE/delta SaO2 (hypoxic sensitivity) during eucapnia, a 39.5% reduction in hypoxic sensitivity at PETCO2 = 46 mm Hg, and 38% reduction at PETCO2 = 50 mm Hg (P less than 0.05). Dopamine also reduced normoxic ventilation at all carbon dioxide levels. There was a greater depression in VE during hypercapnia (25.7% reduction) than during eucapnia (12% reduction). This indicates that dopamine depresses the normoxic ventilatory response to carbon dioxide. Intravenous dopamine reduces the ventilatory response to both hypoxia and hypercapnia but preserves the augmentation of hypoxic ventilatory drive by hypercapnia.
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PMID:Effect of dopamine on hypoxic-hypercapnic interaction in humans. 360 70

Dopamine has been implicated in maintaining tonic inhibition of carotid body activity. We tested this hypothesis by assessing the ventilatory effects of a peripheral dopamine antagonist, domperidone. The effects of this agent on the ventilatory responses to hypoxia and hypercapnia were also examined. The study was performed in awake carotid body intact and carotid body denervated goats. Resting minute ventilation increased while PaCO2 decreased (4 Torr) following domperidone administration (0.5 mg/kg, I.V.) in carotid body intact goats. This response did not occur in carotid body denervated goats supporting the hypothesis that endogenous dopamine provides tonic inhibition in the carotid body. Hypoxic and hypercapnic ventilatory responses were significantly augmented following domperidone administration in the carotid body intact goats. This supports the concept of dopaminergic modulation of the response of the carotid body to stimuli. Domperidone allows study of carotid chemoreceptor dopaminergic activity in awake animals because of its high affinity for carotid body D2 dopamine receptors and its lack of CNS effects.
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PMID:Domperidone-induced potentiation of ventilatory responses in awake goats. 376 21

Carotid bodies and their nerves were excised from rabbits or cats, cleaned of surrounding connective tissue and placed in a chamber through which mammalian saline equilibrated with different gas mixtures was allowed to flow. Single fibers were isolated and identified as chemosensory by their response to hypoxia, hypercapnia, or NaCN. Mass receptor potentials (recorded at some distance from the sensory nerve endings) were evoked by the same stimuli and registered as close as possible to the carotid body. Both cats and rabbits exhibited receptor depolarization and an increased discharge in response to NaCN, hypoxia, hypercapnia and cyanide. However, the effects of some pharmacological agents were quite different in rabbits and cats. In the rabbit, ACh 10-100 microgram and carbachol 1-10 microgram produced receptor hyperpolarization and discharge depression followed by discharge increase. Nicotine 0.3-20 microgram induced receptor depolarization and increased chemosensory discharge frequency. Nicotinic stimulation was antagonized by D-tubocurarine 10(-6)-10(-4) g/ml. Pilocarpine 2-50 microgram hyperpolarized the receptors and depressed discharge frequency. Pilocarpine-induced depression was reduced by atropine 10(-6) g/ml. Dopamine 5-100 microgram depolarized the receptors and increased the chemosensory discharge frequency. This effect of dopamine was reduced by haloperidol (10(-11)-10(-7) M). In the cat, ACh, carbachol and nicotine (same doses as those used in rabbits) induced receptor depolarization and increased the sensory discharge frequency. Pilocarpine (up to 50 microgram) had little effect on either discharge frequency or the receptor potential. Dopamine 5-100 microgram induced receptor hyperpolarization and depression of discharge frequency, and these effects were reduced by haloperidol.
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PMID:A comparative physiological and pharmacological study of cat and rabbit carotid body chemoreceptors. 624 64

Two female patients revived from fulminant attacks of asthma are described. Ventilatory responses to asphyxia in these patients were 0.70 +/- 0.10 l min-1 % SaO2-1 and 0.64 +/- 0.21 l min-1 % SaO2-1 (mean +/- SEM), respectively. These values were significantly less than the responses of seven normal female subjects (1.54 +/- 0.11 l min-1 % SaO2-1 mean +/- SEM; p less than 0.01). Ventilatory responses to hypercapnia of the two patients were in the low normal range. Dopamine-receptor blockade with prochlorperazine significantly increased the ventilatory response to asphyxia in normal subjects (p less than 0.05 or less for each subject) but did not alter the depressed responses in the asthmatic patients. In one patient, naloxone in a dose of 400 micrograms reversed the decreased ventilatory responsiveness; the response to asphyxia was increased from 0.72 l min-1 % SaO-1 to 1.80 l min-1 % SaO2-1 (p less than 0.01) and the response to hypercapnia was increased from 0.90 l min-1 mmHg-1 to 4.80 l min-1 mmHg-1 (p less than 0.01). Naloxone had no effect in the second asthmatic patient nor in five normal subjects. Defective chemoreceptor responses to chemical stimuli may play a role in sudden death from asthma; endogenous opioids may mediate this disorder of ventilatory control.
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PMID:Ventilatory control in two asthmatics resuscitated from respiratory arrest. 659 13

The effect of intravenous dopamine on carotid body chemoreceptor activity was investigated in 6 anesthetized cats which were paralyzed and artificially ventilated. Studies were performed at 4 steady-state PaO2 levels at a constant PaCO2 and at 4 levels of PaCO2 during hyperoxia. Dopamine inhibited carotid chemoreceptors before and excited them after haloperidol. Moderate stimulation of the receptors by hypoxia and hypercapnia augmented dopamine's effects. These results indicate that both inhibitory and excitatory dopamine receptors are present in the carotid body.
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PMID:Inhibitory and excitatory effects of dopamine on carotid chemoreceptors. 677 16

The effects of intravenous infusion of dopamine (20 microgram.min) on the steady-state ventilatory and carotid chemoreceptor responses to successive levels of isocapnic hypoxia and hyperoxic hypercapnia were investigated in cats anesthetized with alpha-chloralose. Dopamine infusion was followed by a maximal decrease in ventilation in about 20 s. Thereafter, the effect diminished and stabilized. Termination of dopamine infusion was promptly followed by an increase in ventilation. These ventilatory responses were smaller than the corresponding carotid chemoreceptor responses. The steady-state effect of dopamine infusion was to diminish ventilation at all levels of arterial O2 tension, the decrease being greater during hypoxia than that during hyperoxia. Bilateral section of the carotid sinus nerves significantly diminished but did not abolish the inhibitory effect of dopamine on ventilation during hyperoxia. Thus the ventilatory depression due to dopamine infusion is not entirely due to its effect on the carotid chemoreceptors. Dopamine decreased ventilatory responses to successive levels of hypercapnia by the same magnitude without changing the slope of the response curves. The steady-state relationship between chemoreceptor activity and ventilation shows that the ventilatory equivalent for carotid chemoreceptor activity is increased during dopamine infusion because of its greater inhibitory effect on carotid chemoreceptor activity than on ventilation with the decrease of arterial O2 tension.
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PMID:Effects of dopamine on chemoreflexes in breathing. 679 Apr 90

The effect of dopamine on the ventilatory response to transient asphyxia was examined to test the hypothesis that dopaminergic mechanisms modulate carotid body function in humans and to determine whether a change in ventilatory responsiveness is effected by changes in tidal volume or breathing frequency. Five healthy adults were subjected to brief episodes of hypercapnic hypoxia before and at the end of a 45-min intravenous infusion of dopamine hydrochloride (5 micrograms/kg/min). Mean ventilatory response to hypercapnic hypoxia decreased from 1.71 +/- 0.33 L/min/% SaO2 (+/- SD) to 1.30 +/- 0.28 L/min/% SaO2 (p less than 0.05) during dopamine infusion. The fall in ventilatory response was due to a fall in the frequency of breathing (p less than 0.01). Dopamine infusion also produced a small decrease in resting minute ventilation (p less than 0.05) and a small increase in resting end-tidal PCO2 (p less than 0.05). No change was noted in the ventilatory response to progressive hypercapnia. These findings suggest that dopamine acts at the carotid body to depress its response to transient hypoxic stimulation and that this effect is to selectively slow the rate of breathing.
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PMID:Ventilatory responsiveness to hypercapnic hypoxia during dopamine infusion in humans. 714 42

Ventilatory acclimatization to high altitude is accompanied by increased hypoxic (HVR) and hypercapnic (HCVR) ventilatory responses which may reflect increased carotid body chemosensitivity. Dopamine is an inhibitory neuromodulator of the carotid body and its activity may be reduced by hypoxic exposure. To determine whether decreased dopaminergic activity could account for the increased chemosensitivity of acclimatization, we examined the response to peripheral dopamine receptor (D2) blockade with domperidone on HVR and HCVR in awake cats before and after exposure to simulated altitude of 14,000 ft for 2 days. During anesthesia, we also examined the effects of domperidone on carotid body responses to hypoxia and hypercapnia in acclimatized and low altitude cats. Two days' exposure to hypobaric hypoxia produced an increase in HVR and HCVR. Before acclimatization, domperidone augmented HVR and HCVR, but there was no effect after acclimatization. In anesthetized low altitude cats, domperidone increased carotid body responses to hypoxia and hypercapnia, but had no effect in acclimatized cats. These results indicate that decreased endogenous dopaminergic activity may contribute to increased ventilatory and chemoreceptor responsiveness to hypoxia and hypercapnia during hypoxic ventilatory acclimatization.
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PMID:Possible role of dopamine in ventilatory acclimatization to high altitude. 774 Feb 13


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