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

The effect of various cardiovascular reflexes and reactions on the plethysmographically recorded penile volume in rabbit was investigated. Stimulation of the aortic nerve or direct stimulation of the carotid sinus produced increase in penile volume, while carotid occlusion produced decrease. Brief volume load or protoveratrine given into the right atrium produced increase in penile volume. Asphyxia, hypercapnia, hypoxia, cyanide and lobeline produced decrease in penile volume, while hypocapnia increased it. Moderate blood taps decreased penile volume, while hypocapnia increased it. Moderate blood taps decreased penile volume. With the exception of the response to asphyxia all these reactions required intact vasomotor nerves. Clonidine increased penile volume if vasomotor nerves were intact but decreased it if the penis was decentralized. Penile volume decreased in shivering animals but increased on warming. Carotid occlusion impaired erectile responses to hypogastric and pelvic nerve stimulation. In certain experiments this effect was more pronounced in the latter case. It is concluded that the medullary neuron pool responsible for penile vasomotor tone participates in general reflex cardiovascular homeostasis and that this may have implications for normal erectile responses.
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PMID:Changes in penile volume during some cardiovascular reflexes and reactions in rabbit. 50 67

Extracellular recordings were made from 127 neurons, identified by antidromic activation from the supraoptic nucleus, in the A1 area of urethan-anesthetized rabbits. The median axonal conduction velocity was 0.7 m/s, and the median discharge rate was 3.9 spikes/s. Raising arterial pressure decreased the discharge rate in 94 of 101 neurons tested. Lowering arterial pressure increased the discharge rate in 50 of 64 neurons tested. Of 70 neurons inhibited by baroreceptor activation, 40 were excited and 25 inhibited by hypercapnic hypoxia. Of 23 neurons excited by hypercapnic hypoxia, all were excited by hypoxia but only 2 were affected by hypercapnia. Of 16 neurons inhibited by hypercapnic hypoxia, 15 were inhibited by hypoxia and 1 was inhibited by hypercapnia. Of 14 neurons excited by hypoxia, 13 were excited by injection of sodium cyanide into the common carotid artery. Of five neurons inhibited by hypoxia, four were inhibited by sodium cyanide. Our results provide electrophysiological evidence that neurons projecting from the A1 area to the supraoptic nucleus increase their discharge rate in response to baroreceptor unloading and decrease their discharge rate in response to baroreceptor activation. These neurons may form part of the central pathway mediating secretion of vasopressin in response to hemorrhage. A high proportion of the neurons also receive peripheral chemoreceptor inputs, and these A1 cells may also be part of the central pathway whereby chemoreceptor stimulation modifies the secretion of vasopressin.
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PMID:Chemoreceptor and baroreceptor responses of A1 area neurons projecting to supraoptic nucleus. 132 16

Brain stem hypoxia caused by vertebral artery injection of sodium cyanide (NaCN) (1-20 micrograms) in artificially ventilated cats depressed phrenic and stimulated sympathetic nerve activity with a simultaneous increase in arterial blood pressure. Larger doses of NaCN caused greater effects. Hypercapnia produced by inhalation of 7% CO2 in O2 tended to reduce NaCN-induced responses on phrenic activity but not on blood pressure or sympathetic activity. Infusion into the vertebral artery with hypoxic saline (3% CO2 in N2) altered blood pressure, also affecting phrenic and sympathetic nerves similarly to NaCN administration. However, washout of CO2 by infusion of 100% O2 bubbled saline at high flow rates (3.6 ml/min) depressed phrenic as well as sympathetic activity and blood pressure. Spinal transection at the first cervical level eliminated sympathetic excitatory response to intravertebral cyanide injection. However, a large dose of NaCN (600 micrograms) given intravenously in spinal animal excited sympathetic activity. We conclude that intravertebral injection of NaCN can be used to study the effects of local hypoxia of the brain stem on cardiorespiratory responses and that hypoxia acts at both these sites (brain stem and spinal cord) to stimulate sympathetic excitation.
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PMID:Cardiorespiratory changes induced by vertebral artery injection of sodium cyanide in cats. 155 49

Carotid body (CB) chemosensory responses to natural and pharmacological stimuli were studied in vitro in the presence and nominal absence of CO2-HCO3- in the perfusion-superfusion media. The CBs obtained from cats (n = 10), anesthetized with sodium pentobarbitone, were simultaneously perfused and superfused with a modified Tyrode solution at 36.5 +/- 0.5 degrees C, equilibrated respectively with PO2 of 120 and less than 20 Torr. The Tyrode, nominally free of CO2-HCO3- (HEPES-NaOH, pH 7.38, 310 mOsm), was used first. Subsequently the Tyrode containing HEPES-HCO3-, equilibrated with PCO2 of 36.8 Torr (pH 7.38) was used. Chemosensory discharges were recorded from the carotid sinus nerve. Both hypoxia (PO2 = 20-25 Torr) and ischemic hypoxia stimulated the discharge in the absence and presence of CO2-HCO3-. However, the presence of CO2-HCO3- significantly raised the baseline activity, augmented the speed, sensitivity and the maximal responses to both types of hypoxia. Hypercapnic perfusate (PCO2 = 65 Torr at pH 7.17) produced a peak response equally promptly in the absence and presence of CO2-HCO3- in the ongoing perfusate but generated a larger and more sustained response. Presence of CO2-HCO3- strongly potentiated the responses to cyanide (10(-10)-10(-7) mol) but less strikingly the responses to nicotine (10(-11)-10(-8) mol). Thus, the extracellular CO2-HCO3- significantly improved the response to hypoxia but was not essential for O2 chemoreception. The underlying mechanisms of the effect of CO2-HCO3- is likely to be mediated by the Cl(-)-HCO3- anion exchanger in the pH regulation of glomus cells.
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PMID:Carotid body chemoreception in the absence and presence of CO2-HCO3-. 166 17

Carotid body chemosensory response to hypoxia is attenuated as a result of prolonged normobaric hyperoxia (NH) in the cat. The effect of NH is likely to be due to high cellular PO2 and O2-related free radicals. Accordingly, the effect would be less if O2 delivery to the chemoreceptor tissue could be compromised. The aortic bodies, which appear to have less of a circulatory O2 delivery, as suggested by their vigorous responses to a slight compromise of O2 flow compared with those of the carotid body, could provide a suitable testing material for the hypothesis. We tested the hypothesis by studying both aortic and carotid body chemoreceptors in the same cats (n = 6) which were exposed to nearly 100% O2 for about 60 h. These chemoreceptor organs were also studied in 6 control cats which were maintained in room air at sea-level. The cats were anesthetized and their carotid and aortic chemosensory fibers were identified by the usual procedure, and their responses to hypoxia and hypercapnia and to bolus injections (i.v.) of cyanide and nicotine were measured. In the NH cats, the carotid but not aortic chemosensory responses to hypoxia and cyanide were attenuated and to hypercapnia (both onset and steady state) augmented. The aortic chemoreceptors were stimulated by hypoxia, hypercapnia, cyanide and nicotine both in the NH and the control cats similarly. The results support the hypothesis that it is presumably a higher tissue blood flow and hence a higher concentration of O2-related free radicals which ultimately led to the specific attenuation of O2 chemoreception in the carotid body.
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PMID:Aortic and carotid body chemoreception in prolonged hyperoxia in the cat. 178 Jun 2

Chemical control of respiration in cats after chronic normobaric hyperoxia (NH; inhalation of 100% O2 for 60-67 h) was compared with that of control rats, anesthetized with pentobarbital. After chronic hyperoxia, induction of moderate hypoxia (PaO2 = 50-60 Torr) increased inspiratory time (TI) often without increasing tidal volume (VT). More intense hypoxia (PaO2 = 40-50 Torr) depressed tidal volume and further increased TI, diminishing the respiratory drive (VT/TI). Hypercapnia, on the other hand, increased tidal volume and shortened respiratory cycle time; but these responses were subnormal. The normal stimulatory effects of intravenous nicotine and inhibitory effect of dopamine on carotid chemo-receptor activity and ventilation were preserved in the NH cats. Cyanide, however, did not stimulate carotid chemoreceptor activity and ventilation. Thus, the changes in the carotid and aortic chemosensory activities elicited appropriate reflex ventilation responses, indicating that the central component of the chemoreflex was not impaired. The ventilatory depression during hypoxia despite an active chemosensory input is consistent with the lack of carotid chemosensory response to and a central depressant effect of hypoxia in the NH cats, and was presumably associated in part with an increased responsiveness of airway reflexes. We conclude that chronic hyperoxia selectively attenuated carotid chemosensory and chemoreflex responses to hypoxia.
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PMID:Chemical respiratory control in chronically hyperoxic cats. 207 96

The hypothesis that augmentation of the carotid chemoreceptor response to hypoxia by almitrine is due in part to an increased response to CO2 was tested by using single or few fiber preparation of carotid body chemosensory fibers in 12 cats anesthetized with alpha-chloralose. To differentiate between the plausible mechanisms of effects, we also tested the responsiveness of the afferents to cyanide and nicotine before and after almitrine. After a saturation dose of almitrine (1 mg.kg-1 followed by 0.5 mg.kg-1.h-1) the chemosensory responses to CO2 strikingly increased even during hyperoxia: the afferents showing an increased transient peak activity at the onset of hypercapnia, an augmented steady-state response to CO2 stimulus, and a decreased arterial PCO2 stimulus threshold. Thus, the effect of almitrine on carotid chemoreceptor response to hypoxia could be explained, at least in part, by its multiplicative stimulus interaction with CO2. After almitrine, the chemoreceptor response to cyanide, which is dependent on arterial PO2, was not particularly augmented relative to those of nicotine. Accordingly, the O2-sensing mechanism does not appear to be the primary site of almitrine effect. The results also indicate that the site of CO2 chemoreception resides downstream from those of hypoxia.
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PMID:Stimulus interaction between CO2 and almitrine in the cat carotid chemoreceptors. 256 54

The present study investigates the nature of tensor veli palatini muscle (TVP) and levator veli palatini muscle (LVP) as accessory respiratory muscles. In the first part of the study, the relation between the muscles' activities as revealed by EMG activities and respiration rhythm was analysed under various combinations of partial pressures of O2 and CO2 in the arterial blood. Furthermore, the effect of sodium cyanide (NaCN) perfused through the carotid sinus was examined. During resting breathing, no EMG activity was recorded from either muscle. In hypercapnic or hypoxemic conditions produced by rebreathing, TVP exhibited a phasic EMG activity during inspiration. LVP showed a phasic EMG activity during expiration in hypoxic conditions (PaO2 less than 40 mmHg). NaCN perfused bilaterally through the carotid sinus induced the phasic EMG activities similar to those observed in hypercapnia and/or hypoxemia. TVP was more sensitive to NaCN than LVP. The second part of the study examined specific roles of the muscles in altered states of breathing. At the time of onset of LVP activity induced by rebreathing, the oral proportion of airflow markedly increased. On the other hand, TVP activity greatly increased in amplitude when negative pressure was applied to the upper airway. The results suggest that both muscles are accessory respiratory muscles and are regulated by chemogenic inputs including those from the carotid body; TVP is an accessory inspiratory muscle that contributes to the maintenance of upper airway patency, and LVP is an accessory expiratory muscle that increases the portion of expiratory airflow through the oral cavity.
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PMID:[Role of the soft palate in respiration: an electromyographic study in the dog]. 263 51

We studied the responses of the ganglioglomerular nerve (GGN) efferents to brief periods of hypoxia and hypercapnia and to several levels of steady-state arterial PO2 and PCO2 and to intravascular injection of cyanide in thirteen anesthetized cats. The cats breathed spontaneously. A branch of the GGN which was cut close to the carotid body was divided into several filaments, and the activity of each filament was tested until clean and identifiable action potentials were obtained. The GGN efferent activity, breath-by-breath inspiratory volume, tracheal PO2 and PCO2 and arterial blood pressure were recorded simultaneously. We found that the GGN contained spontaneously active fibers which showed a range of responses to the respiratory stimuli. Fifty-eight percent of the filaments with dominant cardiovascular rhythm showed the least response to blood gas stimuli. Forty-two percent showed clear responses to hypoxia and hypercapnia. These responses developed slowly with the onset of the stimulus but decreased promptly with the withdrawal of the stimulus. These GGN efferents were also promptly stimulated by sodium cyanide. The steady-state response curve to hypoxia was hyperbolic and to hypercapnia it was linear. Some of these fibers showed stronger respiratory rhythms than others. The responses of these GGN efferents were associated with the respiratory responses to hypoxia and hypercapnia. For the same respiratory drive, however, the steady-state hypoxic stimulus elicited a greater GGN response than did hypercapnia.
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PMID:Responses of ganglioglomerular nerve activity to respiratory stimuli in the cat. 308 75

The experiments were performed on anaesthetized dogs which breathed spontaneously or were artificially ventilated and paralysed. The spontaneous nasal arterial blood flow was measured on one side of the nose while nasal vascular resistance was determined on the other side simultaneously. Nasal arterial blood flow was measured by means of an electromagnetic flow sensor placed around the terminal branch of the internal maxillary artery, the main arterial supply to the nasal mucosa. Nasal vascular resistance was measured by constant-flow perfusion of the terminal branch of the internal maxillary artery. Nasal airway resistance was assessed by monitoring the transnasal pressure at constant airflow through each side of the nose simultaneously. Hypercapnic gas challenge (8% CO2, 30% O2 in N2) to the lungs increased nasal vascular resistance and decreased nasal airway resistance. Similar gas challenge to the nose did not affect nasal vascular resistance but decreased nasal airway resistance. Hypoxic gas challenge (6% O2 in N2) to the lungs did not affect the nasal vascular resistance but decreased nasal airway resistance only when the nasal vascular bed was under controlled perfusion. Similar gas challenge to the nose did not affect either nasal vascular or airway resistance. Arterial chemoreceptor stimulation by intracarotid injection of sodium cyanide increased nasal vascular resistance and decreased nasal airway resistance. The nasal vascular response to hypercapnia and arterial chemoreceptor stimulation was reflex in nature, being abolished by nasal sympathectomy. The nasal airway response to hypercapnia, hypoxia and arterial chemoreceptor stimulation was reflex in nature, being partially or completely abolished by nasal sympathectomy. Hypercapnia probably induced a local vasodilatatory effect on the capacitance vessels whereas hypoxia had no direct action on the vasculature.
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PMID:Effects of hypercapnia and hypoxia on nasal vasculature and airflow resistance in the anaesthetized dog. 309 11


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