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

Patients with breathlessness commonly describe subjective relief when seated near an open window or in front of a fan. Previous studies suggest that a flow of air or application of cold solutions to the face, nasal mucosa, or pharynx may alter ventilation. We hypothesized that a flow of cold air directed against the cheek would reduce the sensation of breathlessness associated with loaded breathing. Sixteen subjects breathed on a device with an inspiratory resistive load (63 cm H2O/L/s) while PCO2 was maintained at 55 torr for 5 min. All studies were performed 4 times with each subject, twice with cold air directed against the cheek (4 degrees to 10 degrees C, 4 km/h) and twice with no flow on the subject. Subjects were asked to rate their breathlessness using a modified Borg scale. Cold air directed on the face reduced breathlessness induced by an inspiratory resistive load and hypercapnia (6.2 +/- 1.7 Borg scale units with no flow, 5.1 +/- 1.7 with cold air; p less than 0.002) without causing a significant reduction in ventilation. This effect was not observed when cold air was directed to the leg and does not appear to be associated with a reduction in the ventilatory response to hypercapnia or with initiation of the diving reflex. We conclude that cold air directed against the cheek significantly reduces dyspnea associated with the combination of hypercapnia and an inspiratory resistive load.
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PMID:Cold facial stimulation reduces breathlessness induced in normal subjects. 360 41

We used mechanical ventilation of the fetal lungs in utero on 11 fetal lambs at 140-145 days gestation to alter fetal blood gases and thus separate the influences of PaO2 and PaCO2 on extrauterine breathing after cord clamping. The fetus was delivered either into a 40 degrees C saline bath or onto a cold table. Mechanical ventilation was stopped 2 min after delivery and the time to onset of continuous air breathing was observed. Also two fetuses were ventilated in utero 5 or more days after chronic instrumentation at 127 days gestation; in these animals the time to onset of breathing (diaphragm EMG) was recorded after stopping the ventilator and occluding the cord. We conclude: (a) hypercapnia is a stimulus to breathing even in hyperoxia and at 40 degrees C; (b) hypocapnia delays the start of extrauterine breathing in hyperoxia at 40 degrees C; (c) hypoxia inhibits breathing in the absence of hypercapnia or cold; (d) cold overrides the effects of hypocapnia in normoxia or moderate hypoxia.
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PMID:Determinants of the onset of continuous air breathing at birth. 366 76

In nine greyhound dogs, anaesthetized with chloralose-urethane, total lung resistance, volume of an isolated cervical tracheal segment and resistance of the isolated larynx were simultaneously measured. Three stimuli were tested: inhalation of a CO2-enriched gas mixture; histamine injected intravenously or administered by aerosol to stimulate primarily lung irritant receptors; and intravenous injection of capsaicin to stimulate primarily lung C-fibre receptors. The stimuli were applied in three successive conditions: neurally-intact animals; denervation of the right lung plus cold block of myelinated fibres in the left cervical vagus nerve; and further blockade of non-myelinated fibres in this nerve. Histamine and capsaicin increased lung and laryngeal resistances, and reduced tracheal volume, and the responses after denervation are consistent with the drugs acting by lung vagal reflexes. In neurally-intact animals, hypercapnia increased total lung resistance, decreased tracheal volume and lowered laryngeal resistance. After elimination of conduction in all myelinated fibres, CO2-induced changes in lung resistance and in tracheal volume were still present. However, the dilating effect of hypercapnia on the larynx diminished markedly. Elimination of all vagal pulmonary afferents abolished the residual laryngeal response to hypercapnia, lowered and delayed changes in tracheal volume and greatly reduced the increase in lung resistance. The results indicate that the laryngeal response to hypercapnia depends on vagal integrity, but the tracheobronchial constrictor effect of CO2 is less affected by vagal denervation.
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PMID:Tracheobronchial and laryngeal responses to hypercapnia, histamine and capsaicin in dogs. 407 57

Nine anesthetized dogs breathed against an expiratory threshold load (ETL) applied by switching the expiratory circuit into a column of H2O to a depth of 20-30 cm. Arterial blood gas tensions were maintained in the normal range by placing the dogs under arteriovenous bypass to avoid any uncontrolled chemostimulation. There was an increase in integrated electromyogram activity of the diaphragm with the ETL. This was rarely observed after cold block of the vagus nerves which also reduced the evoked expiratory activity. The ventilatory response to hypercapnia was greatly depressed under loaded breathing whether vagal afferents were intact or blocked by cold. Both inspiratory drive and ventilatory timing were affected, suggesting that the central integration of chemosensitive afferents was altered. Proof of supraspinal projections of proprioceptive inputs from abdominal muscles was provided by the demonstration of changes in ventilatory timing during selective activation of muscle spindles in abdominal muscles by high-frequency mechanical vibration applied to the linea alba. Thus these observations suggest that during ETL breathing, a possible interaction exists between chemoreflex drive and proprioceptive afferents.
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PMID:Expiratory threshold load under extracorporeal circulation: effects of vagal afferents. 641 63

We studied the response of tracheal slowly adapting stretch receptors (SARs), whose activity was recorded from the peripheral cut end of the right vagus nerve, in newborn and adult dogs during hyperoxic hypercapnia and isocapnic hypoxia. Tracheal receptors only were studied since it was possible to maintain the parasympathetic efferent supply partially intact (contralateral vagus nerve and superior laryngeal nerve). The animals were anesthetized and passively ventilated with the chest open. A stimulatory effect was found in 9 out of 20 puppies for hypercapnia and in 3 out of 10 for hypoxia. The maximum amount of stimulation ranged from 114 to 556% of the control discharge for hypercapnia and from 110 to 387% for hypoxia. In the adult dog CO2 stimulated tracheal SARs in 11 out of 16 dogs (103-404% control) while hypoxia stimulated SARs in 9 out of 13 animals (109-268% control). The stimulatory effect was greater during expiration and, for hypercapnia, decreased in intensity with time. This excitatory action was eliminated by cold block of the contralateral vagus nerve or atropine administration, suggesting that the stimulation was mediated by smooth muscle contraction. These findings support the notion that airway stretch receptors are activated not only by passive distension of the airways, but also by an active contraction of the tracheobronchial smooth muscle.
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PMID:Stimulation of tracheal slowly adapting stretch receptors by hypercapnia and hypoxia. 664 62

17 subjects were carefully selected among 150 patients with COLD: all patients with one or more conditions or diseases that could alter the physiological response to chronic hypercapnia were eliminated. During a period of 13 to 28 days, the acid-base response to slow carbon dioxide changes was studied in the selected patients. Total body buffering capacity was expressed as dH+a/dPaCO2 and showed to be an inverse function of chronic PaCO2 (defined as the value of PaCO2 in clinical and acid-base steady status for each patient), according to the previous suggestions of Weiss and Dulfano and to the report of Ingram and co-workers during acute carbon dioxide changes in the same patients.
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PMID:Relationship between chronic PaCO2 and total body buffering capacity in patients with chronic obstructive lung disease. 677 97

In anaesthetized rabbits the influence of differential vagal cold blockade on the ventilatory response to inhaled CO2 during hyperoxia was investigated. Following total inactivation, the relationship between ventilation (V) and arterial PCO2 (PaCO2) was shifted to the left and steepened slightly over a range of modest hypercapnia, but was progressively flattened as hypercapnia intensified. The latter effect, suggestive of a vagally mediated facilitation of ventilatory CO2 responsiveness, was studied further. Differential vagal cold blockade to a temperature (5-11 degrees C) which abolished the Breuer-Hering inflation reflex (end-inspiratory tracheal occlusion no longer eliciting a prolongation of expiratory duration, TE) had no effect on V either during normocapnia or at a substantial level of hypercapnia. Only with further vagal cooling to 0 degrees C did the ventilatory depression during hypercapnia emerge, largely because TE failed to shorten in response to the hypercapnic stimulus. It is concluded that the integrity of expiratory-terminating mechanisms is crucial for the manifestation of the vagally mediated facilitation of V and its CO2 responsiveness which is evident during hyperoxic hypercapnia. A possible role is suggested for lung epithelial irritant receptors or for the tonic late-expiratory activity from pulmonary stretch receptors.
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PMID:The involvement of expiratory termination in the vagally mediated facilitation of ventilatory CO2 responsiveness during hyperoxia. 678 64

Spontaneous hypertensive rats (SHR) are less prone to develop a dysfunction of the blood-brain barrier (BBB) when exposed to an abrupt increase in blood pressure than normotensive rats (NR), probably as a result of vessel wall hypertrophy and increased vessel wall to lumen ratio. Hemodynamic studies have indicated that structural adaptation develops early as a response to the increased pressure load in renal hypertensive rats (RHR). In the present study RHR (one renal artery constricted and the contralateral kidney intact) were subjected to acute hypertension induced by bicuculline, a drug that induces an abrupt increase in blood pressure concomitant with pronounced cerebral vasodilatation. Protein leakage in the brain, as indicated by Evans blue-albumin and 125IHSA (human serum albumin) extravasation, was not reduced in RHR compared to NR. The cerebrovascular permeability was slightly but significantly (p < 0.01) increased in RHR even in the absence of further blood pressure manipulation. No neurological symptoms were observed in conscious RHR when the BBB dysfunction was aggravated by hypercapnia. The increased cerebrovascular permeability in RHR cold be due to a lower degree of structural adaptation in RHR compared to SHR and/or to some permeability-increasing humoral factor in renal hypertension.
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PMID:The blood brain barrier in renal hypertensive rats. 744 83

Recently, we have described the effects of hypoxia and of hypercapnia on the metabolic (VO2) and ventilatory responses to cold in unanesthetized intact and carotid body-denervated (CBD) rats (Gautier et al., J. Appl. Physiol. 73: 847-854, 1992 and 75: 2570-2579, 1993). In the present paper, we have reanalyzed the above results for a more detailed study of the interactions of hypoxia (FIO2 = 0.12), hypercapnia (FICO2 = 0.04) and changes in VO2 with the ventilatory control. The results show that: (1) Compared to normoxia, in hypoxia increments in V and VT are proportional to VO2 whereas in hypercapnia increments in ventilation (V) and tidal volume (VT) are independent of VO2. In both hypoxia and hypercapnia, increases in respiratory frequency (fR) are independent of VO2; and (2) Interactions of hypoxia, hypercapnia and VO2 with control of V persist in CBD rats but, for a given VO2, V, VT and fR are lower than in intact rats. These interactions are essentially similar to those observed during muscular exercise performed in normoxia, hypoxia or hypercapnia. It is suggested that during cold exposure or muscular exercise, resulting both in increased VO2, there are common integrative structures probably located in the hypothalamus which are involved in the control of breathing.
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PMID:Ventilatory response to CO2 and hypoxia during cold exposure in awake rats. 774 Jan 98

The effects of acute hypercapnia on human thermoregulation during cold exposure were investigated by immersion of eight male subjects to the neck in a 15 degrees C water bath until their core temperatures dropped to 35 degrees C or until 1 h of immersion had elapsed. Air was inspired throughout each experiment, with the exception of a 15-min period commencing with the attainment of an esophageal temperature (Tes) of 36.5 degrees C, during which subjects inspired a gas mixture containing 4% CO2, 20% O2, and 76% N2. Oxygen uptake (VO2, L.min-1), inspired minute ventilation (Vi, L.min-1), esophageal temperature (Tes, degrees C), rectal temperature (Tre, degrees C), mean unweighted skin temperature (Tsk, degrees C), mean heat flux (Q, W.m-2), and electromyographic activity (EMG, mV) of the trapezius and masseter muscles were recorded continuously. VO2 and integrated EMG activity (IEMG) were used as the primary indicators of shivering thermogenesis. Shivering EMG was attenuated immediately following the switch of the inhaled gas mixture from air to 4% CO2. For both the masseter and trapezius muscles the IEMG was significantly suppressed (p < 0.05) during the hypercapnic period. The IEMG values preceding the switch to the hypercapnic mixture were 15% greater than those during the CO2 period. Similarly, IEMG values in the post-CO2 period were 55% greater than during the CO2 period. It is concluded that acute periods of hypercapnia during cold exposure may result in transient suppression of shivering tremor, but this does not appear to affect thermal balance, as reflected in the absence of any significant effect on Tes.
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PMID:Shivering thermogenesis during acute hypercapnia. 806 70


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