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

The changes in the responsiveness of pial arterioles to CO2 and in the composition of cortical cerebrospinal fluid bathing these vessels were studied in the awake rabbit before and after 6 days exposure to hypercapnia (7% CO2) or hypoxia (10% O2). The vasodilator response of pial arterioles to inhalation of 3--10% CO2 was diminished after prolonged hypercapnia and enhanced after prolonged hypoxia. After both hypoxia and hypercapnia, pial arteriolar responsiveness to CO2 was immediately returned toward control levels by washing the brain surface with normal artificial cerebrospinal fluid. The bicarbonate concentration of cerebrospinal fluid bathing the pial vasculature showed a significant decrease after hypoxia and a significant increase after hypercapnia, whereas CSF pH remained unaltered. We conclude that the alteration in responsiveness of pial arterioles to CO2 is due to a change in the chemical composition of the CSF bathing these vessels, involving an adjustment in the concentration of bicarbonate ions.
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PMID:Responses of pial arterioles after prolonged hypercapnia and hypoxia in the awake rabbit. 45 36

Five anesthetized dogs were made severely hypercapnic by stepwise addition of CO2 to their inspired air. Blood PCO2 levels greater than 400 Torr were reached. During hypercapnia, the steady-state end-tidal PCO2 (PaCO2) was always higher than the simultaneous measured arterial PCO2 (PaCO2). The mean ratio PaCO2/PACO2 was 0.861 +/- 0.01. These results are consistent with the predictions of the Charged Membrane Hypothesis, that gas-to-blood PCO2 differences should be directly proportional to the blood H+ activity. The results cannot be explained by delayed equilibration of CO2 between plasma and red blood cells. The latter hypothesis predicts that, under the conditions of these experiments, the PCO2 of arterial blood should be higher than the PCO2 of end-tibal gas. The blood HCO3- during hypercapnia did not increase as much as would be predicted if the blood were exposed to CO2 in vitro. This may reflect movement of blood HCO3- generated by the buffering of carbonic acid into intracellular compartments during hypercapnia.
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PMID:Gas-to-blood PCO2 differences during severe hypercapnia. 46 74

The central control mechanism of respiratory frequency under varied alveolar carbon dioxide pressure (PACO2 20--200 Torr) was investigated in anesthetized, vagotomized, immobilized, and artificially ventilated rabbits. Central inspiratory activity indicated by phrenic motor discharge was tolerant of the extensive hypercapnia. Under light anesthesia the respiratory frequency (f) decreased in a hyperbolic fashion with increasing PACO2. Under deeper anesthesia or after mesencephalic decerebration the hyperbolic f response to PACO2 was abolished or changed to a hill-type f response (initial increase and subsequent decrease in f) and, on the average, the changes in frequency were much less. We conclude that in the absence of vagal control the respiratory frequency is primarily determined by 1) the periodicity of the bulbopontine inspiratory activity, which is little dependent on PACO2, and 2) a suprapontine acceleratory mechanism, which is depressed by increased PACO2 and highly sensitive to anesthetics. The mechanism of changes in the type of f response to CO2 is discussed.
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PMID:Phrenic activity during severe hypercapnia in vagotomized rabbits. 46 79

We have studied the propensity for periodic breathing to occur in cats anaesthetized with pentobarbitone breathing either spontaneously or with the aid of a 'servo-respirator' governed continuously by the efferent phrenic nerve activity. Sustained periodic breathing could be induced increasing 'controller gain', either by increasing the gain of the respirator, or by lung deflation, which reflexly increased controller responses to both hypoxia and hypercapnia. Periodic breathing was potentiated both by hypoxia and by diminishing the central (CO2, H+)-drive by focal cooling at the ventral surface of the medulla, two procedures which increase the relative influence of hypoxic drive. Less hypoxia was needed to produce periodic breathing at high rather than low controller gains. Reducing controller gain to zero by constant artificial respiration always abolished periodic breathing. Periodic breathing was also eradicated when the relative importance of CO2 drive was enhanced by breathing the cats with CO2-enriched gas mixtures or with 100% O2. The results are consistent with theoretical predictions for the occurrence of oscillations in the mechanisms for the chemical control of breathing and indicate that increasing controller gas can produce periodic breathing. The results further emphasize the importance of the (CO2, H+)-drive in preserving ventilatory stability.
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PMID:Experimentally induced Cheyne-Stokes breathing. 47 22

In chronic obstructive pulmonary disease (COPD), the neuromuscular response to an acute increase in airflow produced by external flow resistive loads (FRL) is impaired. The present study compared the response to FRL of 15 subjects with airway obstruction due to asthma and that of 15 normal subjects. FRL were applied during progressive hypercapnia and isocapnic hypoxia produced by rebreathing techniques to permit the response to be assessed at the same degree of CO2 or O2 drive. The neuromuscular response to FRL was assessed from the airway occlusion pressure developed 100 msec after the onset of inspiration (P100), as well as ventilation. During control rebreathing, ventilatory responses to hypercapnia (ratio of change in minute ventilation to change in PCO2, delta VE/delta PCO2) and hypoxia (ratio of change in VE to the change in percentage of O2 saturation, delta VE/deltaSO2) were the same in asthmatic and normal subjects despite differences in the mechanics of breathing. The P100 response to hypercapnia delta P100/delta PCO2) and hypoxia (delta P100/delta SO2) as well as absolute P100 at any given degree of O2 and CO2 drive was greater during control rebreathing in asthmatics than in normal subjects (P less than 0.05). FRL values of 9 and 18 cm H2O per L per sec applied during either hypercapnia or hypoxia increased the occlusion pressure to a greater extent in asthmatics than in normal subjects. Methacholine-induced bronchoconstriction was used to test the effect of acute airway obstruction on the response to FRL. Bronchoconstriction was associated with an increase in the P100 response to hypercapnia and to FRL, despite increases in lung volume and decreases in inspiratory muscle force. We conclude that: (1) asthmatics with airway dysfunction have an increased nonchemical drive to breathe mediated at least in part by sensory receptors in the airways; (2) asthmatics with airway obstruction respond supernormally to acute changes in resistance to airflow, unlike subjects with COPD. The failure of COPD subjects with prolonged airway obstruction to respond to FRL may be due to adaptation of the sensory mechanisms that respond to changes in airway resistance.
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PMID:The respiratory neuromuscular response to hypoxia, hypercapnia, and obstruction to airflow in asthma. 48 28

The effect on CO2 storage and elimination of variations in the slope and intercept of the ventilatory response to CO2 curve was examined. Theoretical and experimental results show that although CO2 elimination rate following a transient ventilatory disturbance is decreased at low ventilatory response slopes, this decrease can be compensated by elevated PCO2 intercepts, or thresholds. Conversely, high CO2 elimination rate following a ventilatory disturbance due to a high ventilatory response slope can be off-set by a depressed PCO2 threshold. The results suggest that elevated thresholds which often accompany depressed ventilatory response slopes may be part of a compensatory mechanism for minimizing transient hypercapnia and acidosis.
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PMID:Transient CO2 elimination and storage as functions of the ventilatory response to CO2. 49 46

We measured cerebral blood flow using both the radioactive microsphere technique and the cerebral venous outflow technique in dogs anesthetized with chloralase. The effect of sympathetic stimulation on cerebral blood flow was observed during both normocapnia and prolonged hypercapnia using both blood flow techniques. The increase in blood flow with hypercapnia was the same with both methods. During hypercapnia the venous outflow method showed a 38% decrease and microspheres an 18% decrease in cerebral blood flow with sympathetic stimulation. At normal CO2, stimulation caused a decrease in cerebral venous flow: no change was observed with the microsphere method. Analysis of the blood flow patterns to extracerebral tissues and evaluation of extracerebral arterial reference samples failed to prove the existence of axial streaming and subsequent skimming of microspheres within the cephalic circulation. It is concluded that direct electrical stimulation of the sympathetic innervation of the cerebral vessels is capable of reducing cerebral blood flow even during a profound hypercapnic vasodilation.
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PMID:Sympathetic modulation of hypercapnic cerebral vasodilation in dogs. 49 41

One subject was exposed for six days to increasing levels of CO2, rising at a constant rate from 0.03 to 3.0% CO2 within a 15-h period followed by 9 h of air breathing. To assess acid-base parameters, arterialized capillary blood was taken from a finger twice daily (at 8 a.m. and 11 p.m.) at times corresponding to the beginning and end of the intermittent exposure to CO2. Venous blood samples were obtained on alternate days at the same times. Urine specimens were collected twice daily. The subject was on a liquid diet. Resting respiratory minute volume (VE), oxygen consumption (VO2), carbon dioxide excretion (VCO2), alveolar carbon dioxide and oxygen tension (PACO2) and PAO2) were measured twice daily. PACO2 and PAO2 were also determined at the end of breath-holding twice daily; CO2 tolerance tests and lung function tests were also carried out. In contrast to the effects of chronic exposure to 3% CO2, the CO2 tolerance tests showed an increased sensitivity (increase of slope) and breath-holding PACO2 did not change, indicating that acclimatization to CO2 did not develop. The ventilatory response to CO2 was not sufficient to prevent CO2 accumulation in the body; this accumulation was eliminated during the nightly air-breathing periods on the fourth and fifth days, indicated by higher values of PaCO2 and PACO2. The known renal response to hypercapnia, consisting of an increased excretion of titratable acidity, ammonia, and hydrogen ion excretion, occurred but was interrupted after the first day and was triggered again on the fourth and fith days when accumulated CO2 was released from body CO2 stores. The second renal response was associated with a marked calcium excretion, which suggests that bone CO2 stores were involved.
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PMID:Effect of intermittent exposure to 3% CO2 on respiration, acid-base balance, and calcium-phosphorus metabolism. 50 20

A recent report (J. Appl. Physiol. 38: 382-388, 1975) suggests that negative blood-gas CO2 partial pressure (PCO2) differences exist in the dog during hypercapnia, as mean expired PCO2 exceeded arterial PCO2 by more than 10 Torr when the CO2 fraction in inspired gas (FICO2) was 0.1. We have reinvestigated this problem in anesthetized dogs breathing spontaneously room air or hypercapnic mixtures (FICO2 = 0.05 or 0.10). During steady state, arterial blood samples were analyzed with electrodes, care being taken to keep the electrode temperature within +/- 0.2 degrees C at the actual aortic temperature of the animal. Respired gas was measured at the tracheostomy by a sensitive low-noise respiratory mass spectrometer. During room air breathing, the arterial-end-expired PCO2 difference, P(a-E')CO2, averaged +5 Torr and decreased to +0.9 Torr and to +0.1 Torr with FICO2 = 0.05 and 0.1, respectively. Hypoxia (FIO2 = 0.10) had no apparent effect on the P(a-E')CO2 difference. We ascribe the decrease in P(a-E')CO2 with hypercapnia to the diminishing effects of alveolar dead space, whereby end expired PCO2 approached arterial PCO2. We then conclude that in blood-gas equilibration lungs, PCO2 in end-capillary blood comes close to alveolar PCO2, and that the negative blood-gas PCO2 differences reported earlier are probably caused by deficiencies in the techniques used.
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PMID:Arterial-expired PCO2 differences in the dog during acute hypercapnia. 51 9

The steady-state arterial CO2 tension (PaCO2) was examined during control and intravenous CO2 loading in awake dogs unencumbered by any breathing apparatus. The dogs inhaled air while undergoing intravenous CO2 loading, and we estimated the gain, delta VA/delta PACO2. CO2 was introduced into the systemic venous blood via a membrane gas exchanger in a femoral arteriovenous shunt circuit, and the extracorporeal blood flow was maintained constant at 0.5 l/min. A total of 11 experiments were performed in 3 dogs comprising 93 control observations and 83 CO2 loading observations. Intravenous CO2 produced a significant increase in the steady state PaCO2, a finding consistent with our previous study in tracheostomized awake dogs. We conclude that intravenous CO2 produces hypercapnia in the awake dog with an intact airway unencumbered by external respiratory apparatus.
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PMID:Arterial PCO2 response to intravenous CO2 in awake dogs unencumbered by external breathing apparatus. 51 11


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