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

Young healthy test subjects showed adaptation to chronic hypercapnia during long-term exposure to an atmosphere containing 0.8--1.8% CO2 at normal atmospheric pressure: bradycardia, increase in vital lung capacity and chest movements, improvement of tests with breathing retention and further decrease in oxyhemoglobin. Simultaneously they exhibited an increase in the alkaline reserve of the blood and of the 2 min step-test index. This can be interpreted both as cause and effect: products of glycolysis are bound by buffer bases, thus reducing oxygen uptake per time unit. Study of adaptation to exercises of increasing workload demonstrated an earlier involvement of anaerobic mechanisms than under normal conditions: linear relationship between the workload and heart rate persisted only up to 150 beats/min. By the end of the second and the beginning of the third month of isolation the test subjects displayed deteriorated health state and work capacity in parallel with compensated acidosis.
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PMID:[Tolerance for controlled physical loading in chronic hypercapnia in man]. 64 21

Approximately isopnoeic conditions (VE=40 l/min) were achieved by the inhalation of asphyxial gas mixtures (PA,O2 60 torr, PA,CO2 40-45 torr) in normothermia after a rise in rectal temperature of 1.6 degrees C had been induced by a heated flying suit. Arterial chemoreceptor drive was transiently reduced by either isocapnic removal of hypoxia (type (1) tests: two breaths of CO2 in O2) or simultaneous withdrawal of both hypercapnia and hypoxia (type (2) tests: two breaths of O2). 8-13 tests of each type were performed at both temperature conditions in 6 expts. on 4 healthy human subjects. Expired volume, total breath duration and inspiratory time were recorded, and minute ventilation and expiratory time subsequently computed breath by breath. In hyperthermia the steady-state ventilation of 40 l/min (at a relatively higher respiratory frequency and a correspondingly lower tidal volume) was achieved at a PA,CO2 which was 5 torr lower than in normothermia. Ventilation decreased significantly in all tests. Tested with a 3-way analysis of variance significant differences between the ventilatory responses at the two temperature conditions, and between the two test types were found. The rate of change of ventilation was greater in hyperthermia than in normothermia, and also greater in type (2) tests than in type (1) tests. Since isopnoeic conditions existed prior to the tests, this implies that the arterial chemoreceptor contribution to the total ventilatory drive is increased in hyperthermia. In type (2) tests a significant lengthening of expiratory time was observed in the first test breath. This finding confirms the effect in man of changes in airway PCO2 on lung stretch receptor discharge.
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PMID:Short-latency ventilatory responses to sudden withdrawal of hypoxia at normal and raised body temperature in man. 64 71

Respiratory drive (deltaP 0.1/deltaPCO2) and ventilatory response (deltaVE/deltaPCO2) to CO2 has been estimated in 20 normal subjects and 28 patients with chronic obstructive pulmonary disease (COPD). In patients with COPD, drive and ventilatory response to CO2 were diminished, but no statistical correlation with FEV1, MBC, TLC, FRC, RV/TLC was found. A statistically negative correlation was found between blood bicarbonate and drive or ventilatory response to CO2. Patients with emphysema and normal PaCO2 demonstrated normal deltaP 0.1/deltaPCO2. In contrast, patients with chronic bronchitis with the same pulmonary function abnormalities and hypercapnia had significant diminution of the deltaP 0.1/deltaPCO2. Therefore, we feel that pulmonary function abnormalities alone cannot explain the deltaP 0.1/deltaPCO2 decrease; in most cases there sould coexist a diminished respiratory sensitivity.
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PMID:Respiratory drive in patients with chronic obstructive pulmonary disease. 67 65

To elucidate the effects of halothane on chemical regulation of ventilation in man, the authors studied the ventilatory responses to isocapnic hypoxia and hyperoxic hypercapnia in 33 human subjects while fully conscious and during sedation or anesthesia with halothane, .1, 1.1, or 2 MAC. In each group, the ventilatory effect of intravenous administration of doxapram, .4 mg/kg, was also measured. Halothane, 1.1 and 2 MAC, totally abolished the hypoxic response and nearly abolished the response to doxapram, while leaving the response to CO2 relatively brisk. Halothane, .1 MAC, decreased the responses to hypoxia and doxapram to less than a third of control, but did not alter the response to CO2. It is concluded that halothane selectivity impairs two ventilatory responses mediated by peripheral chemoreceptors in man.
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PMID:Ventilatory responses to hypoxia and hypercapnia during halothane sedation and anesthesia in man. 69 78

The effects of inspiration of low O2 and/or high CO2 gas mixtures on relative tissue PO2 and perfusion of brain and muscle were studied in 60 pentobarbital-anesthetized spontaneously respiring rats. These animals were studied in intact condition, after administration of phenoxybenzamine hydrochloride, 2 mg/kg, or after bilateral denervation of their carotid bodies. In the intact rats, the relative tissue PO2 ratio of biceps brachii to cerebral white matter always decreased after exposure to the above gas mixtures. This indicated a better maintenance of O2 supply to demand in the brain than in muscle. After either carotid denervation or alpha adrenergic blockade, this change in the ratio was no longer significant. Further, cerebral blood flow responses to these gas mixtures were attenuated (avg + 5.3%) compared to previous work in intact rats. It is concluded that the brain is best protected against hypoxia and/or hypercapnia when the carotid chemoreflex is intact.
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PMID:Blood flow and relative tissue PO2 of brain and muscle: role of carotid chemoreceptors. 70 Nov 27

Experiments on anesthetized chickens were conducted to study interactions between afferent activity from the intrapulmonary and systemic CO2-sensitive chemoreceptors in the generation of respiratory amplitude (RA) and respiratory frequency (f). The thoracoabdominal cavity was opened, air sacs ruptured and each lung independently and unidirectionally ventilated. Intrapulmonary chemoreceptor activity was altered by changing the PCO2 of the ventilatory gas (PICO2) to the vascularly isolated right lung (VIL); systemic chemoreceptor activity was altered by changing the PICO2 to the denervated left gas exchange lung (GEL). Respiratory amplitude and frequency responses to changes in intrapulmonary PCO2 were determined at four levels of systemic arterial PCO2 (PaCO2). The results indicate that elevating PaCO2 shifts the pulmonary CO2-response curves for both RA and f to the left and increases the sensitivity of the RA-CO2 response curve but decreases the sensitivity of the f-CO2 response curve. We conclude that (1) interaction occurs between intrapulmonary and systemic afferent activity in the generation of RA and f, (2) the nature of the interaction is synergism with respect to RA and interference with respect to f, and (3) the interaction is greater during hypocapnia than hypercapnia.
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PMID:Intrapulmonary and systemic CO2-chemoreceptor interaction in the control of avian respiration. 70 70

We have attempted to identify the afferent endings responsible for the pulmonary-CO2 ventilatory reflex. We recorded afferent vagal impulses arising from the left lung in anesthetized dogs with separately ventilated lungs. When the left pulmonary artery was occluded, left lung PCO2 fell to 3 mm Hg and slowly-adapting pulmonary stretch receptor activity increased 46%. Firing declined to its original intensity when left lung PCO2 was raised in steps by administration of CO2, firing decreasing most between 2 and 19 mm Hg, and least between 30 and 50 mm Hg. Irritant receptor activity also increased (from 2.8 to 7.4 impulses/sec) after pulmonary arterial occlusion, the effect being reversed by administration of CO2. These procedures caused trivial changes in pulmonary and bronchial C-fiber activity. Effects on both slowly-adapting stretch receptors and irritant receptors appeared to result from a direct action of CO2 on the endings themselves, rather than from mechanical changes in the lung. Changes in slowly-adapting stretch receptor activity provide an adequate explanation for the pulmonary-CO2 ventilatory reflex, the relationship between impulse frequency and lung PCO2 suggesting that these afferents may have a role in limiting CO2 loss under conditions causing hypocapnia, but be less effective in stimulating breathing during hypercapnia.
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PMID:II. Effect of CO2 on afferent vagal endings in the canine lung. 70 75

In rats, the phenomenon of considerable increase in resistance to acute hypoxia observed after 2-hour stay under conditions of gradually increasing concentration of CO2, decreasing concentration of O2, ANd external cooling at 2--3 degrees seems to be based mainly on changes in concentration of CO2 (ACCORDINGLY, PCO2 and other forms of CO2 in the blood). The high resistance to acute hypoxia develops as well after subcutaneous or i.v. administration of 1.0 ml of water solution (169.2 mg/200 g) NaHCO2, (NH4)2SO4, MgSO4, MnSO4, and ZnSO4 (in proportion: 35 : 5 : 2 : 0.15 : 0.15, resp.) or after 1-hour effect of increased hypercapnia and hypoxia without cooling.
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PMID:[Role of CO2 fixation in increasing the body's resistance to acute hypoxia]. 72 Jun 76

The effects of hyberbaric nitrogen on the responses of ventilation and central inspiratory activity (CIA) to progressive hypercapnia were studied in eight subjects rebreathing a) O2 at an ambient pressure of 1.3 bar (control), and b) air at 6.1 bar (PO2 = 1.3 bar, PN2 = 4.8 bar). Inspiratory occlusion pressure (P0.1), pulmonary ventilation, and end-tidal PCO2 were used for the computation of individual CIA and ventilatory CO2 response curves. Increasing the inspired PN2 to 4.8 bar caused, on the average, a 40% increase of P0.1 at PCO2 = 50 Torr, whereas the slope of the ventilatory CO2 response curve was reduced by 39%. It was concluded that, at raised air and nitrogen pressures, CIA is increased, although not sufficiently to prevent a reduction of ventilation brought about by the increased gas density and consequent increase in airway resistance. The increased airway resistance is thought to be responsible for the increase in CIA by causing a reflex stimulation of the respiratory centers.
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PMID:Dissociated ventilatory and central respiratory responses to CO2 at raised N2 pressure. 73 May 72

An electron microscope study of the left ventricular myocardium from rat acclimatized to chronic hypercapnia was done in order to complete the preceding work concerning general effects of respiratory acidosis. After 15 and 30 days of the acclimatation to 8% CO2 no lesions of the myocardium could be found. The results of the morphometric analysis indicated, however, discrete modifications of heart ultrastructure similar to those found before in hypoxic and failing hearts: namely a decrease of mitochondrial mean diameter and a non significant decrease of mitochondrial fractional volume. The latter was accompanied by a significant decrease of myofibrillar mass. The presence of cellular oedema seems to be suggested by an increase of fractional volume of the cytosol. The mechanism of these changes is not easy to explain. Further work will be necessary to make a choice between two possibilities: (1) depressed contractility related to some direct effect of high pCO2 and (2) tissue hypoxia secondary to local effects of the former.
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PMID:[The rat ventricular myocardium in chronic hypercapnia. Electron microscopic study]. 77 46


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