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Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In progressive exercise increased tidal volume (VT) accompanies increased ventilation (VE) until a VT plateau is reached. We observed in 13 subjects a correspondence between the arrival of the VT plateau and the anaerobic threshold (AT). To examine this association between a mechanical event (the VT plateau) and a metabolic event (the AT), we changed those variables that change at the AT and looked for changes in VT. We found in 13 subjects that CO2 addition to prevent alveolar hypocapnia during cycle ergometer exercise progressing to exhaustion in 12-15 min significantly elevated the VT plateau (mean increase 4.4%; P less than 0.01) as compared with a spontaneous test that induced a mean end-tidal carbon dioxide tension fall of 5.5 Torr. This VT increase was mediated by a significant increase in inspiratory time (TI; P less than 0.02); both the ratio of TI to the total breath duration (TI/Ttot) and the mean rate of inspired airflow (VT/TI) were unchanged at matched VE. Changing other variables known to change at the AT--blood lactate ion concentration and alveolar oxygen tension--left ventilatory pattern unchanged. These results suggest that hypocapnia in severe exercise measurably lowers the VT plateau in normal man.
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PMID:CO2 and exercise tidal volume. 42 48

To study the relationship between proximal tubular reabsorption of bicarbonate, sodium, and chloride, the effects of changes in plasma PCO2 were examined in anesthetized dogs. Distal tubular reabsorption was inhibited by ethacrynic acid; plasma bicarbonate concentration was kept constant at 33.4 +/- 0.3 mM; glomerular filtration rate (GFR) was varied over a wide range to examine glomerulotubular balance (constant fractional reabsorption). Hypercapnia (PCO2, 112.0 +/- 2.5 mmHg) increased bicarbonate reabsorption by about 30%, and hypocapnia (PCO2, 19.8 +/- 0.6 mmHg) decreased reabsorption of bicarbonate by more than 50% and altered reabsorption of sodium, chloride, and bicarbonate in the molar ratios 2.7:1.6:1, respectively. During hypercapnia the range of glomerulotubular balance was extended to a GFR 125% of control. During hypocapnia glomerulotubular balance was present only at GFR below 50% of control; reabsorption of bicarbonate sodium, and chloride was constant at GFR exceeding 50% of control. During metabolic acidosis hypercapnia had no significant effect on reabsorption of bicarbonate, sodium, and chloride. These observations support the hypothesis that bicarbonate reabsorption is the main driving force for osmotic reabsorption of water and NaCl in the proximal tubules.
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PMID:Coupling of NaHCO3 and NaCl reabsorption in dog kidneys during changes in plasma PCO2. 42 65

Acute experiments on cats demonstrated a suppression of the cerebral vessels reaction to hypercapnia under condithacin, while the reaction to hypocapnia persisted. It is assumed that the effects of hypo- and hypercapnia on the cerebral vessels were realized by different mechanisms, i. e. reduction of prostaglandin concentration decreased the cerebral vessels sensitivity to hypercapnia and increased their sensitivity to hypocapnia.
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PMID:[Cerebral blood flow reactions to hypo- and hypercapnia during indomethacin inhibition of prostaglandin biosynthesis]. 42 75

1. In cats under pentobarbitone anaesthesia the effects of focal temperature changes of the ;chemoceptive' areas on the ventral surface of medulla, described by Loeschcke and his associates, were studied with respect to tidal volume, V(T), tidal variation in efferent phrenic activity, Phr(T), and respiratory rate. The cats were either paralysed and ventilated at various constant P(A,CO2) and P(a,O2) levels, or breathing spontaneously.2. It was confirmed that focal bilateral cooling of the intermediate, ;I((S))', areas caused rapid depression of respiration even at constant artificial ventilation. In normocapnic and normoxic conditions apnoea usually ensued at brain surface temperatures of 20-22 degrees C.3. The effects were graded along continuous temperature-response curves with enhancements of ventilation above and depression below normal body temperature.4. The strongest effects on V(T) and Phr(T) were obtained from the I((S)) areas with no or only small effects on inspiratory or expiratory timing in the vagotomized animal. The Hering-Breuer inflation reflex and its effects on timing and amplitudes were not affected by cooling this area.5. Focal cooling of the caudal or the rostral ;chemoceptive' areas, ;C((L))' and ;R((M))' areas, caused smaller effects on V(T) and Phr(T) but produced significant effects on respiratory rate even after vagotomy.6. The effects of focal cooling of these areas could be mimicked by topical application of procaine solution which has been shown not to penetrate deeper than 100 mum from the surface.7. Moderate focal cooling of area I((S)) to temperatures above 28-30 degrees C caused a parallel shift in the CO(2)-response (V(T), Phr(T)) curves to the right with little change in slope. The P(CO2) thresholds for apnoea were correspondingly raised. These focal temperature effects could be compensated by changes in P(CO2) with, on the average, 2.7 torr/ degrees C. Focal temperatures below 28 degrees C usually caused some decrease in slope of the CO(2)-response curves in addition to further shifts.8. Added hypoxic stimulus or electrical stimulation of the carotid sinus nerves caused an almost parallel increase of Phr(T) at all P(CO2) levels and all focal temperatures suggesting an additive type of interaction between the input from the peripheral chemoreceptors and that from the central (CO(2), H(+)) sensing structures whether the latter was altered by changing P(CO2) or by focal temperature changes on the I((S)) areas.9. In contrast to these effects of hypoxia and stimulation of the carotid sinus nerves the reflex increase of inspiratory activity caused by lung deflation or by electrical stimulation of the glossopharyngeal nerve distal to the carotid sinus nerves was CO(2) dependent. These reflex effects decreased with focal cooling of the I((S)) areas as with hypocapnia, suggesting a mainly multiplicative or ;gain-changing' type of interaction with the central chemoceptive drive.10. The close similarities in effect of focal cooling and of hypocapnia on the different respiratory parameters even during constant artificial ventilation indicate that focal temperature changes of the I((S)) areas intervene effectively with the normal ventilatory response to CO(2) without changing the chemical or physical environment of those neural structures in the brain stem which set respiratory pattern.
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PMID:Graded changes in central chemoceptor input by local temperature changes on the ventral surface of medulla. 43 Mar 96

We performed follow-up pulmonary function studies on three patients with acute pulmonary histoplasmosis over a period of several months, and found that the disease is benign and usually responds well to treatment or is self-limiting. There are four major changes in lung function, namely a restrictive defect, an impairment of diffusing capacity, stiff lung, and obstruction in small airways. These changes usually lead to disturbance of ventilation-perfusion ratios and impaired gas transport across alveolar capillary membranes, resulting in arterial hypoxemia. There is also hypocapnia from alveolar hyperventilation commonly found in restrictive and stiff lung syndrome.
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PMID:Pulmonary function studies in acute pulmonary histoplasmosis. 44 69

To clarify the problems of altitude tolerance in birds, we studied the combined effect of hypocapnia and hypoxia on cerebral blood flow (CBF) in ducks. CBF was measured by the xenon clearance method. Normocapnic hypoxia causes CBF to increase when the arterial O2 tension (PaO2) falls below 60--70 mmHg. Hypocapnic hypoxia significantly shifts the blood flow curve so that blood flow does not increase until a lower PaO2 (50--60 mmHg) is reached. This gives the appearance that hypocapnia suppresses the hypoxia-induced increase in CBF. However, due to the Bohr effect, the hypocapnic blood contains significantly more O2 than does the normocapnic blood at the same PaO2. Therefore, when CBF is expressed as a function of O2 content, rather than PO2, CBF in the hypocapnic group does not differ significantly from the CBF in the normocapnic group. We interpret this to mean that because of the significantly greater oxygen content of the hypocapnic blood at a given PaO2, the degree of hypoxia experienced by these brains is not as severe as that experienced by the normocapnic brains.
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PMID:Avian cerebral blood flow: influence of the Bohr effect on oxygen supply. 44 97

Injection of subconvulsive doses of strychnine blocking the inhibitory synapses significantly increases the reflex activity of the respiratory muscle evoked by stimulation of the sciatic nerve as well as by inhalation of hypercapnic gas mixture. Thus the inhibitory synapses prevent the extreme hypocapnia evoked by hyperventilation.
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PMID:[Hyperventilation and inhibitory synapses]. 46 79

We studied the effects of hypocapnia and methacholine on small airways resistance (Rsaw) and collateral ventilation in anesthetized paralyzed dogs. The animals were ventilated with air while either 10% CO2 or air (hypocapnia) was infused through a segment obstructed with a fiber-optic bronchoscope. Measurements were made before and after instillation of methacholine into the obstructed segment. Collateral resistance (Rcoll) and Rsaw increased with hypocapnia and methacholine. The time constant for collateral ventilation increased with hypocapnia, but did not change with methacholine because of decreases in the compliance of the obstructed segment. We conclude that collateral channels respond to methacholine and hypocapnia in a manner similar to small airways and that local parasympathomimetic stimulation, unlike lung deflation does not increase the time constant for collateral ventilation.
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PMID:Effects of methacholine and hypocapnia on airways and collateral ventilation in dogs. 46 15

Eight awake cats have been studied before and after carotid denervation during air and oxygen breathing, and during hypercapnia. Analysis of the variables that characterize the spirogram shows that carotid denervation consistently results in a decrease of the mean inspiratory flow (VT/TI), causing a decrease in tidal volume (VT) and ventilation with a relative alveolar hypercapnia. In carotid-denervated animals, inhalation of oxygen results in an increase in ventilation due to an augmentation of VT/TI and VT and a relative hypocapnia. TI does not significantly change in the different conditions whereas TE is significantly affected. TE seems therefore to be more closely related to the rate of rise of inspiratory activity than to inspiratory duration.
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PMID:Effects of carotid body denervation on respiratory pattern of awake cats. 46 36

The ventilatory effects of graded reductions in brain bloow flow (BBF) were studied in unanesthetized goats. At a BBF of 85% of control (PVO2 = 29.2 Torr, PVCO2 = 47.3 Torr) there were no clear ventilatory effects. At BBF of 70% of control (PVO2 = 25.2, PVCO2 = 50.5) and 50% of control (PVCO2 = 22.3, PVCO2 = 53.0) there was hyperpnea, due primarily to an increase of tidal volume. Further reduction of BBF (avg of 42% of control) first produced intense tachypnea and then (30--40% of control) caused apnea that was reversible. At 50% BBF there was a reduction of brain O2 consumption, (4.67--4.00 ml/min) and an increase in systemic O2 consumption. beta-Adrenergic blockade prevented the increase in systemic O2 consumption and reduced the hyperpnea by two-thirds at 50% BBF; the residual hyperpnea was associated with hypocapnia in contrast to the hyperpnea prior to beta-adrenergic blockade, which was virtually isocapnic. The data suggest that hyperpnea due to brain ischemia is a result of both brain acidosis and systemic hypermetabolism. The similarity of the pattern of responses to that previously reported for progressive carboxyhemoglobinemia suggests that brain hypoxia is a determinant of the ventilatory responses to brain ischemia.
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PMID:Effects of graded reduction of brain blood flow on ventilation in unanesthetized goats. 46 49


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