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

Graded degrees of both chronic hyper- and hypocapnia are known to induce renal responses that significantly alter plasma bicarbonate concentration. These findings have raised the possibility that even normal variations in PaCO2 play an important role in determining the exact level of bicarbonate in plasma. To test this hypothesis, we examined the relationship between resting levels of PaCO2 and the plasma bicarbonate concentration in two groups of normal dogs, one ingesting a normal salt diet and the other a salt-restricted diet. The results indicate that values for bicarbonate within the normal range are highly dependent on the prevaling level of carbon dioxide tension ([HCO3-] = 0.35 PaCO2 + 9.0, r = 0.72). Accordingly, approximately 50% of the normal variance in bicarbonate concentration is explained simply by the variance in PaCO2. The joint confidence region for bicarbonate concentration and PaCO2, which can be derived from these data, provides a new and more rigorous definition of the normal range for acid-base values in the dog.
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PMID:Effect of natural variations in PaCO2 on plasma [HCO3-] in dogs: a redefinition of normal. 3 8

In 660 supine, intubated and anaesthetized, healthy patients scheduled for various elective surgical procedures, the distribution of arterial carbon dioxide tension (PaCO2) was investigated during manual non-monitored ventilation. The study comprised six equal groups: group 1: ventilation with a circle circuit absorber system; group 2: ventilation with the Hafnia A circuit using a total fresh gas flow (FGF) of 100 ml . kg-1 . min-1; groups 3-6: ventilation with a Hafnia D circuit with fresh gas flows of 100, 80, 70 and 60 ml . kg-1 . min-1, respectively. The mean PaCO2's of the first three groups were situated in the lower range of normocapnia (the observations in the first group having the greatest total range), whereas the rebreathing (Hafnia A and D) circuits resulted in a clustering of observed data. Employing the rebreathing circuits, protection against hypocapnia can be achieved by lowering the fresh gas flow. The most satisfying result was obtained with the Hafnia D circuit with a fresh gas flow of 70 ml . kg-1 . min-1 resulting in normocapnia with a modest and limited spread towards hypo- and hypercapnia. FGF in excess of this level must be considered as wasted. The study indicates that corrections of fresh gas flows for age are superfluous. Use of relaxants and type of surgery had no influence on the observations.
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PMID:Arterial carbon dioxide tensions during anaesthesia with manual ventilation. A descriptive study of the effects of various non-polluting circuits. 3 15

Responses of aortic chemoreceptor afferents to a range of arterial carbon dioxide tension (Paco2) changes at various levels of arterial oxygen tension (Pao2) were investigated in 18 cats anesthetized with alpha-chloralose and maintained at 38 degrees C. Aortic chemoreceptor activity, end-tidal oxygen pressure, end-tidal carbon dioxide pressure, and arterial blood pressure were continuously monitored. Arterial blood gases were measured in steady states. Single or a few clearly identifiable afferents were studied during changes and steady states of Pao2 and Paco2. All the aortic chemoreceptor afferent discharge rates increased with Paco2 increases from hypercapnia (10-15 Torr) to normocapnia and moderate hypercapnia (30-50 Torr) and with Pao2 decreases from above 400 to 30 Torr. Hypoxia augmented the response to Paco2 most effectively in the range of 10-40 Torr. At any Pao2, the discharge rate reached a plateau with sufficient intensity of hypercapnia. The Paco2 stimulus threshold at a Pao2 of 440 Torr was about 15 Torr, and at a Pao2 of 60 Torr it was 10 Torr. In the transition from hypocapnia to hypercapnia, responses increased gradually, usually without an overshoot. The steady-state responses to Paco2 of the majority of aortic chemoreceptors resembled those of carotid chemoreceptors. The responses of both receptors can be attributed to the same basic type of mechanism.
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PMID:Aortic body chemoreceptor responses to changes in PCO2 and PO2 in the cat. 4 29

Separate and combined effects of acute metabolic acidosis and hypocapnia were determined in skeletal and cardiac muscles of intact rats. Normocapnic metabolic acidosis, imposed by intraperitoneal injection of hydrochloric acid (6 mEq/kg), did not change skeletal muscle intracellular acid--base parameters. Hypocapnia, induced by mechanical hyperventilation, resulted in intracellular alkalosis within skeletal muscle during both respiratory alkalosis and compensated metabolic acidosis; changes of skeletal muscle intracellular bicarbonate concentration per unit change in carbon dioxide tension were identical during these two experimental procedures. These data suggest that processes other than physicochemical buffering neutralize protons taken into skeletal muscle cells during acute metabolic acidosis. The acid--base state of the heart was quite stable during these experimental manipulations; thus, it appears that cardiac muscle has an extraordinary buffering ability. Moreover, our data suggest that processes other than physicochemical buffering maintain cardiac intracellular pH normal during hypocapnia.
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PMID:Effect of hypocapnia on intracellular pH during metabolic acidosis. 4 59

To investigate the influence of variations in arterial oxygen tensions (PaO2), arterial carbon dioxide tensions (PaCO2), and arterial pH on long bone medullary pressures, seven anaesthetized dogs were investigated. Comparing the control medullary pressures, i.e. the mean medullary pressures obtained at the normal range of PaO2 (75--110 mmHg) with the mean medullary pressures corresponding to the range of PaO2 of less than 75 mmHg, statistically significant (P less than 0.05) decreases were seen in both epiphyseal, metaphyseal and diaphyseal medullary pressures, from 27.6 +/- 5.0 to 15.5 +/- 3.6 mmHg, from 23.5 +/- 2.9 to 13.9 +/- 2.3 mmHg and from 27.7 +/- 3.9 to 18.3 +/- 2.5 mmHg (all mean values +/- s.e. mean), respectively. Hyperoxia, hypocapnia, hypercapnia or metabolic acidosis had no effect on medullary pressures in any of the regions studied.
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PMID:Observations on long bone medullary pressures in relation to arterial PO2, PCO2 and pH in the anaesthetized dog. 4 59

Intravenous injection of CT 1341 (a mixture of alphaxalone and alphadolone dissolved in cremophor el) induced a decrease in cerebral blood flow (CBF) measured by 133Xe clearance in cats with artificial respiration (the mean reduction in CBF was 2 ml/100 g/mn for 1,2 mg/kg or CT 1341. So, CBF was decreased by 22% when CT 1341 (7,2 mg/kg) was intravenously injected, (mean Pa CO2 equals 30 mm Hg). Changes in CBF following CT 1341 intravenous injection seems to be caused by cerebral vascular constriction evidenced by the direct observation of pial vessels. Following intravenous injection of CT 1341 (from 7, 2 mg/kg to 19,2 mg/kg), the cerebrovascular reactivity to hypercapnia or hypocapnia was not affected, but autoregulation of cerebral blood flow was transiently abolished. In animals with free respiration, CBF was increased in relation with the elevation in Pa CO2 caused by the depression of respiration.
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PMID:[Effects of combination alfaxalone and alfadolone, anesthetic derivatives of pregnanedione, on cerebral hemodynamics in cats]. 12 19

Nitroglycerin was administered to a group of 11 patients with chronic obstructive pulmonary disease in a dose of 0.4 mg sublingually. Arterial blood gases and blood pressure and pulse were measured at 5-min intervals for 30 min after nitroglycerin. There was a slight decrease in arterial O2 tension for the duration of the study; the maximal change was from a mean pre-nitroglycerin value of 53.5 mm Hg to 50.3 mm Hg at 20 min. In addition, there was a slight reduction in arterial CO2 tension and bicarbonate for 25 min. It is postulated that decreased O2 transport (due to increased hypoxemia and probably decreased cardiac output) plus hypocapnia were a sufficient stimulus to raise blood lactate. It is recommended that in patients receiving nitroglycerin who have obstructive airway disease, attention be directed toward the effect on arterial blood gases.
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PMID:The effect of nitroglycerin in gas exchange on chronic obstructive pulmonary disease. 23 14

The effects of halothane, enflurane, and methoxyflurane on hypocapnic bronchoconstriction (increased airway resistance and decreased compliance of the lung) were studied in vivo in the isolated left lower lobe of the canine lung. Hypocapnic bronchoconstriction, induced by altering the concentration of CO2 in gas ventilating the lobe, was repeated in the presence and absence of various concentrations of anesthetic gases (halothane: 0.5, 1.0, and 3.0 per cent; enflurane: 1.0, 3.0, and 5.0 per cent; methoxyflurane: 0.25, 0.50, and 1.0 per cent). In the higher concentrations, all three drugs blocked the bronchoconstrictor effect produced when the inspired CO2 was decreased from 5 to 0 per cent. In lower concentrations, halothane was the most effective blocking drug. Propranolol did not affect the ability of the three anesthetics to block hypocapnic bronchoconstriction, nor did the beta-receptor blocking drug sotalol affect the blocking effects of halothane. The ability of these anesthetics to block hypocapnic bronchoconstriction probably is mediated not through an adrenergic mechanism but by one that is nonspecific. (Key words: Lung, bronchoconstriction; Carbon dioxide, hypocarbia; Anesthetics, volatile, halothane; Anesthetics, volatile, enflurane; Anesthetics, volatile, methoxyflurane.)
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PMID:Hypocapnic bronchoconstriction and inhalation anesthetics. 24 37

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

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


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