Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

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

A marked increase in the prostaglandin E (PGE) content in the cerebrospinal fluid (CSF) and the arterial blood of cats was observed under conditions of 3-minute hypocapnia. During 30-minute hypocapnia a restoration of the initial PGE level was seen. The PGE content in CSF increased while in the arterial blood it decreased comparatively to the control under conditions of 3-minute hypercapnia. In 30-minute hypercapnia the PGE amount in the CSF and the blood dropped in comparison with 3-minute hypercapnia being below the basal level in the blood. It is suggested that in hypocapnia PGE should limit its constrictive effect on the cerebral vessels while under conditions of hypercapnia they are to promote the realization of the cerebral vessel reaction to CO2.
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PMID:[Variations in prostaglandin E content in the arterial blood and cerebrospinal fluid under conditions of hypo- and hypercapnia]. 51 23

1. Extracellular micro-electrodes were used to measure the responses of expiratory bulbospinal neurones to CO2 in anaesthetized, paralyzed cats, ventilated with O2. Simultaneous measurements were made of phrenic nerve and intercostal nerve filament discharges. 2. Hypocapnia produced tonic activity in some of the expiratory neurones and in expiratory filaments but rendered the phrenic and inspiratory filaments silent. 3. A graded excitatory effect of CO2 on tonic activity of both the neurones and the filaments was seen which progressed smoothly and continuously to rhythmic activity as CO2 was increased and to zero as CO2 was decreased. 4. Increases in blood pressure produced effects which were opposite to those produced by CO2, and which had a faster time course. 5. The CO2 response curves of those units showing tonic activity were indistinguishable from the CO2 response curves of those which did not. 6. A mid line lesion in the medulla interrupted inspiratory activity, converting activity of expiratory bulbospinal neurones from periodic to ionic firing patterns. 7. Following such lesions the CO2 threshold for rhythmic excitation of medullary neurones was elevated and the slopes of their CO2 response curves were reduced. 8. These findings fully confirm the hypothesis put forward by Bainton, Kirkwood & Sears (1978b) that bulbospinal respiratory neurones convey both tonic and rhythmic excitation to spinal respiratory motoneurones and that the rhythmic excitation of expiratory muscles derives from a period inhibition of expiratory bulbospinal neurones which are subjected to a tonic CO2 dependent excitation which is continuously variable over the physiological range.
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PMID:The effect of carbon dioxide on the tonic and the rhythmic discharges of expiratory bulbospinal neurones. 52 96

Recent studies have indicated that the breathing frequency responses to inspired CO2 in part result from changes in pulmonary stretch receptor activity. Pulmonary CO2 may alter frequency by direct inhibition of stretch receptor discharge, or secondarily, by changes in airway mechanics. The vascularly isolated left lower lobe (LLL) of the canine lung was used to determine the effect of hypocapnic airway constriction on the pulmonary CO2 reflex. The upper and middle lobes of the left lung were removed and the right vagus nerve sectioned. Blood was recirculated through the LLL. Diaphragm electromyogram was used as an index of respiratory center activity and to trigger ventilation of the left lower lobe. Lobar hypocapnia increased peak airway pressure and reduced respiratory rate. However, infusion of isoproterenol or the use of a mechanical overflow system to block the airway pressure response prevented the frequency changes associated with CO2. Although both the direct and mechanical effects of CO2 on stretch receptors may contribute to the reflex, in the LLL preparation the mechanical effects predominate.
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PMID:Breathing frequency responses to pulmonary CO2 in an isolated lobe of the canine lung. 53 90

1. Electromyography was used to measure the response of the diaphragm and intercostal muscles to CO2 in artificially ventilated decerebrate cats. 2. Hypocapnia produced tonic activity in either inspiratory or expiratory muscles or both, according to the preparation. 3. A graded effect of CO2 on both rhythmic and tonic activity was observed and for the latter this could be seen at as low as 10 torr PA,CO2. 4. In one human subject tonic firing of expiratory motoneurones was also induced by hypocapnia and this activity showed a graded increase with increasing (CO2. 5. A saggital incision of the medulla aimed at interrupting inspiratory bulbospinal axons abolished activity in inspiratory muscles and at eupnoeic levels of CO2 converted the activity of expiratory muscles from a periodic to a topic firing pattern. 6. Following such lesions the threshold for rhythmic excitation of expiratory muscles was elevated and this revealed that the graded effect of CO2 on tonic expiratory activity extends to as high as 60 torr. 7. The tonic activation of respiratory muscles in response to CO2 ceased after cervical cord transection or when the saggital incision in the medulla was extended caudally to the first cervical segment. 8. It is concluded that the CO2 dependent activation of spinal respiratory motoneurones is conveyed by bulbospinal axons which decussate in the vicinity of the obex and that this activation can be rhythmic or tonic. 9. It is suggested that the rhythmic excitation of expiratory muscles derives from a periodic inhibition of expiratory bulbospinal neurones which are subjected to a tonic CO2 dependent excitation which is continuously variable over the physiological range.
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PMID:On the transmission of the stimulating effects of carbon dioxide to the muscles of respiration. 69 Aug 72

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


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