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

1. In four awake dogs we measured EMG activity of three inspiratory and four expiratory muscles during sustained central chemoreceptor stimulation (CO2 inhalation), and peripheral chemoreceptor stimulation (intravenous infusion of almitrine bismesylate (almitrine)). By using this selective pharmacological stimulation of the peripheral chemoreceptors and reversibly cold-blocking pulmonary stretch receptors, we were able to determine the effects of each type of stimulation on respiratory muscle recruitment in the absence of such complicating influences as pulmonary stretch receptor feedback, cerebral hypoxia or hypocapnia, and differences in breathing pattern. 2. During 10 min of steady-state hyperpnoea (minute ventilation VI, approximately twice eupnoea) caused by either hypercapnia or isocapnic stimulation of the carotid bodies with almitrine, all three inspiratory and all four expiratory muscles demonstrated significant and sustained elevations in EMG activity. 3. With both types of chemoreceptor stimulation, as tidal volume, VT, increased, so did the mean electrical activities of the crural diaphragm (r = 0.88), costal diaphragm (r = 0.93), parasternals (r = 0.82), triangularis sterni (r = 0.74), transversus abdominis (r = 0.77), external obliques (r = 0.68) and internal intercostals (r = 0.75). 4. In each dog, the response of ventilation and of the diaphragmatic EMG to a given level of central or peripheral chemoreceptor stimulation is highly reproducible from one test day to the next. On the other hand, accessory inspiratory and expiratory abdominal and rib cage muscles in two of the four dogs showed highly significant changes from day to day in the amount of their EMG activity at any given VT. 5. During steady-state ventilatory stimulation, 2 min intervals were chosen during which the two types of chemoreceptor stimulation had caused hyperpnoeas with similar values for VT, total time per breath (TTOT) and inspiratory time divided by the total time (TI/TTOT). Comparison of EMG activities during these matched hyperpnoeas revealed that there were no differences in the activities of any of the muscles between the two forms of stimulation. We conclude that peripheral chemoreceptor stimulation causes significant and sustained recruitment of expiratory muscles even in the absence of pulmonary feedback and that both expiratory and inspiratory muscles are recruited to the same extent during peripheral chemoreceptor stimulation as they are during an identical hyperpnoea caused by central chemoreceptor stimulation.
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PMID:Respiratory muscle recruitment during selective central and peripheral chemoreceptor stimulation in awake dogs. 159 81

Previous reports suggest that isometric exercise (2-min handgrip at 50% maximal voluntary contraction [MVC]) substantially lowers intraocular pressure (IOP). The authors questioned whether the mechanism for lowered IOP in exercise is secondary to hyperventilation. Accordingly, in this study 11 subjects, with elevated IOP (greater than or equal to 18 mm Hg) and otherwise healthy, did 2 min of handgrip exercise at 50% MVC with and without carbon dioxide supplementation to maintain isocapnic conditions. Compared with a control experiment that involved neither exercise nor CO2 addition, exercise induced a fall in IOP from 18.3 to 15.6 mm Hg (P less than 0.001). This statistically significant decline in IOP persisted for 15 min after the exercise session. At the point of minimum IOP (1 min after the end of exercise), the minute ventilation was elevated from 6.5-8.1 l/min (P less than 0.05), and the end-tidal partial pressure of CO2 (PCO2) was reduced from 37.0 to 33.7 mm Hg (P less than 0.05) with respect to control values. By contrast, adding CO2 sufficient to maintain isocapnic conditions (experimental end-tidal PCO2 = 38.9 versus 38.5 mm Hg in the control study; P = not significant) abolished the exercise-induced ocular hypotension (experimental IOP = 17.8 versus 18.1 mm Hg in the control study; P = not significant). It was concluded that prevention of hypocapnia during isometric handgrip exercise blocks the subsequent fall in IOP, suggesting both that isometric exercise per se has no direct influence on IOP and that therapy for ocular hypertension could involve manipulation of blood gases.
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PMID:Isocapnia blocks exercise-induced reductions in ocular tension. 160 33

Circulatory and metabolic homeostasis in patients with hypoplastic left heart syndrome is dependent on a delicate balance between systemic and pulmonary blood flow. Hypocarbia can result in a marked decrease in pulmonary vascular resistance accompanied by pulmonary overcirculation, systemic hypotension, metabolic acidosis, and death. This report illustrates that early and precise control of the arterial carbon dioxide tension using inspired carbon dioxide can be effective in preventing or treating instability arising during management of a patient with hypoplastic left heart syndrome.
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PMID:Carbon dioxide prevents pulmonary overcirculation in hypoplastic left heart syndrome. 161 Feb 28

Ventilatory acclimatization (VA) to hypoxia alters cerebrovascular responses to arterial blood gas perturbations. For example, after VA, cerebral blood flow (CBF) is elevated, at a given arterial CO2 tension (PaCO2), compared to CBF before VA. This experiment examined the effects of VA to 72 h of normobaric hypoxia [arterial O2 tension (PaO2) approx. 40 mmHg, O2 saturation in arterial blood approx. 50%] on total and regional cerebrovascular resistance (CVR and rCVR) and cerebral O2 extraction fraction (OEF) in 32 conscious sheep. Four different O2-CO2 gas combinations were sequentially administered to each sheep before and after VA. CVR and rCVR were calculated from CBF (radiolabeled microspheres) and arterial and cerebral downstream pressures; OEF was calculated from arterial and cerebral venous O2 contents. After VA, during hyperoxia, CVR and rCVR tended to be lower during both hypocapnia and hypercapnia. During hypoxia, although CVR and rCVR were slightly less during hypocapnia, CVR and rCVR during hypercapnia were surprisingly increased. The post-VA increases in mean CVR and mean rCVR during hypoxic gas combinations differed from the post-VA decreases during hyperoxic gas combinations (0.04 less than or equal to P less than or equal to 0.11). In contrast, although VA decreased OEF during three of four gas combinations (P less than or equal to 0.003), there was a greater mean post-VA decrease in OEF during hypercapnic gas combinations than during hypocapnic gas combinations (P = 0.025); decreases in OEF were correlated with decreases in cerebral O2 consumption. The post-VA CVR responses may reflect altered neurocirculatory control by the arterial chemoreflex; the OEF responses suggest relative cerebral hyperperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Acclimatization to hypoxia alters cerebral convective and diffusive O2 delivery. 161 32

Unanaesthetized rats whose arterial chemoreceptors were stimulated by an one hour acute exposition to hypoxic gaseous mixtures with various carbon dioxide concentrations, presented depletion of the catecholamines content of their adrenal glands only when hypocapnia or increased pH was present (non compensated hypoxia). Moreover, exposition to simultaneous hypoxia and hypercapnia increased the epinephrine stock of the adrenal glands. No changes were found in the myocardium amine content in the same conditions. When anaesthetized rats were treated by iv injection of almitrine bismesylate, a peripheral chemoreceptors stimulating drug, adrenal catecholamines content was insignificantly reduced. In the myocardium, the amines remained at control levels. The most powerful factor related to catecholamines depletion in the adrenals seems to be the hypocapnia or the alkalosis induced by the hyperventilation provoked by glomic stimulation. No indication has been found in favor of an effective adrenergic stimulation caused directly by chemoreceptors stimulation.
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PMID:[Chemostimulation and catecholamine content of the rat adrenal medulla]. 171 97

The responses of intracranial pressure (ICP) to hyperbaric oxygen (HBO) therapy and arterial gas pressures were investigated. ICP was measured through a ventricular or spinal drainage catheter in patients with brain tumor or cerebrovascular disease. Changes in ICP, heart rate (HR), arterial blood pressure (ABP), and transcutaneous partial pressure of carbon dioxide (PtcCO2) or oxygen (PtcO2) were recorded continuously during air or 100% O2 breathing at 1 and 2.5 atmospheres absolute (ATA). HR and PtcCO2 decreased and mean ABP was unchanged during HBO inhalation. ICP was reduced at the beginning and tended to increase gradually during HBO inhalation. The change from air to O2 without altering respiratory frequency and volume caused a gradual increase of ICP and PtcCO2 with a transient ICP reduction in an artificially respirated patient. Intentionally reduced respiration to maintain PtcCO2 at the value at 2.5 ATA with air caused the ICP to return to near the value at 2.5 ATA with air even during HBO inhalation. These findings suggest that reduced ICP is initially due to direct cerebral vasoconstriction caused by hyperoxia and is maintained mainly by induced hypocapnia during HBO inhalation. Care is required when giving HBO therapy to patients with a high ICP and/or who are respirated artificially.
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PMID:Intracranial pressure responses during hyperbaric oxygen therapy. 172 71

To evaluate the role of different vasomotor stimuli for the measurement of cerebrovascular vasomotor reactivity (VMR), 47 patients (i.e., 93 hemispheres) with various degrees of internal carotid artery (ICA) occlusive disease were studied. Patients were divided into clinical [asymptomatic, transient ischemic attack (TIA) or completed stroke] as well as angiological subgroups. Low-grade or high-grade unilateral ICA lesions were compared to bilateral ICA occlusive disease. Relative flow velocity changes within the middle cerebral artery were measured by means of transcranial Doppler during hyper- and hypocapnia (VMRTOT), during hypercapnia alone (VMRCO2), and after injection of 1 g acetazolamide (VMRACE). VMR was expressed as the percentage change in flow velocity after stimulus application as compared with flow velocity at rest. There was a close and statistically highly significant correlation of CO2-induced with acetazolamide-induced VMR (r = 0.69 in VMRTOT versus VMRACE and 0.79 in VMRCO2 versus VMRACE; P less than 0.0001; linear regression), indicating a strong similarity of the vasodilatative effects of CO2 and acetazolamide on cerebral arteries. Both stimulation techniques highly significantly differentiated between asymptomatic patients and those with TIA or completed stroke. Angiological subgroups were separated best by the acetazolamide test. Reclassification of patients into angiological subgroups by linear discriminant analysis was equally good with all three methods. We conclude that both acetazolamide- and CO2-induced stimulation of the cerebral vasomotors are valid techniques to measure reduction in perfusion reserve due to extracranial cerebrovascular occlusive disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Evaluation of cerebral vasomotor reactivity by various vasodilating stimuli: comparison of CO2 to acetazolamide. 172 37

We have previously shown that airway hypocapnia induced bronchoconstriction in the guinea pig lung by releasing tachykinins. To examine whether airway hypocapnia could also cause an increase in airway microvascular leakage, a tracheal segment was isolated in vivo in anesthetized guinea pigs and unidirectionally ventilated (200 ml/min) for 1 h with fully conditioned air (0% CO2) or isocapnic gas (5% CO2). The lungs were ventilated through a distally placed tracheal cannula. Microvascular leakage was quantitated by the injection of Evans blue (EB) and its extraction from the tracheal segment. EB extravasation was increased in tracheae exposed to 0% CO2 (52.3 +/- 2.0 micrograms/g wet tissue) compared with tracheae exposed to 5% CO2 (26.4 +/- 2.9 micrograms/g; p less than 0.05) and to tracheae from spontaneously breathing guinea pigs (25.2 +/- 2.3 micrograms/g; p less than 0.05). Groups of animals in which trachea were unidirectionally ventilated with 0% CO2 were then pretreated with a range of drugs in an attempt to determine the mediators responsible for the microvascular leakage with 0% CO2. Capsaicin and morphine pretreatment did not significantly alter 0% CO2-induced EB extravasation, and phosphoramidon prevented rather than increased extravasation, suggesting that tachykinins did not play a role. The hypocapnia-induced increase in microvascular leakage was, however, prevented by indomethacin pretreatment and significantly attenuated by dazmegrel, a thromboxane synthetase inhibitor. We conclude that airway hypocapnia causes microvascular leakage in the guinea pig trachea and that this effect is mediated by prostaglandins and/or thromboxane.
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PMID:Airway hypocapnia increases microvascular leakage in the guinea pig trachea. 173 4

An enclosed afferent reservoir breathing system (EAR) designed by Ohmeda was evaluated during anaesthesia with controlled ventilation in 104 healthy children. Carbon dioxide production and arterial carbon dioxide tension were measured in 12 children in order to determine the proportion of fresh gas (VF) involved in gas exchange. When the ratio of minute volume ventilation to fresh gas flow (VE:VF) exceeded 1.5, fractional utilization of fresh gas with the EAR was 0.92. This value and values of carbon dioxide production obtained from 43 children were used to derive a simple formula relating fresh gas flow requirements to body weight. The formula, VF = 0.6 x weight 0.5, was assessed in 49 children weighing 10-70 kg. The mean end-tidal partial pressure of carbon dioxide in these patients was 4.5 kPa (range 3.8-5.2 kPa). We conclude that the EAR has an efficiency of 92% in the use of fresh gas during controlled ventilation in healthy children, provided the VE:VF ratio is greater than 1.5. Under these conditions, normocapnia to mild hypocapnia was produced accurately using the formula VF = 0.6 x weight 0.5.
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PMID:Fresh gas requirements of an enclosed afferent reservoir breathing system during controlled ventilation in children. 832 78

The main disadvantages of the to-and-fro system (the bulky canister and the progressive increase in apparatus deadspace) may be overcome by the use of a smaller canister. In this laboratory study, we have evaluated a 160 g canister in a low-flow to-and-fro system (fresh gas flow 1 litre/minute). Two carbon dioxide productions of 150 and 200 ml/minute were simulated. The mean times to exhaustion, defined here as a 0.5 kPa rise in end-tidal PCO2, were 112 and 79 minutes in the 150 and 200 ml/minute carbon dioxide groups respectively. Ventilation to normacapnia or hypocapnia did not affect the times to exhaustion. The soda lime absorbed 16 litres of carbon dioxide before exhaustion, and this was not affected by minute volume or carbon dioxide production. A small soda lime canister is suitable for carbon dioxide absorption in a low-flow to-and-fro system for ventilated adults.
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PMID:Evaluation of a small soda lime canister in a to-and-fro system. 175 May 99


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