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)

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

The breathing frequency response to changes in airway CO2 of a vascularly isolated lobe of the canine lung has previously been shown to be primarily dependent on CO2-mediated changes in airway pressure. This study was carried out to determine what contribution changes in airway pressure make in the whole lung airway CO2-mediated breathing frequency response. Mongrel dogs were anesthetized and placed on cardiopulmonary bypass. Diaphragm electromyogram (EMG) was used to monitor respiratory center output and to trigger ventilation of the lungs. Isoproterenol administered to the lungs prevented hypocapnic airway constriction but only partially blocked the decrease in breathing frequency, suggesting that in the whole lung preparation, airway CO2 in part alters breathing frequency through a direct effect on pulmonary receptors. At constant positive end-expired pressures (1-6 Torr), 0% airway CO2 produced greater increases in expiratory time than 10% CO2. Thus airway CO2 can affect breathing frequency in the absence of CO2-related changes in airway pressure at pressures that would produce lung volumes similar to those observed at end expiration in the intact animal. An argument is presented that the receptors directly affected by CO2 are probably not located in the airways constricted by hypocapnia.
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PMID:Interrelationships among airway CO2, airway pressure, and breathing frequency. 680 Sep 86

To quantify any mechanical inhibitory effect of nasal intermittent positive pressure ventilation (IPPV) on inspiratory activity of the diaphragm we ventilated five conscious relaxed subjects on two occasions at respiratory rates similar to quiet breathing (QB) and at three levels of applied pressure (Pappl)--6, 9 and 12 cmH2O, each during hypocapnia (P(CO2) allowed to decrease) and eucapnia (CO2 added to inspired gas). Diaphragm activity was assessed from transdiaphragmatic pressure (esophageal and gastric balloons) and diaphragm EMG (surface electrodes) both integrated with time (integral(Pdi x dt) and integral(EMGdi x dt), respectively). Neural inspiratory time (Tin) was measured as onset to peak of the integral(EMGdi x dt) signal. Relative to QB, integral(Pdi x dt) was 50-69% less during eucapnic IPPV 6-12 cmH2O (P < 0.005) and 67-85% less during hypocapnic IPPV (P < 0.005). Tin decreased (P < 0.05) with IPPV and, on ceasing IPPV, there was apnoea (prolonged expiratory time) on 23 of 27 occasions; these changes were independent of P(CO2). Integral(EMGdi x dt) decreased (P < 0.05) at Pappl 12 cmH2O during eucapnia and at all Pappl during hypocapnia. The repeatability of integral(EMGdi x dt) was substantially less than integral(Pdi x dt) (F = 42, P << 0.01). We conclude that, during non-invasive IPPV in awake healthy subjects mechanical factors are of major importance in inhibiting inspiratory activity of the diaphragm.
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PMID:Diaphragm inhibition with positive pressure ventilation: quantification of mechanical effects. 1064 59