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)

We have attempted to identify the afferent endings responsible for the pulmonary-CO2 ventilatory reflex. We recorded afferent vagal impulses arising from the left lung in anesthetized dogs with separately ventilated lungs. When the left pulmonary artery was occluded, left lung PCO2 fell to 3 mm Hg and slowly-adapting pulmonary stretch receptor activity increased 46%. Firing declined to its original intensity when left lung PCO2 was raised in steps by administration of CO2, firing decreasing most between 2 and 19 mm Hg, and least between 30 and 50 mm Hg. Irritant receptor activity also increased (from 2.8 to 7.4 impulses/sec) after pulmonary arterial occlusion, the effect being reversed by administration of CO2. These procedures caused trivial changes in pulmonary and bronchial C-fiber activity. Effects on both slowly-adapting stretch receptors and irritant receptors appeared to result from a direct action of CO2 on the endings themselves, rather than from mechanical changes in the lung. Changes in slowly-adapting stretch receptor activity provide an adequate explanation for the pulmonary-CO2 ventilatory reflex, the relationship between impulse frequency and lung PCO2 suggesting that these afferents may have a role in limiting CO2 loss under conditions causing hypocapnia, but be less effective in stimulating breathing during hypercapnia.
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PMID:II. Effect of CO2 on afferent vagal endings in the canine lung. 70 75

Three patients with paralytic poliomyelitis have been ventilated via tracheostomy with uncuffed silver cannula for 21 years, with high tidal volumes of atmospheric air (8.3, 7.2, and 5.4 ml/kg b.wt.), at a frequency of 20, passive expiration, and without periodic hyperinflation. No pulmonary complications were seen during the whole of this period. The total compliance was significantly decreased. The pulmonary physiological shunt relative to the total pulmonary blood flow (Qs/Qt) was slightly increased. PaO2 was nevertheless normal, probably due to a high alveolar PO2 caused by the hyperventilation. The physiological dead space realtive to the tidal volume (VD/VT) was within the noraml range, but VD was high in one case. Two of the patients disclosed an extremely low CO2 production and a PaCO2 averaging 12 mmHg, with small fluctuations during a 24-hour study. This profound respiratory alkalosis was only partly compensated in the arterial blood (pH: 7.54 and 7.50), suggesting a new state of acid-base equilibrium. The cerebrospinal fluid lactate was significantly increased to about 4 mmol/l, but the patients revealed no signs of impaired cerebral function. A reduction of the degree of hypocapnia by the use of a mechanical dead space is recommended.
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PMID:Artificial hyperventilation during 21 years in three cases of complete respiratory paralysis. 81 38

The purpose of this investigation was to assess the relative contributions of hyperpnea and hypocapnia in the induction of postexercise asthma. To achieve these ends, eight young asthmatics were exercised on a treadmill while minute ventilations (VE) and end-tidal CO2 (PET CO2) tensions were continuously recorded. The subjects were then restudied using a partial rebreathing technique that allowed separation of minute and alveolar ventilations so that independent evaluations could be made of the relative effects of bulk airflow on pulmonary mechanics as well as a systematic study of hypocapnia in a dose-response fashion. Sustained hyperpnea with VEidentical to those recorded during exercise was totally without effect when the mean PET CO2 was isocapnic or lowered to approximately 30 Torr. Reduction in PETCO2 to 21.3 +/-0.9 Torr brought about significant changes in mechanics, but in every variable measured, exercise produced the greatest alterations and did so at PETCO2 values that had no effect when studied in a controlled fashion. Consequently, neither high VE per se, nor hypocapnia can be considered as the mechanisms underlying exercise induced asthma.
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PMID:Relative contributions of hypocarbia and hyperpnea as mechanisms in postexercise asthma. 83 72

Increased body temperature stimulates hyperventilation in man but little is known about its effects on ventilatory responsiveness to hypoxia. Hence this study examined the effects of hyperthermia on hypoxic ventilatory response (HVR), hypercapnic ventilatory response (HCVR), and oxygen consumption (VO2). Six fasting subjects had these variables measured under basal conditions and at two levels of hyperthermia. Hypoxic ventilatory response was measured as the shape paramater A of the VE/PAO2 curves. Since hyperthermia produces hyperventilation and, therefore, hypocapnia, HVR was measured at the hyperthermic (hypocapnic alveolar CO2 tension (PACO2) and at the basal (normothermic) PACO2. Hypoxic ventilatory response (A) increased when measured at basal PACO2 levels, from 113 +/- 8.8 (S.E.M.) to 189 +/- 21.8 at 0.7 degrees C. and 240 +/- 34.0 at + 1.40 degrees C. (P less than 0.005). HVR measured during hyperthermic hypocapnia also increased at each temperature level but did not reach statistical significance (P = 0.1). Hypercapnic ventilatory response, as measured by the slope S of VE/PACO2 lines, increased significantly at each temperature elevation (P less than 0.025). We conclude that raising body temperature causes a significant augmentation of ventilatory responses to hypoxia (during normothermic PACO2 conditions) and to hypercapnia.
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PMID:Effects of hyperthermia on hypoxic ventilatory response in normal man. 83 15

Two groups of patients with similar degrees of chronic airway obstruction exhibited different degrees of increased arterial oxygenation with CO2-induced hyperpnea versus voluntary increases in ventilation matched for ventilatory pattern. Patients who failed to increase arterial PO2 as much with voluntary hyperventilation as with CO2 challenge also had a lower dynamic compliance with the voluntary maneuver, whereas those with similar increases in arterial PO2 had similar dynamic compliances during the 2 periods of increased minute ventilation. The differences between the 2 groups are believed to be related to different effects of hypocapnia on collateral ventilation.
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PMID:Arterial oxygenation differences with carbon dioxide-induced versus voluntary increases in minute ventilation in chronic airway obstruction. 88 70

The effect of hypercapnia on coronary vascular resistance (CVR) was studied in seven open-chest dogs. Coronary blood flow was supplied to the cannulated left main coronary artery from the femoral artery by a precision pump. Coronary arterial PCO2 was locally controlled with a small membrane oxygenator in the coronary perfusion circuit. Each PCO2 change was made at a constant coronary flow, and CVR was calculated from the ratio of perfusion pressure to flow. Coronary sinus (CS) PCO2 and PO2 were recorded continuously from blood withdrawn through a CS catheter. Normocapnia (PCO2 = 42.3 +/- 2.8 mm Hg) was obtained with a membrane oxygenator gas composition of 95% O2-5% CO2, and hypocapnia was produced with 100% O2-0% CO2. In addition to physiology normal coronary flow (determined by a CS PO2 of 20-30 mm Hg) relatively high and low flow states were studied. At a normal control CS PO2, a decrease in coronary arterial PCO2 from 42.3 +/- 2.8 to 23.8 +/- 1.3 mm Hg caused CVR to increase by 84.2%, from 1.27 +/- 0.06 to 2.30 +/- 0.04 units. Since pH was inversely related to PCO2, the effect on CVR may have been mediated through a pH change. CS PCO2 decreased from 65.2 +/- 1.9 to 39.4 +/- 1.3 mm Hg. myocardial oxygen consumption was unchanged. Increases in CVR of 74.5, 119.5, and 69.3% occurred during hypocapnia in three additional experiments in which control arterial PO2 was maintained at 52-90 mm Hg. When CS PO2 was greater than 30 mm Hg, the normocapnic CVR was high, and was only minimally increased by hypocapnia. When coronary flow was reduced to an ischemic level there was little response in CVR to hypocapnia. Thus the level of arterial PCO2 can have an important effect on CVR independent of changes in O2 consumption. Myocardial PCO2, derived from metabolically produced CO2 and contributed to by arterial CO2, may be a major factor in normal control of coronary flow.
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PMID:The response of canine coronary vascular resistance to local alterations in coronary arterial P CO2. 96 40

In each of ten healthy young subjects breathing different concentrations of CO2 in O2, four alveolar CO2-tension levels were obtained, ranging from about 20 mmHg when hyperventilating in O2 to 50 mmHg. Maximum expiratory flows at 60% total lung capacity were measured at each level and corrected for the influence of the expired gas on the flow. The corrected maximum flow decreased significantly when the alveolar CO2 tension was below 30-35 mmHg, while there was only slight or no influence of CO2 on the maximal flow when the tension was above 35 mmHg. The decrease is taken as evidence of a constrictor effect on peripheral bronchi of hypocapnia.
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PMID:The effect of CO2 on peripheral airways. 98 28

This study was designed to determine blood flow to the liver during hypercapnia and combined hypercapnia-hypoxia with the portal vein and hepatic artery intact except for placement of an electromagnetic flow probe around these vessels. Twenty mongrel dogs weighing 30-45 kg were anesthetized with pentobarbital and flow probes and occluders were surgically implanted. Ten of these dogs were subjected to hypercapnia alone. During inspiration of 6% CO2 in room air, portal vein flow increased from 588 +/- 73 ml/min to 731 +/- 113 ml/min (p less than .05), while hepatic artery flow did not change significantly from its control mean of 221 +/- 38 ml/min. In the remaining dogs, inhalation of 6% O2 resulted in a reduction of portal blood flow within 30 min from 527 +/- 55 ml/min to 381 +/- 41 ml/min (p less than .01). Again, mean hepatic artery flow did not increase significantly above its control of 273 +/- 43 ml/min. Subsequent inhalation of 6% CO2 plus 6% O2 (combined hypercapniahypoxia) for 30 min in these same animals resulted in a significant increase of portal vein blood flow from 514 +/- 46 ml/min to 716 +/- 116 ml/min (p less than .05). Thus, hypercapnia alone increases total liver blood flow, primarily by an increase in portal vein flow. Hypoxia results in a decrease in portal vein flow. The superimposition of hypercapnia on hypoxia restores blood flow to a level close to that found with hypercapnia alone. Hypercapnia in the range of 63 +/- 4 mmHg PCO2 overwhelms the tendency toward a reduction of portal vein blood flow induced by an arterial PO2 of 42 +/- 5 mmHg in the presence of mild hypocapnia (PCO2 : 30.2 +/- 1 mmHg).
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PMID:Carbon dioxide and liver blood flow. 101 83

The cardiovascular system of the anaesthetized dog has been used as an experimental model for studying the mechanisms of the haemodynamic responses to hypoxia. Together with aortic and left circumflex coronary artery blood flow (electromagnetic flow transducers), aortic and left ventricular pressures have been recorded and blood has been sampled from the aorta and the coronary sinus (PO2, PCO2, pH). During short periods of hypoxia an improvement of myocardial performance has been observed both before and after administration of a beta-adrenergic receptor blocker and a marked reduction of coronary sinus PCO2 has been noted. When hypoxia was caused by a mixture of nitrogen (95%) and CO2 (5%) an improvement of performance was observed only before administration of the beta-blocker. The slope of the relationship between PCSCO2 and cardiac performance was found to be similar before and after administration of the beta-blocker and also similar to that observed in studies of the response of the isolated heart muscle to acute hypocapnia. Besides beta-adrenergic receptor stimulation, a reduction of coronary sinus PCO2 (CO2 wash-out due to an increase of coronary blood flow) could be a factor contributing to the maintenance of myocardial performance in the face of hypoxia.
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PMID:[CO2 "wash-out" : a factor contributing to increase myocardial performance in the face of hypoxia (author's transl)]. 101 80

The respiratory frequency, tidal volume and ventilization responses of 20 conscious cats to hypoxia, at controlled levels of alveolar CO2, revealed a characteristic steady state response in the majority of animals which indicated a negative interaction of stimuli on tidal volume and minute volume of ventilation, but a positive interaction on frequency. Another series of studies, conducted on seven conscious cats, sought to identify hypoxic response thresholds and depression thresholds, by determining responses over a wide range of hypoxic stimulus intensities, and at different controlled alveolar PCO2. Response threshold was at about 65 torr PAO2. Under eucapnic conditions, ventilation began to fail at PAO2 about 30 torr due to failure of tidal volume. The frequency continued to increase even in the lowest range of PAO2. With hypocapnia no failure of ventilation, frequency, or tidal volume was seen even at the lowest PAO2, but with hypercapnia, the tidal volume began to fail at PAO2 about 50 torr. The minute volume however, continued to increase into the lowest range of PAO2, because the frequency continued to respond at a rate greater than the tidal volume was failing. The results are discussed in terms of interactive depression manifest through the coupled responses of peripheral and central mechanisms.
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PMID:Hypoxia and carbon dioxide as separate and interactive depressants of ventilation. 101 31


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