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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Eight awake cats have been studied before and after carotid denervation during air and oxygen breathing, and during hypercapnia. Analysis of the variables that characterize the spirogram shows that carotid denervation consistently results in a decrease of the mean inspiratory flow (VT/TI), causing a decrease in tidal volume (VT) and ventilation with a relative alveolar hypercapnia. In carotid-denervated animals, inhalation of oxygen results in an increase in ventilation due to an augmentation of VT/TI and VT and a relative hypocapnia. TI does not significantly change in the different conditions whereas TE is significantly affected. TE seems therefore to be more closely related to the rate of rise of inspiratory activity than to inspiratory duration.
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PMID:Effects of carotid body denervation on respiratory pattern of awake cats. 46 36

The effects of analgesic doses of morphine on ventilation, arterial blood gas tensions, chemical control of breathing, and the ventilatory response to exercise were studied in six normal subjects. After administration of 0.2 mg/kg morphine, resting ventilation decreased primarily because of a reduction of tidal volume. Ventilatory responses to carbon dioxide and hypoxia were significantly reduced to one-half and one-third of control, respectively. Ventilatory responses at any given level of exercise were significantly reduced after morphine. However, since oxygen consumption during exercise was similarly reduced after morphine, the relationship between ventilation and metabolic rate during steady-state exercise was not altered by the drug. In addition, morphine prolonged the attainment of steady-state ventilation in four of the six subjects, similar to that reported for chemodenervated subjects. The findings suggest that blunting of chemoreception for hypoxia and hypercapnia has no effect upon the link between metabolic rate and ventilation during steady-state exercise, but the hypoxia chemoreflex may be involved in determining the dynamic characteristics of the response.
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PMID:Effects of morphine on ventilatory response to exercise. 46 50

Using ten normal dogs, the right upper lobe of the lung was isolated in vivo by a balloon catheter and was artificially ventilated with nitrogen, air, 60% oxygen in nitrogen, and 60% oxygen and 20% carbon dioxide in nitrogen, while the rest of the lungs maintained a spontaneous breathing of ambient air. Aminophylline did not show a vasodilating action under severe alveolar hypoxia (PAO2: ca. 40 mmHg); on the contrary, it seemed to potentiate hypoxic pulmonary vasoconstriction. When the regional alveolar oxygen tension became less hypoxic (PAO2: ca. 70 mmHg) or higher than that in the rest of the lungs which spontaneously breathed ambient air, aminophylline showed a definite vasodilating action. Aminophylline also showed a vasodilating action in alveolar hypercapnia in the presence of alveolar hyperoxia.
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PMID:Effect of aminophylline on regional perfusion distribution in the lungs. 48 2

The influence of regional alveolar oxygen and carbon dioxide tensions on the distribution of lung blood flow and gas exchange was studied in unanaesthetised sheep. Right apical lobe (RAL) hypoxia, induced by administering nitrogen or nitrogen/oxygen mixtures to the lobe, stimulated a prompt, graded and well sustained reduction in lobar blood flow. Maximum hypoxia was accompanied by an approximate 65% reduction in perfusion, a significant fall in RAL carbon dioxide tension and output, a reversal of lobar oxygen flux and an average 13 Torr fall in arterial oxygen tension. The reduction in perfusion and gas exchange persisted in the face of elevated systemic oxygen tensions produced by giving pure oxygen instead of air to the remainder of the lung (RL). Mild RAL hypercapnia potentiated the hypoxia-induced change in perfusion and gas exchange. During lobar hypoxia RL blood flow and gas exchange increased to maintain total pulmonary gas exchange at an essentially constant level. RAL hyperoxia did not significantly alter the distribution of perfusion or gas exchange.
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PMID:Regional alveolar gas composition and lung function in sheep. 49 47

Cerebral blood flow and cerebral oxygen uptake were studied during severe arterial hypoxia in anesthetized dogs. It was shown that the hypoxic vasodilatation in the brain reaches a limit at an arterial oxygen saturation at about 25% and that this vasodilatation is less than that which may be induced by hypercapnia. A further deepening of the arterial hypoxia at a maintained cerebral perfusion pressure is combined with a continuous decrease in cerebral venous oxygen tension and a reduced oxygen uptake.
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PMID:Cerebral blood flow, cerebrovascular resistance and cerebral metabolic rate of oxygen in severe arterial hypoxia in dogs. 49 40

A homogeneous sample of 14 patients with advanced chronic bronchitis and emphysema complicated by secondary polycythaemia and pulmonary hypertension was examined. Eight patients who were receiving long-term oxygen therapy (LTO2) for 15-20 h in the 24 h day showed a significantly faster, that is more normal, frequency of the dominant EEG activity and a higher level of arterial oxygenation when breathing air than six similar patients not receiving LTO2. Acute administration of oxygen (2 1/min) for 15 min did not change the EEG pattern in either group of patients. The frequency of the dominant EEG activity in all 14 patients showed a significant positive correlation with the arterial oxygen saturation and negative correlation with the level of polycythaemia. Occurrence of intermixed EEG show activity theta and delta was positively correlated both with hypoxaemia and hypercapnia. The results suggest that the LTO2 in patients with chronic ventilatory failure has a beneficial effect on cerebral function as measured by EEG.
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PMID:The effects of long-term oxygen therapy on the EEG in patients with chronic stable ventilatory failure. 49 89

The responses to hypocapnia and to hypercapnia of both the systemic and the coronary circulations have been studied in the dog during intermittent positive pressure ventilation under halothane anaesthesia. In the absence of significant variations of myocardial contractility, the reduction of cardiac output, because of hypocapnia, was determined by the increase of systemic vascular resistance, while the increase of cardiac output because of hypercapnia was determined by an increase of heart rate without change of stroke volume. The alterations of coronary blood flow (reduction following hypocapnia, augmentation following hypercapnia) were considerably larger than the changes of cardiac output and of myocardial oxygen consumption. Such disparity between oxygen supply and demand, together with the effect of pH and PCO2 on the oxyhaemoglobin dissociation curve led to a marked reduction of coronary sinus PO2 in response to hypocapnia and a marked increase of coronary sinus PO2 in response to hypercapnia. The data suggests that PCO2 (or respiratory alterations of pH) may have a direct effect on the regulation of coronary blood flow. The low coronary sinus PO2 observed at hypocapnia may suggest the risk of myocardial ischaemia.
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PMID:Effect of CO2 on the systemic and coronary circulations and on coronary sinus blood gas tensions. 49 91

One subject was exposed for six days to increasing levels of CO2, rising at a constant rate from 0.03 to 3.0% CO2 within a 15-h period followed by 9 h of air breathing. To assess acid-base parameters, arterialized capillary blood was taken from a finger twice daily (at 8 a.m. and 11 p.m.) at times corresponding to the beginning and end of the intermittent exposure to CO2. Venous blood samples were obtained on alternate days at the same times. Urine specimens were collected twice daily. The subject was on a liquid diet. Resting respiratory minute volume (VE), oxygen consumption (VO2), carbon dioxide excretion (VCO2), alveolar carbon dioxide and oxygen tension (PACO2) and PAO2) were measured twice daily. PACO2 and PAO2 were also determined at the end of breath-holding twice daily; CO2 tolerance tests and lung function tests were also carried out. In contrast to the effects of chronic exposure to 3% CO2, the CO2 tolerance tests showed an increased sensitivity (increase of slope) and breath-holding PACO2 did not change, indicating that acclimatization to CO2 did not develop. The ventilatory response to CO2 was not sufficient to prevent CO2 accumulation in the body; this accumulation was eliminated during the nightly air-breathing periods on the fourth and fifth days, indicated by higher values of PaCO2 and PACO2. The known renal response to hypercapnia, consisting of an increased excretion of titratable acidity, ammonia, and hydrogen ion excretion, occurred but was interrupted after the first day and was triggered again on the fourth and fith days when accumulated CO2 was released from body CO2 stores. The second renal response was associated with a marked calcium excretion, which suggests that bone CO2 stores were involved.
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PMID:Effect of intermittent exposure to 3% CO2 on respiration, acid-base balance, and calcium-phosphorus metabolism. 50 20

Oxygen for therapy of chronically hypoxemic patients can be supplied by an oxygen concentrator (De Vilbiss, DeVO2). By these means longterm oxygen therapy can be carried out on a round-the-clock-basis without risk of hypercapnia and without the need of handling the refill of oxygen containers. 9 patients in severe respiratory failure were treated with 2 to 4 l/min from the concentrator through 4 hour 4 days. Serial bloodgas analyses showed marked improvement of hypoxemia in all patients and prevention of exercise-induced failure in one patient. The oxygen concentrator therefore is suitable for the home treatment of patients with severe hypoxemia.
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PMID:[Oxygen therapy by means of an oxygen concentrator (author's transl)]. 50 95

We measured ventilatory responses to CO2 (delta VI/delta PCO2) and transient hypoxia (delta VI/delta SaO2) during reductions of brain blood flow (BBF) to 70% and 50% of control in unanesthetized goats. Increase in inspiratory volume per change in CO2 tension (delta VI/delta PCO2) was measured during rebreathing with sampling of both arterial and cerebral venous blood; increase in inspiratory volume per fall in arterial oxygen saturation (delta VI/delta SaO2) was assessed by the transient N2 inhalation method. Delta VI/delta SaO2 did not significantly change at 70% BBF, but was depressed at 50% BBF. Delta VI/delta PCO2 increased (0.94 +/- 0.18 to 1.29 +/- 0.24 l . min-1 . Torr-1) at 70% BBF if arterial CO2 tension were used to represent the CO2 stimulus but was unchanged if venous CO2 tension were used. At 50% BBF, delta VI/delta PCO2 was depressed (0.38 +/- 0.13 l . min-1 . Torr-1) for both representations of the CO2 stimulus. Brain ischemia increased blood pressure and heart rate but blunted the increase in BBF caused by hypercapnia. We conclude that 1) moderate brain ischemia (70% BBF) does not affect chemosensitivity to hypoxia and CO2, 2) delta VI/delta PCO2 may not be accurately determined from PaCO2 during brain ischemia because cerebrovascular reactivity to CO2 is depressed, and 3) severe brain ischemia (50% BBF) blunts delta VI/delta SaO2 and delta VI/delta PCO2, probably as a consequence of hypoxic depression of the respiratory neurons.
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PMID:Effects of graded reduction of brain blood flow on chemical control of breathing. 53


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