Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Sympathoadrenal activity was studied in 13 young piglets during hypoxia. The piglets were anaesthetized with chloralose/urethane, tracheostomized, paralyzed with gallamine and artificially ventilated. A femoral artery catheter was inserted and used for blood sampling. The piglets were challenged with 6 min of 6% CO2, 10 min of 12% O2 and 6 min of 6% O2 before and after theophylline (an adenosine receptor antagonist) treatment 20 mg/kg (n = 9) or saline (n = 4). Plasma samples were obtained before, during and after each hypercapnic or hypoxic period and analysed for their content of noradrenaline, adrenaline and neuropeptide Y. Hypercapnia with 6% CO2 and moderate hypoxia with 12% O2 did not lead to any significant increase of either noradrenaline (NA), adrenaline (A) or neuropeptide Y (NPY). However, severe hypoxia with 6% O2 increased the NA level from 30 to 66 nmol/l; the A level from 1 to 28 nmol/l and NPY from 140 to 213 pmol/l. After treatment with theophylline the baseline NA increased from 27 to 40 nmol/l, A rom 1.5 to 4.0 and NPY concentration from 65 to 171 pmol/l. Theophylline moderately enhanced the release of NPY, NA and A during the 12% O2 challenge. However, during the severe hypoxia (6%), the increase of NA (from 49 to 333 nmol/l), A (from 8 to 214 nmol/l) and NPY (from 184 to 385 pmol/l) showed considerably enhancement after the theophylline treatment. The results obtained before and after saline were similar showing that the duration of the experiments per se did not change the baseline levels or the effect of the challenges on NA, A or NPY levels.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Neuropeptide Y and catecholamine release in the piglet during hypoxia: enhancement by theophylline. 130 59

Theophylline is commonly believed to stimulate central respiratory centers. We studied the effect of oral theophylline therapy on ventilatory responses to hypercapnia and hypoxia during a double-blind placebo-controlled trial with a slow release oral theophylline preparation. We measured hypercapnic and hypoxic ventilatory responses using rebreathing techniques in 15 subjects (21 to 41 yr of age, with normal lung function) on three occasions: baseline, after 4 days of Drug 1, and after 4 days of Drug 2. For subjects receiving theophylline, the mean serum theophylline level was 11.3 + 1.3 (SE) micrograms/ml (range, 5.3 to 22.1). Unpleasant side effects were reported by 11 of the 15 subjects (nausea, jitteriness, and agitation) while receiving theophylline but not while receiving placebo. The mean hypercapnic ventilatory response with placebo was 4.3 +/- 0.9 L/min/mm Hg PACO2 and with theophylline it was 4.5 +/- 0.7 L/min/%SaO2 and with theophylline it was -2.7 +/- 0.4 L/min/%SaO2. Hypoxic responses for each subject were measured at similar PvCO2. There were no significant changes in ventilatory responses with theophylline. We conclude that theophylline use, at a dose sufficient to cause side effects, does not affect chemoreceptor responsiveness.
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PMID:Theophylline does not increase ventilatory responses to hypercapnia or hypoxia. 145 55

We studied the effect of aminophylline on twitch tension (TT) and intracellular pH (pHi) in isolated rat diaphragm strips that were fatigued, hypercapnic, or hypoxic. Superfused muscles were directly stimulated at 0.5 Hz. The pHi was measured from distribution volumes of dimethyl-oxazolidinedione. Fatigue was induced by intermittent tetanic stimulation. Hypercapnia and hypoxia were produced by altering superfusate carbon dioxide tension (PCO2) or oxygen tension (PO2). Aminophylline (1.0 mmol.l-1) reversed the twitch decay seen during fatigue or hypercapnic acidosis, and caused partial recovery of twitch depression during hypoxia. Muscle fatigue was not due to an intracellular acidosis. Both hypercapnia and hypoxia lowered pHi. Aminophylline did not alter pHi in unstimulated muscles, but caused a significant fall in pHi in stimulated muscles that were fatigued or hypoxic. High dose aminophylline improved twitch tension in diaphragm strips that were fatigued, acidotic, or hypoxic. Twitch potentiation was not due to an intracellular alkalosis. Aminophylline lowered pHi in stimulated muscle, and thus, theoretically, could sometimes be harmful in the treatment of muscle fatigue.
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PMID:The effect of aminophylline on function and intracellular pH of the rat diaphragm. 228 69

Variations of arterial PCO2 and pH are known to influence myocardial blood flow (MBF) in that hypercapnia results in a coronary vasodilatation, while hypocapnia possibly decreases MBF. The present study was performed to examine if hypocapnia and hypercapnia might influence the sensitivity to exogenous administration of adenosine. Aminophylline, an adenosine receptor blocking agent, was administered to rule out the effect of endogenously liberated adenosine during variations of PCO2 and pH. In the last part of the study, it was examined whether verapamil, a calcium-channel blocker, might influence the MBF response to variations in PCO2 and pH. Closed-chest dogs were anaesthetized with pentobarbital, and hypocapnia induced by hyperventilation. Carbon dioxide was added to the inspiratory gas to create normocapnia and hypercapnia. In the control group hypocapnia did not significantly reduce MBF although a decrease in coronary sinus (CS) SO2 indicated a coronary vasoconstriction. During continuous adenosine infusion (7.5 +/- 0.3 mg/kg/h) which increased MBF 116% during normocapnia, creating hypocapnia caused a 40% decrease in MBF. Hypercapnia seemed to potentiate the vasodilating effect of adenosine. During administration of aminophylline hypocapnia did not cause any decrease in MBF, while hypercapnia increased MBF by 39%, and these results are in harmony with the results obtained in the control group without aminophylline. Verapamil did not result in any altered MBF response to hypocapnia and hypercapnia when compared to the unblocked control group. These observations do not support the idea of any major influence of the Ca2+ fluxes blocked by verapamil as the cause of MBF changes during variations in PCO2 and pH.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Adenosine modifies canine myocardial blood flow response to hypocapnia and hypercapnia, while aminophylline and verapamil do not. 312 Mar 3

A 17-year old boy presented with severe, predominantly central sleep apnoeas secondary to structural damage in the medulla. At low O2 saturation, the electroencephalogram showed the sudden onset of slow waves. Hypercapnic ventilatory response was low and hypoxic ventilatory response was absent. Low flow oxygen therapy dramatically improved the apnoea score, probably by relieving hypoxic brain depression. Slow waves also disappeared with oxygen therapy. Aminophylline was effective on apnoea score and duration (p less than 0.001). This beneficial effect could be explained by an improvement of the normal oscillations of respiration at the onset of sleep, a change in arousability or a stimulation of the ascending reticular system. These findings suggest a possible role of hypoxic depression in the manifestations of central sleep apnoeas and demonstrate the beneficial effect of low flow oxygen and aminophylline in treating certain central sleep apnoeas.
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PMID:Effect of aminophylline and relief from hypoxia on central sleep apnoea due to medullary damage. 360 31

The present study reviews 62 children who where admitted to the department of pediatrics for acute bronchiolitis. We adopted the following therapeutic protocol: treatments were applied randomly and we administered a fast action theophylline solution (Theophylline Bruneau R) or a placebo solution every six hours by oral route or stomach probe at 10 mg/kg between 2 and 6 months, 12 mg/kg between 6 and 12 months and 16 mg/kg between 12 and 24 months. Evaluations of theophylline levels were systematically carried out (immunoenzymatic method) for every infant on day 1, day 3, and day 4 two hours after morning administration and the results studied to see if any changes were necessary. This treatment was well tolerated. Statistical analysis was performed before removal of blind. The homogeneity of the two groups was respected if we considered ages (placebo group: 7.1 months +/- 1.0, theophylline group: 5.6 months +/- 0.6), the initial seriousness as evidenced by hypoxemia (placebo group 61 +/- 2 Torr, theophylline group: 58 +/- 3 Torr) hypercapnia (placebo group: 37.8 +/- 1.0, theophylline group: 35.5 +/- 2) and chest retractions.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Treatment of acute bronchiolitis in infants by oral suspension theophylline. Double-blind study in 62 children]. 389 10

The diseases which are commonly complicated by hypercapnic respiratory failure also compromise the respiratory muscles in several ways. Increased work of breathing, mechanical disadvantage, neuromuscular disease, impaired nutritional status, shock, hypoxemia, acidosis, and deficiency of potassium, magnesium, and inorganic phosphorus are the major non-neurologic factors which contribute to respiratory muscle fatigue and failure. Respiratory muscle fatigue has two components. High frequency fatigue occurs rapidly with intense contractile efforts but is usually not severe. It also recovers rapidly with rest. Low frequency fatigue develops more slowly but is severe and requires hours for recovery. Since the spontaneous rate of neural stimulation is predominantly in the low frequency range, this component of fatigue is of particular clinical importance. Fatigue of the inspiratory muscles leads to acute respiratory acidosis, but before carbon dioxide retention occurs, it can be recognized from characteristic symptoms and signs. These include dyspnea which responds to mechanical ventilation, rapid shallow breathing, and asynchronous movements of the chest and abdomen. Inspiratory muscle fatigue must be treated by putting these muscles to rest, by mechanically supporting ventilation. In addition, underlying metabolic nutritional and circulatory abnormalities must be corrected and infection treated. Aminophylline and isoproterenol can restore inspiratory muscle contractility, but controlled clinical trials remain to be done regarding their application in acute and chronic respiratory failure. Inspiratory muscle training improves strength and endurance in patients with obstructive lung disease, cystic fibrosis, and spinal cord injury, but does not always improve physical exercise performance. Again, more work is needed to develop the indications for inspiratory muscle training and to determine the optimum type and duration of the training regimen.
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PMID:Respiratory muscle failure. 634 27

The role of adenosine in the regional cerebral blood flow (rCBF) response to hypoxia was evaluated in young (6 month) and aged (26-28 month) F344 rats using theophylline, an adenosine antagonist. Regional CBF was measured with radioactive microspheres under control anesthetized conditions (70% N2O, 30% O2) and at two levels of hypoxia (CaO2 = 8.7-9.0 ml . 100ml-1 and 3.2-3.7 ml . 100ml-1). Without theophylline infusion, CBF increases were similar between young and aged rats during moderate hypoxia but were increased more in young during severe hypoxia. Intracerebrovascular theophylline infusion significantly attenuated the increase in CBF during both moderate and severe hypoxia and decreased the difference between young and aged rats. Theophylline infusion produced no significant effect on the increase in CBF produced by hypercapnia, indicating the specificity of the treatment for hypoxic induced CBF changes and adenosine release. Intracerebrovascular infusion of adenosine had no effect on CBF, presumably due to the presence of the blood brain barrier. The results suggest that adenosine plays a major role in CBF increases during both moderate and severe hypoxia and in the difference in response to hypoxia between young and aged rats.
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PMID:The role of adenosine in CBF increases during hypoxia in young vs aged rats. 669 16

This study investigated the effect of acute changes in blood gases and pH on theophylline kinetics. Groups of 6 conscious rabbits were exposed to air (control) or to a high CO2 and/or low O2 atmosphere for 570 minutes, or received 47 ml/kg of 0.3N HCl by gavage. Once blood gases or pH were stabilized, they received 2.5 mg/kg theophylline intravenously. Urine, blood samples, and cerebrospinal fluid were collected. Metabolic acidosis did not modify theophylline kinetics. Theophylline serum concentrations increased with hypercapnia (p less than 0.05), hypoxemia (p less than 0.01), and hypercapnia combined with hypoxemia (p less than 0.001), compared with those in control animals. These increases were related to a decrease in theophylline nonrenal clearance (Clnr). Thus, Clnr decreased from 1.52 +/- 0.05 ml/min/kg in control animals to 1.13 +/- 0.13 in hypercapnia (p less than 0.01), 1.09 +/- 0.09 in hypoxemia (p less than 0.001), and 1.02 +/- 0.02 in hypoxemia combined with hypercapnia (p less than 0.001). Theophylline protein binding was not affected by any of the experimental conditions. The ratio of central nervous system to serum theophylline concentration was increased by 16% (p less than 0.05) with hypercapnia combined with hypoxemia. It was concluded that both hypercapnia and/or hypoxemia decreased theophylline biotransformation. Such a decrease may be the cause of toxicity.
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PMID:Influence of hypercapnia and/or hypoxemia and metabolic acidosis on theophylline kinetics in the conscious rabbit. 672 Dec 73


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