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

1. The influence of hypoventilation or hyperventilation on blood pressure and pulse rate responses to verapamil and nifedipine was studied in chloralose-anaesthetized rats. 2. Artificial ventilation with room air at a fixed volume of 10 ml kg-1 successfully induced combinations of hypoxaemia, hypercarbia and acidosis at a ventilator rate of 37 strokes min-1 and of hyperoxaemia, hypocarbia and alkalosis at 160 strokes min-1. 3. Hypoventilation caused significant decreases in both the blood pressure and pulse rate, whereas hyperventilation produced significant increases in these parameters. 4. In the controls, intravenous injections of graded doses of either verapamil or nifedipine caused dose-dependent decreases in mean blood pressure. The effects on pulse rate were not marked. 5. The hypotensive effects of verapamil were significantly more intense in hyperventilated rats, whereas those of nifedipine were significantly less pronounced in hypoventilated animals. The hypoventilated rats exhibited a significant dose-dependent decrease in pulse rate in response to verapamil administration. 6. It is concluded that cardiovascular responses to verapamil, nifedipine and probably other calcium antagonists are altered in the presence of blood gas abnormalities.
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PMID:Cardiovascular responses to verapamil and nifedipine in hypoventilated and hyperventilated rats. 237 53

1. The aim of the present study was to assess the effects of hypercapnia or hypoxia on plasma concentrations of atrial natriuretic factor (ANF) in conscious unrestrained dogs. 2. For this purpose, chronically instrumented dogs were exposed in a random order to either room air, or to an atmosphere containing 21% O2/10% CO2/69% N2 to produce hypercapnia, or 10% O2/3% CO2/87% N2 to produce hypoxia without respiratory alkalosis. 3. Plasma concentrations of ANF did not change significantly during hypoxia. 4. In contrast, during hypercapnia, plasma concentrations of ANF increased by more than 100% and returned to baseline at the end of hypercapnia. 5. Hypercapnia, but not hypoxia, induced an increase in left atrial and central venous pressures. 6. We conclude that hypercapnia increases plasma ANF concentration, and that this increase may be secondary to an increase of the left and right atrial pressures. These phenomena may explain the increase in diuresis and natriuresis which has been described during hypercapnia.
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PMID:Effects of hypoxia and hypercapnia on atrial natriuretic factor and plasma renin activity in conscious dogs. 252 64

Respiratory insufficiency of any cause has significant effects on the nervous system. Headache, mental status changes, papilledema, and numerous motor abnormalities including asterixis are commonly seen. Abnormalities in ventilation and gas exchange result in hypoxia, hypercapnia, and respiratory acidosis, and these, in turn, interfere with cerebral metabolism, increase CBF, and may raise intracranial pressure. Chronic respiratory insufficiency can persist for many months with minimal neurologic symptoms, as numerous compensatory mechanisms, particularly renal, may take effect. Treatment includes restoring adequate ventilation and improving gas exchange and may require tracheal intubation and assisted ventilation. Supplemental oxygen therapy should be carefully monitored, as high rates of flow may suppress the hypoxic drive for respiration and lead to significant carbon dioxide retention. The sleep apnea syndromes are a group of disorders in which abnormal respiratory patterns during sleep result in hypercapnia and hypoxemia. Intermittent obstruction of the upper airway and abnormalities of brainstem respiratory centers cause frequent nocturnal awakenings and apneas in these patients. Treatments vary and include weight loss in obese subjects, respiratory stimulants, tracheostomy, and diaphragmatic pacing. Rapid ascent to high altitudes may result in headache, changes in mental status, papilledema, and other neurologic symptoms in certain individuals: a syndrome known as high-altitude sickness. Hypoxia leading to cerebral edema, nocturnal periodic breathing, and hypobaria produces neurologic symptoms in these individuals. Acetazolamide and dexamethasone may be effective in minimizing symptoms of this disorder. Sustained hyperventilation produces acral and circumoral paresthesias and lightheadedness in anxious individuals and can be maintained by relatively normal ventilatory patterns once established. These symptoms are due to hypophosphatemia and respiratory alkalosis, the latter reducing CBF and causing localized tissue hypoxia. Rebreathing into a paper bag at the first awareness of symptoms is the most effective form of treatment.
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PMID:Neurologic manifestations of pulmonary disease. 267 37

Respiratory acid-base disorders elicit physiological responses that alter O2 delivery to various tissues. We have used a near infrared (NIR) optical technique to monitor cytochrome a,a3 oxidation state, tissue O2 store (relative hemoglobin plus myoglobin oxygenation), and regional blood volume in intact resting skeletal muscle during respiratory acid-base disturbances in anesthetized cats. Hypercapnic acidosis and hypocapnic alkalosis were produced in separate groups of animals by ventilation with increasing concentrations of CO2 (n = 13) or hyperventilation (n = 8). Respiratory acidosis decreased oxygen availability to hindlimb muscle while respiratory alkalosis did not change tissue oxygenation. Inspired CO2 progressively decreased muscle blood volume, cytochrome a,a3 oxidation level, and muscle oxygen store. These optical responses were greatly attenuated both by pre-treatment with bretylium and by hemorrhagic hypotension, suggesting mediation through sympathetic vasoconstriction. Metabolic acidosis, produced by intravenous HCl infusion (n = 8), did not reproduce the hindlimb optical responses mediated by CO2. These experiments demonstrate that hypercapnic acidosis significantly decreases oxygen supply to resting skeletal muscle in the anesthetized cat, probably via neuroregulatory responses to CO2 which do not depend on changes in arterial [H+] in the tested pH range.
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PMID:Skeletal muscle oxygen availability during respiratory acid-base disturbances in cats. 282 60

1. The effect of varying artificial respiratory volume (at a fixed rate of 54 min-1) on cardiac output, its distribution and tissue blood flows were determined with tracer microspheres in control pithed rats or during pressor responses to either the alpha 1-adrenoceptor agonist phenylephrine or the alpha 2-agonist xylazine. Phenylephrine was investigated in the presence of propranolol (3 mg kg-1). The rats were pithed under halothane anaesthesia. 2. A respiratory volume of 15 ml kg-1 produced modest hypercapnia (PaCO2 = 47 mmHg), hypoxia (PaO2 = 60 mmHg) and acidosis (pH = 7.35) relative to control animals respired at 20 ml kg-1 (PaCO2 = 32 mmHg; PaO2 = 77 mmHg; pH = 7.47). In rats respired at 15 ml kg-1, total peripheral resistance was lower, and cardiac output greater (due to increased stroke volume), than in the controls. Lowering respiratory volume reduced distribution of cardiac output to the kidneys, increased it to the large intestine and also increased blood flow through the gastrointestinal tract, skin and spleen. A respiratory volume of 30 ml kg-1 gave mild hypocapnia (PaCO2 = 19 mmHg), hyperoxia (PaO2 = 101 mmHg) and alkalosis (pH = 7.59) compared to 20 ml kg-1 but had no effect on cardiac output distribution or organ blood flow although heart rate was 29% greater at 30 ml kg-1. 3. Xylazine (500 micrograms bolus followed by 100 micrograms min-1 infusion) at all three respiratory volumes gave well-sustained mean pressor responses of 62-64 mmHg by increasing both total peripheral resistance and cardiac output (resulting from increased stroke volume). It increased the proportion of cardiac output passing to the liver, reduced that going to the spleen and gastrointestinal tract and increased cardiac, renal and hepatosplanchnic blood flows. 4. The secondary, relatively sustained, pressor effect of phenylephrine (5 micrograms bolus followed by 0.4 micrograms min-1 infusion, i.v.) varied at the 3 respiratory volumes with mean values from 32 to 53 mmHg. This response was due to both increased total peripheral resistance and cardiac output (resulting from greater stroke volumes and/or heart rates). Phenylephrine increased the proportion of cardiac output passing to the gastrointestinal tract, heart, kidneys and hepatosplanchnic bed and increased cardiac, hepatosplanchnic, renal and gastrointestinal blood flows. 5. Respiratory volume had no effect on the cardiovascular effects of xylazine. However, respiratory volume modified the effects of phenylephrine on heart rate and changed the relative contributions of stroke volume and heart rate to the increased cardiac output. It also influenced the effects of phenylephrine on cardiac output distribution to the liver, epididimides and hepatosplanchnic bed and on blood flow through skeletal muscle and the large intestine. 6. Changes in respiratory volume of air ventilated pithed rats thus influence cardiac output, its distribution and regional blood flows. Such changes can also differently influence the responses of various vascular beds to phenylephrine whilst having no effect on their responses to xylazine.
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PMID:Effect of artificial respiratory volume on the cardiovascular responses to an alpha 1- and an alpha 2-adrenoceptor agonist in the air-ventilated pithed rat. 289 57

Bicarbonate reabsorption by the immature kidney in response to acute acid-base changes was assessed in 50 anesthetized newborn rabbits before the end of nephrogenesis. The normal newborn rabbit (age 5-12 days) is in a state of hypochloremic metabolic alkalosis (PHCO3-, 31.9 +/- 0.6 mmol/l; PCl-, 83.1 +/- 1.0) and excretes a hypertonic (Uosmol = 578 +/- 41 mosmol/kgH2O), alkaline (UpH = 7.40 +/- 0.15) urine containing 50 +/- 9 mmol/l Cl- and 13 +/- 4 mmol/l Na+. The alkalosis is probably generated by an alkaline load contained in the mother's milk and maintained by a state of chloride wasting and volume contraction. In this alkalotic model, bicarbonate reabsorption, expressed per milliliter glomerular filtration rate (GFR), correlates positively with arterial CO2 pressure (PaCO2). The ability of the immature kidney to reclaim filtered bicarbonate in response to an elevation of the plasma carbon dioxide tension remains unlimited up to PaCO2 of 110 mmHg (y = 20.7 + 0.15 x, r = 0.82, P less than 0.001). Hypercapnia is associated with a marked fall in GFR, so that the positive correlation between bicarbonate reabsorption and PaCO2 vanishes when the bicarbonate reabsorption rate is expressed in absolute terms. Bicarbonate reabsorption is strongly dependent on the filtered load during both acutely induced metabolic acidosis and alkalosis. The acid-base state of the newborn rabbit is in sharp contrast with that of most animal species, and the renal handling of bicarbonate as a function of GFR does not show signs of tubular immaturity.
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PMID:Bicarbonate reabsorption by the kidney of the newborn rabbit. 291 64

The compensated chronic respiratory acidosis in a girl with cystic fibrosis changed into a mixed respiratory acidosis and metabolic alkalosis under the influence of therapeutic measures. As a consequence respiratory insufficiency worsened. Conservative management of the alkalosis alone both improved hypoxemia and hypercapnia without needing artificial ventilation.
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PMID:[Respiratory insufficiency in mucoviscidosis. Pathophysiologic aspects of conservative drug therapy]. 292 95

To further study the relationship between ventilatory response (VR) and exercise performance, and to investigate to what extent progesterone is responsible for ventilatory changes in the luteal phase of the menstrual cycle, we administered medroxyprogesterone acetate (MPA) to 10 normal males (20 mg three times a day for 5 doses) and compared results with those obtained in a similar study of females. With MPA, there was an increase in the resting VR to hypercapnia; the resting VR to hypoxia was not changed. There was a respiratory alkalosis at rest. During exercise, the PaCO2 remained lower but the pHa was not different because of a tendency toward lower bicarbonate concentration with MPA. Ventilation, when related to CO2 output, was increased at all exercise loads, indicating increased VR to endogenous CO2. However, ventilation was only minimally (3%) increased when related to oxygen uptake or workload. This apparent disparity is because of slightly lower CO2 output at a given oxygen uptake with MPA. As in females, maximal duration of exercise and maximal oxygen uptake were unchanged. Except for degree, MPA induced all the ventilatory changes seen in the menstrual cycle. Increased VR does not adversely affect exercise performance.
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PMID:Progesterone-induced changes in exercise performance and ventilatory response. 295 62

The influence of blood gases on alpha 1- and alpha 2-adrenoceptor-mediated pressor responses was studied in the pithed rat by varying the inspired gas mixture or the ventilation stroke volume. Acidosis favoured the peak responses to the alpha 2-adrenoceptor agonist, xylazine, while alkalosis favoured the peak responses to the alpha 1-adrenoceptor agonist, phenylephrine. A combination of hypoxia and hypercapnia greatly depressed the alpha 1 response to phenylephrine whereas the alpha 2 response to xylazine remained relatively unaffected. When Pao2 was varied in either acidotic or alkalotic conditions the response to the phenylephrine increased as Pao2 increased. To prevent hypoxia in air ventilated rats, large stroke volumes were required. This caused alkalosis and hence decreased responsiveness to xylazine. Consequently, air ventilated pithed rats gave poorer responses to xylazine than did those ventilated on 100% O2. The results show that alpha 1- and alpha 2-adrenoceptor-mediated pressor responses can be differentially affected by blood gases. The relative contribution of alpha 1- and alpha 2-adrenoceptors to vascular tone may be either under- or over-estimated depending on the arterial blood gases.
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PMID:The influence of blood gases on alpha 1- and alpha 2- adrenoceptor-mediated pressor responses in the pithed rat. 299 76

Hypercapnia is common in chronic respiratory failure (IRCO), and may be further increased in a significant way by oxygen therapy, used for severe hypoxaemia in acute exacerbations. The determinants of PaCO2 are metabolic (hence importance of alkalosis) and ventilatory. In chronic airflow obstruction, CO2 production and ventilation are normal; thus the factor responsible for hypercapnia is essentially the fraction of total ventilation lost in the anatomical and alveolar (VD/VT ratio) dead space, whose effect on PaCO2 is all the more marked on account of the high starting point. From the time of administering pure oxygen hypercapnia is only weakly linked to changes in total ventilation (which, after a few minutes returns to its initial level) and only slightly to the correction of hypoxaemia and desaturation (Haldane effect). On the other hand, the ventilation-perfusion ratios are altered, as evidenced by increased VD/VT ratios. The exact mechanisms are ill understood, but one could consider the worsening venous admixture effect by the reduction of hypoxic vasoconstriction and micro-atelectasis in the poorly ventilated zones, as well as the rise in the anatomical dead space (broncho-dilatation) and alveolar dead space (redistribution of ventilation to poorly perfused zones). In comparison with standard ideas, the genesis of hypercapnia from oxygen therapy depends more on an AIR/BLOOD mis-match, than on the suppression of the hypoxic ventilatory stimulus.
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PMID:[Relationship between hypercapnia and hypoxemia in chronic obstructive respiratory insufficiency]. 314 Mar 17


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