UMLS:C0020440 - FACTA Search

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Query: UMLS:C0020440 (hypercapnia)
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The most common causes of hypoxic cor pulmonale are chronic bronchitis and emphysema. Although the clinical situation in some patients is characterized early by hypoxemia, oedema is rare in patients with an arterial pO2 above 60 mm Hg. The presence of oedema can be regarded as an unfavorable prognostic indicator. For many years, peripheral oedema had been considered an expression of congestive cardiac failure; it may be assumed, however, that neither right nor left ventricular failure is prerequisite to the development of oedema. Oedema formation can be attributed to excessive retention of salt and water or a redistribution of body water into the extracellular compartment. Hypercapnia and acidosis affect direct stimulation of renal hydrogen ion secretion. The resulting electrochemical imbalance is compensated by reabsorption of sodium. Hypercapnia and, in acute phases possibly, hypoxia lead to a fall in renal blood flow mediated by alpha-adrenergic stimulation through activation of the renin-angiotensin-aldosterone system. An increase in plasma ADH may also contribute to development of oedema. The development of cor pulmonale or respiratory insufficiency can be enhanced by nocturnal hypoventilation and hypoxia during sleep as well as by sleep apnoea. Nocturnal hypoxia, smoking and reduced oxygen tension in the relevant kidney cells responsible for erythropoietin release promote the occurrence of secondary polycythaemia. For treatment of acute exacerbations in cor pulmonale associated with infections bronchitis antibiotics such as amoxycillin and cotrimoxacol are drugs of first choice. While the use of digoxin is of doubtful value, the cautious administration of diuretics may bring symptomatic relief. In addition to physiotherapy, beta-2-selective bronchodilators and nebulized bronchodilator therapy can be useful; theophyllines dilate airways and increase cardiac output but they can cause arrhythmias and a deterioration of arterial blood gases in hypoxic patients. If the patient has been treated chronically with corticosteroids, the dosage will have to be incremented; if asthma is suspected, corticosteroid treatment is essential. Controlled oxygen therapy is the most important single therapy aimed at relief of severe arterial hypoxaemia. Oxygen should be titrated initially (for the first one or two days) to achieve an arterial tension of at least 48 mm Hg. Thereafter, the oxygen flow should be increased to yield an arterial tension in excess of 60 mm Hg during continued treatment for two to three weeks.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Hypoxic cor pulmonale: a review. 294 54

The abdominal muscles accelerate airflow during expiration and may also influence the end-expiratory volume and configuration of the thorax. Although much is known about their electrical activity, the degree to which they change length during the respiratory cycle has not been previously assessed. In the present study we measured respiratory changes in transverse abdominis length using sonomicrometry in 14 pentobarbital sodium-anesthetized supine dogs and compared length changes to simultaneously recorded tidal volume and transverse abdominis electromyograms (EMG). To determine muscle resting length at passive functional residual capacity (LFRC), the animals were hyperventilated to apnea. The transverse abdominis was electrically active in all animals during resting O2 breathing (eupnea). During inspiration the transverse abdominis lengthened above resting length in all 14 dogs by a mean of 3.7 +/- 1.1% LFRC; during expiration the transverse abdominis shortened below resting length in 13 of 14 dogs by a mean of 4.2 +/- 0.9% LFRC. Increasing hyperoxic hypercapnia (produced in 9 animals) progressively heightened transverse abdominis EMG and progressively increased the extent of muscle shortening below resting length (to 12.6 +/- 3.2% LFRC at a PCO2 of 90 Torr). During single-breath airway occlusion substantial inspiratory lengthening of the transverse abdominis occurred, both during O2 breathing and during CO2 rebreathing.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Transverse abdominis length changes during eupnea, hypercapnia, and airway occlusion. 296 75

This study was designed to establish the relationship between urinary pCO2 and systemic blood pCO2 during acute hypercapnia and to investigate the significance of this relationship to collecting duct hydrogen ion (H+) secretion when the urine is acid and when it is highly alkaline. In rats excreting a highly alkaline urine, an acute increase in blood pCO2 (from 42 +/- 0.8 to 87 +/- 0.8 mmHg) resulted in a significant fall in urine minus blood (U-B) pCO2 (from 31 +/- 2.0 to 16 +/- 4.2 mmHg, P less than 0.005), a finding which could be interpreted to indicate inhibition of collecting duct H+ secretion by hypercapnia. The urinary pCO2 of rats with hypercapnia, unlike that of normocapnic controls, was significantly lower than that of blood when the urine was acid (58 +/- 6.3 and 86 +/- 1.7 mmHg, P less than 0.001) and when it was alkalinized in the face of accelerated carbonic acid dehydration by infusion of carbonic anhydrase (78 +/- 2.7 and 87 +/- 1.8 mmHg, P less than 0.02). The finding of a urinary pCO2 lower than systemic blood pCO2 during hypercapnia suggested that the urine pCO2 prevailing before bicarbonate loading should be known and the blood pCO2 kept constant to evaluate collecting duct H+ secretion using the urinary pCO2 technique. In experiments performed under these conditions, sodium bicarbonate infusion resulted in an increment in urinary pCO2 (i.e., a delta pCO2) which was comparable in hypercapnic and normocapnic rats (40 +/- 7.2 and 42 +/- 4.6 mmHg, respectively) that were alkalemic (blood pH 7.53 +/- 0.02 and 7.69 +/- 0.01, respectively). The U-B pCO2, however, was again lower in hypercapnic than in normocapnic rats (15 +/- 4.0 and 39 +/- 2.5 mmHg, respectively, P less than 0.001). In hypercapnic rats in which blood pH during bicarbonate infusion was not allowed to become alkalemic (7.38 +/- 0.01), the delta pCO2 was higher than that of normocapnic rats which were alkalemic (70 +/- 5.6 and 42 +/- 4.6 mmHg, respectively, P less than 0.005) while the U-B pCO2 was about the same (39 +/- 3.7 and 39 +/- 2.5 mmHg). We further examined urine pCO2 generation by measuring the difference between the urine pCO2 of a highly alkaline urine not containing carbonic anhydrase and that of an equally alkaline urine containing this enzyme. Carbonic anhydrase infusion to hypercapnic rats that were not alkalemic resulted in a fall in urine pCO(2) (from 122+/-5.7 to 77+/-2.2 mmHg) which was greater (P <0.02) than that seen in alkalemic normocapnic controls (from 73+/- 1.9 to 43+/-1.3 mmHg) with a comparable urine bicarbonate concentration and urine nonbicarbonate buffer capacity. CO(2) generation, therefore, from collecting dust H(+) secretion and titration of bicarbonate, was higher in hypercapnic rats that in normocapnic controls. We conclude that in rats with actue hypercapnia, the U-B p(CO(2)) achieved during bicarbonate loading greatly underestimates collecting duct H(+) secretion because it is artificially influenced by systemic blood pCO(2). the deltapCO(2) is a better qualitative index of collecting duct H+ secretion that the U-B pCO(2), because it is not artificially influenced by systemic blood pCO(2) and it takes into account the urine PCO(2) prevailing before bicarbonate loading.
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PMID:Relationship of urinary and blood carbon dioxide tension during hypercapnia in the rat. Its significance in the evaluation of collecting duct hydrogen ion secretion. 298 5

To examine the effect of carbonic anhydrase inhibition on proximal tubular electrolyte reabsorption, plasma pH was altered before and after acetazolamide administration in six volume-expanded dogs during continuous infusion of ethacrynic acid to inhibit transcellular NaCl reabsorption. Plasma pH was altered by changing PCO2, keeping plasma bicarbonate concentration and glomerular filtration rate constant. Linear inverse relationships were obtained between electrolyte reabsorption and plasma pH. Before acetazolamide administration, a change in plasma pH of 0.1 unit from pH 7.4 altered bicarbonate reabsorption by about 10% and sodium and chloride reabsorption remaining during ethacrynic acid infusion by about 6.5%. Administration of acetazolamide (30 mg/kg b.wt.) caused a reduction in electrolyte reabsorption at all plasma pH levels examined. A further reduction occurred after increasing the dose to 100 mg/kg b.wt. The absolute inhibitory effects were almost twice as large during hypercapnia as during hypocapnia whereas the reduction in fractional reabsorption was the same at all plasma pH levels. Both variations in plasma pH and administration of acetazolamide altered the reabsorption of bicarbonate, chloride and sodium in molar ratios of about 1:2:3. Hence, acetazolamide inhibits a constant fraction of the NaHCO3 reabsorption and the associated NaCl reabsorption in the proximal tubules independent of changes in plasma pH.
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PMID:Inhibitory effect of acetazolamide on renal tubular reabsorption of NaHCO3 and NaCl in dogs varies inversely with plasma pH. 299 93

The rise in urinary pCO2 above blood pCO2 which occurs in response to bicarbonate loading (i.e. the urine to blood (U-B) pCO2 gradient), is used with increasing frequency as an index of collecting duct hydrogen ion secretion. We recently proposed, however, that the U-B pCO2 gradient is not an appropriate index of collecting duct hydrogen ion secretion when blood pCO2 is altered acutely. This issue was further investigated by examining the effect of chronic hypercapnia on urinary pCO2 generation. In rats exposed to chronic hypercapnia induced by breathing 10% CO2 for 3 days in an environmental chamber, acute sodium bicarbonate infusion resulted in a U-B pCO2 lower than that of normocapnic control rats (11 +/- 4.6 and 30 +/- 1.8 mm Hg, p less than 0.001). This finding could be interpreted to indicate that collecting duct hydrogen ion secretion is depressed in rats with chronic hypercapnia. The urinary pCO2 of rats with chronic hypercapnia was lower than that of the blood (54 +/- 6.0 and 86 +/- 1.2 mm Hg, p less than 0.005, respectively). In these rats, NaHCO3 infusion, while blood pCO2 was kept constant, elicited a marked rise in urine pCO2 (from 54 +/- 6.0 to 104 +/- 6.0 mm Hg, p less than 0.005) which was not significantly different from that observed in normocapnic control rats. The infusion of carbonic anhydrase resulted in a comparable fall in urine pCO2 in hypercapnic and normocapnic rats (-27 +/- 5 and -30 +/- 3 mm Hg).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Urinary pCO2 as an index of collecting duct hydrogen ion secretion during chronic hypercapnia. 299 36

To study both temporal and quantitative effects of hypercapnia on the extent of pH compensation in the arterial blood, specimens of carp (Cyprinus carpio) were exposed to a PCO2 of about 7.5 mmHg (1 mmHg = 133.3 Pa) (1% CO2) in the environmental water for several weeks, and a second group of animals was subjected to an environmental PCO2 of about 37 mmHg (5% CO2) for up to 96 h. A third series of experiments was designed to test the possibility that infusion of bicarbonate would increase the extent of plasma pH compensation. Dorsal aortic plasma pH, PCO2 and [HCO3-], as well as net transfer of HCO3- -equivalent ions, NH4+, Cl- and Na+, between fish and ambient water, were monitored throughout the experiments. Exposure to environmental PCO2 of 7.5 mmHg resulted in the expected respiratory acidosis with the associated drop in plasma pH, and subsequent compensatory plasma [HCO3-] increase. The compensatory increase of plasma bicarbonate during long-term hypercapnia continued during 19 days of exposure with plasma bicarbonate finally elevated from 13.0 mmoll-1 during control conditions to 25.9 mmoll-1 in hypercapnia, an increase equivalent to 80% plasma pH compensation. Exposure to 5% hypercapnia elicited much larger acid-base effects, which were compensated to a much lesser extent. Plasma pH recovered to only about 45% of the pH depression expected at constant bicarbonate concentration. At the end of the 96-h exposure period, plasma [HCO3-] was elevated by a factor of 2.5 to about 28.2 mmoll-1. The observed increase in plasma bicarbonate concentration during 5% hypercapnic exposure was attributable to net gain of bicarbonate equivalent ions from (or release of H+-equivalent ions to) the environmental water. Quantitatively, the gain of 15.6 mmol kg-1 was considerably larger than the amount required for compensation of the extracellular space, suggesting that acid-base relevant ions were transferred for compensation of the intracellular body compartments. The uptake of bicarbonate-equivalent ions from the water was accompanied by a net release of Cl-and, to a smaller extent, by a net uptake of Na+, suggesting a 75% contribution of the Cl-/HCO-3 exchange mechanism. Infusion of bicarbonate after 48 h of exposure to 7.5 mmHg PCo2 had only a transient effect on further pH compensation. The infused bicarbonate was lost to the ambient water, and pre-infusion levels of bicarbonate were reattained within 24 h. Repetition of the infusion did not result in a notable improvement of the acid-base status.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Acid-base regulation and ion transfers in the carp (Cyprinus carpio): pH compensation during graded long- and short-term environmental hypercapnia, and the effect of bicarbonate infusion. 302 33

We studied the responses of the ganglioglomerular nerve (GGN) efferents to brief periods of hypoxia and hypercapnia and to several levels of steady-state arterial PO2 and PCO2 and to intravascular injection of cyanide in thirteen anesthetized cats. The cats breathed spontaneously. A branch of the GGN which was cut close to the carotid body was divided into several filaments, and the activity of each filament was tested until clean and identifiable action potentials were obtained. The GGN efferent activity, breath-by-breath inspiratory volume, tracheal PO2 and PCO2 and arterial blood pressure were recorded simultaneously. We found that the GGN contained spontaneously active fibers which showed a range of responses to the respiratory stimuli. Fifty-eight percent of the filaments with dominant cardiovascular rhythm showed the least response to blood gas stimuli. Forty-two percent showed clear responses to hypoxia and hypercapnia. These responses developed slowly with the onset of the stimulus but decreased promptly with the withdrawal of the stimulus. These GGN efferents were also promptly stimulated by sodium cyanide. The steady-state response curve to hypoxia was hyperbolic and to hypercapnia it was linear. Some of these fibers showed stronger respiratory rhythms than others. The responses of these GGN efferents were associated with the respiratory responses to hypoxia and hypercapnia. For the same respiratory drive, however, the steady-state hypoxic stimulus elicited a greater GGN response than did hypercapnia.
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PMID:Responses of ganglioglomerular nerve activity to respiratory stimuli in the cat. 308 75

The aims of this study were to investigate the effect of changes in arterial blood gases and pH on furosemide pharmacodynamics and kinetics. Five groups of conscious rabbits were used: a control group breathing air with normoxia and normocarbia; a second group with hypercapnia and respiratory acidosis; a third with hypoxemia; a fourth with hypercapnia and respiratory acidosis combined with hypoxemia (HCHO); and the fifth group with metabolic acidosis. All experimental conditions, except hypoxemia, increased sodium tubular reabsorption and therefore, decreased urinary excretion of sodium. Renal blood flow was decreased by HCHO and metabolic acidosis. In response to 5 mg/kv i.v. of furosemide, natriuresis and diuresis were decreased by an average of 44% in animals with HCHO (P less than .05). The kinetics of furosemide were not affected by any of the experimental conditions except HCHO, in which the renal clearance of furosemide was reduced from 7.5 +/- 1.4 ml/min/kg (controls) to 2.7 +/- 0.7 ml/min/kg (P less than .05). The reduction in renal clearance of furosemide was associated with a decrease in urinary excretion of sodium (P less than .05). The reduction in renal clearance of furosemide was probably secondary to the decrease in renal blood flow and an increase in furosemide tubular reabsorption. Finally, HCHO did not decrease plasma volume, suggesting that the reduction in renal blood flow was secondary to blood flow distribution. In conclusion, only hypercapnia and respiratory acidosis combined with hypoxemia decreases the natriuretic and diuretic effect of furosemide.
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PMID:Furosemide pharmacodynamics: effect of respiratory and acid-base disturbances. 308 62

The experiments were performed on anaesthetized dogs which breathed spontaneously or were artificially ventilated and paralysed. The spontaneous nasal arterial blood flow was measured on one side of the nose while nasal vascular resistance was determined on the other side simultaneously. Nasal arterial blood flow was measured by means of an electromagnetic flow sensor placed around the terminal branch of the internal maxillary artery, the main arterial supply to the nasal mucosa. Nasal vascular resistance was measured by constant-flow perfusion of the terminal branch of the internal maxillary artery. Nasal airway resistance was assessed by monitoring the transnasal pressure at constant airflow through each side of the nose simultaneously. Hypercapnic gas challenge (8% CO2, 30% O2 in N2) to the lungs increased nasal vascular resistance and decreased nasal airway resistance. Similar gas challenge to the nose did not affect nasal vascular resistance but decreased nasal airway resistance. Hypoxic gas challenge (6% O2 in N2) to the lungs did not affect the nasal vascular resistance but decreased nasal airway resistance only when the nasal vascular bed was under controlled perfusion. Similar gas challenge to the nose did not affect either nasal vascular or airway resistance. Arterial chemoreceptor stimulation by intracarotid injection of sodium cyanide increased nasal vascular resistance and decreased nasal airway resistance. The nasal vascular response to hypercapnia and arterial chemoreceptor stimulation was reflex in nature, being abolished by nasal sympathectomy. The nasal airway response to hypercapnia, hypoxia and arterial chemoreceptor stimulation was reflex in nature, being partially or completely abolished by nasal sympathectomy. Hypercapnia probably induced a local vasodilatatory effect on the capacitance vessels whereas hypoxia had no direct action on the vasculature.
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PMID:Effects of hypercapnia and hypoxia on nasal vasculature and airflow resistance in the anaesthetized dog. 309 11

The physiological role of carbonic anhydrase III in slow-twitch skeletal muscle was investigated using isolated mouse soleus (N = 30) contracting once every 1.7 min for 75 min in Krebs-Henseleit solution gassed with either 95% oxygen - 5% carbon dioxide (normocapnia) or 90% oxygen - 10% carbon dioxide (hypercapnia). Each contraction was 500 ms in duration at 50 Hz. When muscles contracted in normocapnic solution (pH 7.42), the developed tension decreased an average of 6.1 +/- 0.8% over 25 min. For the next 50 min, 15 muscles remained normocapnic, while the remainder contracted in hypercapnic solution (pH 7.20). Tension decreased significantly more with hypercapnia. For the last 25 min, both normocapnic and hypercapnic muscles were divided into three treatment groups (N = 5). One group continued in the same environment, while acetazolamide (final concentration of 10(-5) M) was added to the bath of the second and sodium cyanate (final concentration of 10(-5) M) was added to the bath of the third group. Acetazolamide had no effect on tension in either carbon dioxide environment. Sodium cyanate significantly decreased tension from the hypercapnic control but had no effect in normocapnia. Thus carbonic anhydrase III inhibition with sodium cyanate increased the effect of hypercapnia implying that carbonic anhydrase III assists in the regulation of free hydrogen ion concentration in slow-twitch skeletal muscle.
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PMID:Carbonic anhydrase III inhibition in normocapnic and hypercapnic contracting mouse soleus. 310 51

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