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

The cricothyroid muscle serves as an accessory muscle of respiration in anesthetized animals. The functional significance of this activity is unknown. To determine respiratory cricothyroid muscle activity in conscious humans, cricothyroid muscle electromyogram was measured percutaneously, along with posterior cricoarytenoid muscle electromyogram and esophageal pressure in six volunteers. Low level cricothyroid muscle activity with quiet breathing was observed in four subjects. In all subjects, cricothyroid muscle activity was recruited by voluntary deep breathing, brief airway occlusion, and hypercapnia. Continuous positive airway pressure at 7.5-cm H2O increased expiratory cricothyroid muscle activity in all subjects, and suppressed inspiratory activity in five. These results indicate that respiratory reflexes of the cricothyroid muscle are operative in conscious humans.
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PMID:Respiratory activity of the cricothyroid muscle in conscious humans. 240 47

The upper airway (UAW) is intrinsically unstable and susceptible to collapse when the negative inspiratory intraluminal pressure exceeds the stabilizing forces which prevent obstruction. In the present study we evaluated mechanisms by which UAW patency is maintained in the presence of increased inspiratory flows when respiration is stimulated. In seven anesthetized dogs breathing spontaneously through a low tracheostomy, the UAW was isolated by a second tracheostomy directed rostrally. UAW pressure-flow relationship and stability against collapse were evaluated during steady flow in the inspiratory direction while the animals were breathing 100% O2 or a hypercapnic gas mixture. The pressure-flow curves of the isolated UAW demonstrated the characteristic pattern of collapsible tubes. Steady state hypercapnia resulted in lower UAW resistance during both inspiration and expiration. UAW resistance decreased linearly as PCO2 and ventilation increased over the course of CO2 rebreathing. In addition, during hypercapnia the critical negative intraluminal pressure required to induce UAW collapse and obstruction increased from -4.3 +/- 0.9 to -8.5 +/- 1.5 SE cm H2O (p less than 0.01), indicating increased stability of the UAW. Since hypercapnia is known to stimulate UAW muscles, our findings suggest that increased UAW muscle activity improves UAW patency both by decreasing their resistance to airflow, and by increasing UAW walls rigidity and stability against collapse.
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PMID:Effect of hypercapnia on upper airway resistance and collapsibility in anesthetized dogs. 249 2

In chronic experiments on rabbits, the effect of hyperthermia growing up to 41 degrees C upon the cerebral circulation system, was studied. Cortical blood flow decreased by 20-25% due to hypercapnia and constriction of arterioles whereas the blood flow in the thalamus and hypothalamus either remained the same as initial one or increased insignificantly. The reactivity of cerebral vessels in CO2 inhalation and orthostatic load decreased along with the rise of body temperature. The signs of lesion of the hemato-encephalic barrier and an increase of the water content by 3-4% in the cortex and white matter were revealed in hyperthermia. The impedance data corroborated extracellular character of cerebral oedema. Comparative study of vasodilators euphylline, cavinton and flunaresine has revealed that the calcium blocking agent flunaresine provides the best restoration of the cerebral blood flow level and the reactivity of cerebral vessels in hyperthermia.
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PMID:[Functioning of the cerebral circulatory system in rabbits during hyperthermia]. 251 12

The steady-state responses of upper-airway dilating muscles and diaphragm activity to elevation of lung volume induced by positive end-expiratory pressure loading were studied in 9 pentobarbital-anesthetized dogs with vagus nerves intact. The early and late effects of 5 min of expiratory threshold loads upon upper airway dilating muscle activity (the alae nasi, the genioglossus and the posterior cricoarytenoid) were compared to their effects on diaphragm activity. During resting O2 breathing, application of 5 and 10 cm H2O of positive end-expiratory pressure produced no significant change in the peak electrical activity of the upper-airway dilating muscles and diaphragm (p greater than 0.05). No qualitative differences were found in the upper-airway dilating muscles and diaphragm responses to expiratory threshold loads when the animals breathed 3 or 7% CO2 in O2, compared to when they inspired 100% O2. Furthermore, no differences were found in the electrical activity of the upper-airway dilating muscles and diaphragm at any given end-tidal CO2 when unloaded responses were compared with loaded responses during progressive hypercapnia. However, positive end-expiratory pressure loading caused significant prolongation of expiratory duration, which gradually returned toward control levels when the loads were maintained. In animals who developed periodic breathing by increasing levels of anesthesia, positive end-expiratory pressure loading eliminated the periodicity and made the pattern of breathing regular. Based on these results, it can be concluded that under the conditions of these experiments, increases in lung volume produced by expiratory threshold loads do not reduce the activity of upper-airway dilating muscles. The maintenance of the electrical activity of the upper-airway dilating muscles might be caused by excitatory reflex mechanisms or central habituation.
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PMID:Responses of upper-airway dilating muscles and diaphragm activity to end-expiratory pressure loading in anesthetized dogs. 260 63

Renal function was assessed in 89 patients with advanced chronic obstructive pulmonary disease and chronic cor pulmonale, 62 of them had respiratory failure, 18 health aged served as control. The results showed that the creatinine clearance and the free water clearance were decreased in 82.3% and 69.5% of patients with respiratory failure respectively. The renal function was impaired in case of hypoxia, PaO2 less than or equal to 6.0 kPa (45 mmHg), mean 5.33 kPa (40 mmHg). Hypercapnia was one of the most important factors that effected the renal function. There was a clinical threshold which effected the renal function, i.e. PaCO2 equals more than 8.67 kPa (65 mmHg). Renal function was greatly impaired if hypercapnia and hypoxia exist at the same time. The impairment of renal function was further marked when right heart failure and acidosis developed. The causes and effects of the abnormality of renal function were preliminarily discussed.
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PMID:[Influence of acute respiratory failure on renal function in advanced chronic obstructive pulmonary disease and chronic cor pulmonale]. 263 31

In the proximal tubules, fractional reabsorption remains essentially unchanged during variations in glomerular filtration rate (GFR). Glomerulotubular balance (GTB), defined as the linear relationship between proximal tubular reabsorption and GFR, is quantitatively the most important regulator of tubular reabsorption, which may be stopped by inhibiting Na, K-ATPase activity completely. However, ouabain in doses inhibiting 80% of the Na, K-ATPases, exerts no effect on proximal reabsorption of water, NaCl and NaHCO3. At constant plasma pH, the same relationship between filtered and reabsorbed bicarbonate is obtained whether bicarbonate reabsorption is altered by varying GFR or plasma concentration of bicarbonate. In contrast, a selective rise in plasma NaCl concentration at constant plasma pH (hypernatremia) reduces NaHCO3 reabsorption and fails to stimulate NaCl reabsorption. Other characteristics of proximal tubular reabsorption are that nonreabsorbable solutes, such as mannitol, inhibit water and NaCl reabsorption with little or no change in NaHCO3 reabsorption and renal oxygen consumption. Mannitol reduces the slope of the GTB curve for NaCl but not for NaHCO3. Hypertonic NaHCO3 exerts an osmotic effect on proximal water and NaCl reabsorption comparable to that of mannitol, whereas hypertonic NaCl is without osmotic effect. By reducing plasma pH (hypercapnia at high plasma bicarbonate concentration), the slope of the GTB curves for NaCl and NaHCO3 can be greatly increased. By raising plasma pH either by hypocapnia or bicarbonate loading, proximal reabsorption of NaHCO3 and NaCl is greatly depressed and remains almost unaltered during variations of GFR (abolished GTB). Similarly, carbonic anhydrase inhibitors, such as acetazolamide, reduce the reabsorption of NaCl and NaHCO3 in the same proportion as a rise in plasma pH, and abolish GTB. Examinations of proximal tubular oxygen consumption indicate that the energy requirement for NaHCO3 reabsorption is as expected for transcellular transport by Na, K-ATPases, whereas proximal NaCl reabsorption requires no additional energy. These data indicate that transcellular energy-requiring NaHCO3 reabsorption provides the main osmotic force across the tight junction for paracellular reabsorption of proximal tubular fluid containing NaCl and other solutes of low reflection coefficient. The main factors influencing GTB are the filtered load of bicarbonate, plasma pH and nonreabsorbable solutes in the proximal tubular fluid.
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PMID:Essentials of glomerulotubular balance. 267 97

Plasma ADH, PA and PRA in patients with respiratory failure (RF) were studied. RF patients were divided into 4 groups, i.e. acute RF (ARF) and chronic RF (CRF), with or without hypercapnia. The levels of these hormones were significantly higher in RF than those in control subjects, moreover, they were markedly elevated in ARF than those in CRF. In multiple regression analysis, ADH correlated with PaO2, pH and PRA in RF patients, but correlated with serum osmolality in control subjects. It was considered that ADH in RF was affected by the direct effect of blood gases and circulatory disorder. The mechanism of elevated PA and PRA in RF probably was mediated through restriction of intake of water and Na, reduction of renal blood flow and decreased ACE often occurred in RF. Abnormally elevated hormones are more often recognized in edematous patients than in nonedematous patients. It was suggested that many patients with RF develop heart failure or edema due to hormonal abnormalities.
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PMID:[ADH (anti-diuretic hormone), aldosterone (PA) and renin activity (PRA) in patients with respiratory failure]. 269 88

We studied the spontaneous breathing patterns of 10 normal adult volunteers during high-frequency chest wall oscillation (HFCWO), accomplished by inflating and deflating a vest worn around each subject's thorax at 2.5 Hz. Tidal volumes generated by HFCWO averaged 100 ml. Mean vest pressure was maintained at approximately 35 cm H2O throughout each experiment, even when HFCWO was not applied. During HFCWO, subjects were instructed occasionally to exhale deeply to obtain end-tidal samples representative of PACO2. HFCWO increased the breath-to-breath variability of spontaneous respiration in all subjects, prolonging expiratory pauses and producing short apneas in some cases. PACO2 decreased significantly (p less than 0.05). The effects on minute ventilation, tidal volume, and inspiratory and expiratory durations remained variable across subjects, even when differences in PACO2 between control and HFCWO states were reduced through inhalation of a low CO2 mixture. None of the changes were statistically significant, although average expiratory duration increased by 29%. Ventilatory responses to CO2 with and without HFCWO were also measured. Normocapnic (PACO2 = 40 mm Hg) ventilatory drive increased significantly (p less than 0.05) in six subjects (Type 1 response) and decreased substantially in the others (Type 2 response); with hypercapnia, the changes in drive were attenuated in both groups. Consequently, CO2 sensitivity decreased in Type 1 subjects and increased in Type 2 subjects. A simple analysis based on this result shows that with HFCWO, Type 2 subjects breathing air will tend to have a lower spontaneous minute ventilation and become hypercapnic. Type 1 subjects will become hypocapnic, but minute ventilation may be higher or lower than control.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of high-frequency chest wall oscillation on respiratory control in humans. 271 50

The concentrations of plasma catecholamines, epinephrine and norepinephrine, were monitored in rainbow trout (Salmo gairdneri) after acute (30 min) exposure to various levels of external hypercapnia (water PCO2 (PwCO2) = 0-11.3 Torr) under normoxic (water PO2 (PwO2) = 153 +/- 1.1 Torr) or hyperoxic (PwO2 = 653 +/- 27.0 Torr) conditions. Whole blood pH decreased to a similar extent as a function of external carbon dioxide tensions in both the normoxic and hyperoxic hypercapnic groups. Arterial oxygen content, however, declined only during normoxic hypercapnia. Similarly, plasma catecholamines (primarily epinephrine) increased only during normoxic hypercapnia in proportion to the severity of the whole blood acidosis. Epinephrine levels were elevated 10-fold from 0.70 +/- 0.06 nM to 7.06 +/- 3.7 nM at the highest concentration of external CO2 (11.3 Torr) whereas norepinephrine increased 3-fold from 0.56 +/- 0.07 nM to 1.62 +/- 0.40 nM. The absence of catecholamine release into the circulation during hyperoxic hypercapnia was not due to inhibition of the 'catecholamine-releasing process' by abnormally elevated arterial oxygen tensions (PaO2 = approximately 400 Torr) because acutely anaemic and thus hypoxemic fish (haematocrit = 4.9 +/- 0.7%) displayed identical elevations of plasma catecholamines under both normoxic and hyperoxic conditions. The results of these experiments demonstrate that arterial hypoxemia, rather than blood acidosis per se, is the proximate stimulus causing catecholamine mobilization in rainbow trout during short-term environmental hypercapnia.
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PMID:Evidence that hypoxemia promotes catecholamine release during hypercapnic acidosis in rainbow trout (Salmo gairdneri). 278 Nov 70

The presence of a peripheral myopathy in hypothyroidism has been well recognized. Involvement of the diaphragm has been suggested recently but the clinical spectrum never clearly defined. We studied three patients with hypothyroidism presenting with fatigue, dyspnea, exercise limitation, and in two, chronic alveolar hypoventilation (PaCO2 of 51 and 75 mm Hg) before and after thyroid hormone replacement. In all patients diaphragmatic strength as determined by the maximal transdiaphragmatic pressure was low (2, 13, and 64 cm H2O) and improved with therapy (86, 84, and 90 cm H2O). Similarly, all patients manifested a fatiguing breathing pattern, as determined by the diaphragmatic tension time index. These values (0.22, 0.55, and 0.36) decreased after hormone replacement (0.16, 0.20, and 0.15). These changes were associated with the correction of hypercarbia in the two patients with hypoventilation and an improvement in lung volumes and exercise endurance in all patients. This study confirms that in patients with hypothyroidism diaphragmatic dysfunction occurs more frequently than has been suspected and might be of varying severity. This dysfunction reverses with adequate hormone replacement.
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PMID:Hypothyroidism. A reversible cause of diaphragmatic dysfunction. 280 37


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