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

We have investigated, in six healthy male volunteers, the effect of high thoracic extradural anaesthesia on the ventilatory pattern and hypercapnic ventilatory response. Ventilatory variables were determined using a respiratory inductive plethysmograph. Duration of inspiration, rib cage excursion and its contribution to tidal volume decreased significantly following extradural anaesthesia, while mean inspiratory flow rate and minute ventilation increased. End-tidal PCO2 and the tidal excursion of the abdomen were unchanged. Hypercapnic ventilatory response decreased significantly following extradural anaesthesia, principally because of the rib cage component. The slope of the abdominal component did not change significantly. The results indicate that mechanical impairment of rib cage movement can produce decreased ventilatory response to carbon dioxide. The ventilatory impairment and the changes in breathing pattern induced by the high thoracic extradural anaesthesia probably reflect blockade of the efferent or afferent pathway (or both) of the intercostal nerve roots.
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PMID:Effect of high thoracic extradural anaesthesia on ventilatory response to hypercapnia in normal volunteers. 249 10

The blood flow to the diaphragm, external and internal intercostal muscles, abdominal oblique muscles, and other rib-cage and abdominal muscles was measured, using radio-labelled microspheres, in 6 newborn lambs quietly breathing in air and during 3 different levels of CO2 induced hypercapnic hyperpnoea (inspired gas containing 4%, 5.5%, or 7% CO2). We also calculated the oxygen uptake of the diaphragm (VO2di). While the lambs were breathing air diaphragmatic blood flow (Qdi, 38.2 +/- 4.0 SEM ml.min-1.100 g-1) was similar to external intercostal muscle blood flow (Qei, 37.1 +/- 8.1 ml.min-1.100 g-1), and both were greater than internal intercostal muscle blood flow (Qii, 24.8 +/- 6.1 ml.min-1.100 g-1; P less than 0.05). During hyperpnoea Qdi, Qei, and Qii were augmented with Qdi equal to 200.1 +/- 12.2 ml.min-1.100 g-1 in 7% CO2 and Qei equal to 88.4 +/- 14.1 ml.min-1.100 g-1 in 7% CO2 (Qdi was greater than Qei, P less than 0.01). Qii was 40.7 +/- 5.6 ml.min-1.100 g-1 in 7% CO2 being less than Qdi (P less than 0.01) and Qei (P less than 0.05). The abdominal oblique muscles also had augmented flow in response to hyperpnoea. The level of hypercapnia that resulted in an augmentation of Qdi (5.5% inspired CO2) was lower than that which augmented Qei and Qii (7% inspired CO2). VO2di was linearly related to Qdi (r = 0.98). Our results suggest that in the newborn lamb the diaphragm is the dominant respiratory muscle in response to hypercapnia.
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PMID:Blood flow to the respiratory muscles during hypercapnic hyperpnoea in the newborn lamb. 272 19

The present study compared the responses of rib cage and abdominal expiratory muscles to chemical and mechanical stimuli. In pentobarbital-anesthetized spontaneously breathing dogs, electromyograms (EMG) were recorded from the triangularis sterni (TS) and transverse abdominis (TA) muscles using bipolar intramuscular wire electrodes. During resting oxygen breathing, both muscles were electrically active during expiration. Progressive hyperoxic hypercapnia significantly augmented the expiratory activity of both the TA and the TS. However, the mean percent increases in electrical activity in response to CO2 were substantially greater for the TA than for the TS at all PCO2 levels greater than 50 Torr (P less than 0.01). Occlusion of the airway at end inspiration significantly delayed the onset of TS EMG (from 0.35 +/- 0.07 to 3.35 +/- 0.67 sec; P less than 0.002) and decreased TS EMG rate of rise (P less than 0.002), but did not significantly alter these parameters for the TA. Esophageal distension increased TS EMG in all dogs (by mean of 220 +/- 64%; P less than 0.01), but in contrast decreased TA EMG in all dogs (by a mean of 63 +/- 12%; P less than 0.001). The response to esophageal distention occurred in a graded manner and appeared to be mediated predominantly via vagal afferents. We concluded that expiratory muscles of the rib cage and abdomen manifest substantial differences in their electrical responses to chemoreceptor, pulmonary stretch receptor, and esophageal mechanoreceptor stimuli.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Rib cage and abdominal expiratory muscle responses to CO2 and esophageal distension. 296 76

The main cause of secondary pulmonary hypertension in the view of a pulmonologist is alveolar hypoventilation - eventually potentiated by acidosis and hypercapnia - which leads to reflectory hypoxemic vasoconstriction of the small pulmonary arteries. Anatomic changes in the pulmonary vessels may be absent or may be limited to medial hypertrophy of the arterioles. If the underlying cause of the hypoxia can be corrected, this reflectory pulmonary hypertension is reversible. In diffuse progressive lung disease, interstitial fibrosis with destruction of the alveolar wall and capillaries may occur, leading to restriction of the pulmonary vascular bed. In such cases pulmonary hypertension may not be completely reversible. The most frequent causes of pulmonary hypertension in childhood are obstructive (e.g. Cystic Fibrosis) or restrictive lung diseases (e.g. interstitial fibrosis). Rare but important in the differential diagnosis are upper airway obstruction, thoracic cage deformity, neuromuscular disorders, high altitude and respiratory center dysfunction. The therapy is elimination of the underlying disease or optimal treatment. In addition prophylactic or therapeutic longterm application of oxygen is more efficient than treatment with pulmonary vasodilators or modern substances like Almitrine. Right heart decompensation should be treated by diuretics. The longterm prognosis is dependent of the underlying disease and is poor in a chronic progressive lung disease like cystic fibrosis and certain types of lung fibrosis.
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PMID:[Pulmonary hypertension from the viewpoint of the pediatric pulmonologist]. 310 Dec 91

The aim of this study was to investigate (i) whether bilirubin encephalopathy with lasting sequelae could be created in a rat model, and (ii) putative differences in brain toxicity between bound and unbound bilirubin. Hyperbilirubinemia was produced by infusing bilirubin 20 mg/kg/h during 3 h into 6-week-old male Sprague-Dawley rats. In addition to the hyperbilirubinemia, different groups were created by exposing the rats to hyperosmolality, hypercarbia, and sulfisoxazole. Three weeks after the infusion the rats were studied in an open-field apparatus during 10 daily sessions of 15 min duration. A data collection program was used to study the following measures of activity: crossings in cage, peeks, rearing, latency to enter field, crossings in middle and in outer field, and time outside cage. The data were subjected to multivariate analyses of variance (MANOVA). Generally, the level of activity was higher in the bilirubin-treated rats as compared to the control animals. The difference in activity between bilirubin-treated and control rats changed systematically both between and within sessions. The data show that both unbound and albumin-bound bilirubin are neurotoxic, but they indicate a more pronounced effect of unbound bilirubin. The sequelae of bilirubin brain toxicity appear to include changes in stimulus processing. This is compatible with findings from neuropsychological tests of children who have had significant neonatal hyperbilirubinemia.
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PMID:Open-field behavior of rats previously subjected to short-term hyperbilirubinemia with or without blood-brain barrier manipulations. 369 Mar 1

We measured, in 11 healthy volunteers, the contributions of rib cage and abdomen--diaphragm compartments to increased ventilation caused by hypercapnia, hypoxia, and exercise to determine whether different stimuli produce similar or different patterns of ventilation with respect to the motion of rib cage and abdominal compartments. Progressive hyperoxic hypercapnia and progressive isocapnic hypoxia were induced by rebreathing methods and graded exercise performed on a treadmill, and compartmental tidal volume (VT) was measured by respiratory inductive plethysmography. For each stimulus, the wide range of VT responses among individuals was determined primarily by the range of rib cage contributions to VT, the abdominal compartment VT response slopes accounting for less of this range. There were no significant differences between hypercapnia and hypoxia in either rib cage or abdominal contributions to ventilation (for both, p less than 0.3). However, exercise rib cage and abdominal contributions to ventilation were significantly different from those during chemically driven breathing: for the rib cage compartment, p less than 0.0001 and for the abdominal compartment, p less than 0.05. Whereas, in 8 of 10 subjects the rib cage contribution to VT during exercise was similar to or exceeded that during rebreathing, in 7 of 10 subjects the abdomen-diaphragm contribution fell below that measured during both hypercapnia and hypoxia. There was a significant correlation between hypercapnia and hypoxia in the VT contribution of each compartment at equivalent levels of ventilation (rib cage, p less than 0.0001; abdomen, p less than 0.0005), but there was no significant correlation in the VT contribution of either compartment between exercise and hypercapnia or exercise and hypoxia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Thoracoabdominal motion during hypercapnia, hypoxia, and exercise. 398 3

This study compared the respiratory responses to ventilatory loading in 8 normal subjects and 11 quadriplegic patients with low cervical spinal cord transection. Progressive hypercapnia was produced by rebreathing. Rebreathing trials were carried out with no added load and with inspiratory resistive loads of 5 and 16 cmH2O. l-1 X s. Measurements were made of ventilation and of diaphragmatic electromyographic activity. Base-line hypercapnic ventilatory responses were significantly lower than normal in the quadriplegic patients, but the effects of resistive loading on the ventilatory responses were comparable in the two groups. The change in peak moving-average diaphragmatic electrical activity (DI peak) for a given change in CO2 partial pressure (PCO2) and DI peak at PCO2 55 Torr increased significantly with resistive loading both in the normal subjects and the quadriplegic patients. In the normal subjects, but not in the quadriplegic patients, inspiratory duration increased progressively with increasing resistance. The increase in DI peak during ventilatory loading in the normal subjects was a consequence of inspiratory prolongation. In contrast, in the quadriplegic patients during breathing against the larger resistive load, there was a significant increase in the average rate of rise (DI peak divided by the time from onset to peak) of diaphragmatic activity. The change in DI rate of rise for a given change in PCO2 increased to 137 +/- 13% (SE), and the DI rate of rise at PCO2 55 Torr increased to 128 +/- 8% (SE) of control values. These results indicate that compensatory increases in diaphragmatic activation during ventilatory loading occur in quadriplegic patients in whom afferent feedback from rib cage receptors is disrupted.
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PMID:Respiratory responses to ventilatory loading following low cervical spinal cord injury. 407 83

To determine whether the rib cage and abdomen-diaphragm contributions to tidal volume (VT) during CO2 rebreathing are affected by postural change, using respiratory inductive plethysmography, we measured in eight healthy volunteers the compartmental VT responses to progressive hypercapnia in both seated and supine postures. The ventilatory, frequency, and VT responses to CO2 of the total respiratory system were not significantly different between postures. VT responses, corrected for body size, ranged from 1.67 to 3.71% vital capacity (VC) X Torr-1 (mean 2.27) in seated subjects and from 1.08 to 3.79% VC X Torr-1 (mean 2.06), in supine subjects. In both postures, the VT response of the abdominal compartment was nearly uniform among subjects and independent of the total respiratory system VT response (slope = 0.091, r = 0.210 P greater than 0.3 seated; slope = 0.043, r = 0.077, P greater than 0.3 supine), whereas the VT response of the rib cage varied among subjects and was significantly correlated to the total VT response (slope = 0.815, r = 0.84, P less than 0.01, seated; slope = 1.125, r = 0.859, P less than 0.01, supine). Thus high tidal volume responses to CO2 rebreathing are determined largely by recruitment of the rib cage compartment in both seated and supine postures.
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PMID:Effect of posture on thoracoabdominal movements during CO2 rebreathing. 622 9

The ventilatory and occlusion pressure (P100) responses to hypercapnia, maximal inspiratory airway and transdiaphragmatic pressures, and the separate volume contributions of the rib cage and abdomen to tidal breathing were evaluated in 16 patients with chronic stable interstitial lung disease. Compared with those in the normal subjects, ventilation and P100 at a PCO2 = 55 mmHg were significantly higher (p less than 0.05 and p less than 0.01, respectively) in the patients with interstitial lung disease. However, the ventilatory and occlusion pressure responses to hypercapnia (delta VE/delta PCO2 and delta P 100/delta PCO2, respectively) were not significantly different between the groups. Maximal inspiratory airway pressure was significantly reduced in the patient group (p less than 0.05); maximal transdiaphragmatic pressure was also reduced but not significantly. At any given level of ventilation, tidal volume was decreased and breathing frequency increased in the patients with interstitial lung disease (p less than 0.05). The greater respiratory frequency was caused by reductions in both expiratory and inspiratory time. Because of smaller tidal volumes, rib cage expansion was reduced in the group of patients when compared with that in normal subjects during both spontaneous breathing and when compared at the same level of hypercapnia; abdomen volume was reduced to a lesser extent. We conclude that in patients with interstitial lung disease, non-chemical, presumably neural, mechanisms, increase respiratory drive and alter the breathing pattern. We speculate that both vagal mechanisms and mechanoreceptors in the chest wall sensitive to rib cage expansion contribute to these responses.
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PMID:Occlusion pressure and breathing pattern in patients with interstitial lung disease. 640 5

The aim of the present study was to determine whether acute changes in blood gases and pH alter sulfamethazine (SMZ) kinetics. Groups of conscious rabbits were exposed for 270 min either to air or to a high CO2 and (or) low O2 atmosphere to produce hypercapnia, hypoxemia, or both. Another group of rabbits received 47 mL/kg of 0.3 M HCl by gavage tube to induce metabolic acidosis. Once the blood gases were stabilized, the rabbits received 20 mg/kg SMZ i.v. Multiple blood samples were drawn for 180 min to assess SMZ kinetic parameters, SMZ protein binding, and blood gases. Fifteen minutes after the administration of SMZ, a suboccipital puncture was performed to determine the concentration of SMZ in the cerebrospinal fluid (CSF). Urine was collected for the first 180 min through a sterile catheter and for the next 21 h in a metabolic cage. Hypercapnia alone did not significantly influence SMZ kinetics. Hypoxemia, hypoxemia combined with hypercapnia, and metabolic acidosis increased the SMZ apparent volume of distribution (V) and total body clearance (CL). This increase in the SMZ V correlated positively (p less than 0.01) to the ratio of SMZ concentration in CSF to SMZ concentration in plasma. The increase in SMZ CL was mainly due to an increase in nonrenal clearance, although a slight increase in SMZ renal clearance was also observed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Influence of hypercapnia and (or) hypoxemia and metabolic acidosis on sulfamethazine kinetics in the conscious rabbit. 649 28


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