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)

Experiments were conducted to test the hypothesis that one or more interrenal steroids are active in regulatory responses to respiratory acidosis in the toad, Bufo marinus. Toads were divided into four experimental groups. The first group received sham injections. The second group received 1-3 mg of aminoglutethimide (AG) every 8 hr. AG inhibits the conversion of cholesterol to pregnenolone, thus inhibiting all steroid hormone synthesis. The third group received AG + 5 micrograms of aldosterone on the same schedule. The fourth group received AG + 25 micrograms of corticosterone on the same schedule as the other groups. All four groups were subjected to hypercapnia using 5% CO2 to induce a respiratory acidosis. The sham-operated animals displayed the normal compensatory pattern of producing a metabolic alkalosis (elevated plasma HCO3-) after 24 hr. AG-treated toads failed to elevate plasma HCO3-. Administration of interrenal steroids produced compensation in varying degrees. Aldosterone produced a small compensation while corticosterone produced a compensation similar to that seen in sham-operated animals. Analysis of steroid titers in toad plasma during hypercapnia showed that Bufo marinus does not elevate aldosterone during respiratory acidosis, but that corticosterone is elevated. AG blocked the corticosterone elevation, however. AG also produced a hyponatremia that was corrected with aldosterone or corticosterone. Normocapnic controls showed that AG does not produce deleterious effects on pH or blood gases in toads in the absence of a respiratory acidosis. We conclude that corticosterone is important in acid-base regulatory responses to respiratory acidosis in this amphibian.
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PMID:Acid-base-electrolyte balance responses of Bufo marinus to aminoglutethimide, corticosterone, and aldosterone during hypercapnia. 150 25

We compared the effects of pressure support ventilation (PSV) with those of assist control ventilation (ACV) on breathing patterns and blood gas exchange in six patients with status asthmaticus. Both PSV and ACV delivered adequate minute ventilation (PSV: 7.5 +/- 1.4 l/min/m2, ACV: 7.3 +/- 1.3 l/min/m2) to correct respiratory acidosis (pH = 7.33 +/- 0.12 during both PSV and ACV) and prevent hypoxia. Peak airway pressure during PSV was significantly lower with the same tidal volume than that during ACV (PSV: 30 +/- 10 cmH2O (2.9 +/- 1.0 kPa), ACV: 50 +/- 13 cmH2O (4.9 +/- 1.3 kPa)). The lower airway pressure during PSV was due to persistent inspiratory muscle activity. The oxygen cost of breathing estimated by oxygen consumption was equivalent in both modes. We conclude that PSV is effective in supplying tidal volumes adequate to improve hypercarbia at markedly lower airway pressures than ACV.
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PMID:Effectiveness of pressure support ventilation for mechanical ventilatory support in patients with status asthmaticus. 153 79

Problems facing a patient with severe dyspnea secondary to diaphragmatic herniation are hypoxia, hypercarbia and respiratory acidosis, and cardiovascular instability. It is easy to precipitate a crisis in these patients during anesthetic induction as a result of stress, bad positioning, induction of pneumothorax, or inappropriate anesthetic technique. These patients require a smooth, stress-free perianesthetic period with preoxygenation, positioning with the affected side down, rapid intravenous induction, endotracheal intubation, and mechanical ventilation. Maintenance with isoflurane is preferred, and nitrous oxide should be avoided. Close monitoring of the cardiovascular and pulmonary systems is essential. Recovery from anesthesia should include oxygen supplementation, pleural drainage, and local analgesia if required.
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PMID:Anesthesia for patients with diaphragmatic hernia and severe dyspnea. 158 3

The independence of the central and peripheral chemoreflexes has been tested in humans. Acute metabolic acidosis generated by a prior bout of brief, hard exercise was used to stimulate primarily the peripheral chemoreceptors, and respiratory acidosis generated by inhaled CO2 was used to stimulate both central and peripheral chemoreceptors. Seven healthy young men were studied. Ventilation and arterial pH, PCO2 and PO2 were recorded. Peripheral chemoreflex sensitivity to hypoxia during acute metabolic acidosis was repeatedly determined by measuring ventilation in euoxia (PETO2 = 100 Torr) and hypoxia (PETO2 = 50 Torr) as the subject recovered from exercise-induced acidosis. Peripheral chemoreflex sensitivity to hypoxia during CO2 inhalation was repeatedly determined by measuring ventilation in euoxia and hypoxia at two levels of hypercapnia (PETCO2 = 45 Torr and PETCO2 = 50 Torr). The ventilatory sensitivity to hypoxia at matched arterial pH values was not significantly different between conditions of high (CO2 inhalation) and low (metabolic acidosis) central chemoreceptor activity. We therefore conclude that interaction between central and peripheral chemoreflexes was non-significant in all subjects.
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PMID:An assessment of central-peripheral ventilatory chemoreflex interaction in humans. 162 48

Exposure of adult brown bullheads Ictalurus nebulosus (120-450 g) to environmental hypercapnia (2% carbon dioxide in air) and subsequent recovery caused transient changes in whole body net sodium flux (JnetNa+) and net chloride flux (JnetCl-) resulting largely from changes in whole body sodium influx (JNa+in) and chloride influx (JinCl-). Scanning electron microscopy (SEM) revealed that the fractional area of chloride cells (CCs) on the interlamellar regions was reduced by 95% during environmental hypercapnia. During post-hypercapnic recovery, gill filament CC fractional area increased. The changes in JinCl- during and after environmental hypercapnia were closely associated with the changes in CC fractional area while the changes in JinNa+ did not correspond to the changes in CC fractional area. Transmission electron microscopy (TEM) supported the SEM observations of CC surface area changes and demonstrated that these changes were caused by covering/uncovering by adjacent pavement cells (PVCs). Lamellar and filament PVC microvilli density increased during hypercapnia while there was a subsequent reduction in the posthypercapnic period. These data suggest that an important mechanism of acid-base regulation during hypercapnic acidosis is modification of the chloride cell-associated Cl-/HCO3- exchange mechanism. We suggest that bullheads vary availability, and thus functional activity, of this transporter via reversible morphological alterations of the gill epithelium. The increase in density of PVC microvilli may be associated with sodium uptake and/or acidic equivalent excretion during acidosis.
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PMID:Evidence for a morphological component in acid-base regulation during environmental hypercapnia in the brown bullhead (Ictalurus nebulosus). 162 10

We measured intracellular pH (pHi) of single epithelial cells in situ in the urinary bladder epithelium using microspectrofluorometry and the cytoplasmically trapped pH-sensitive fluorophore, 2',7'-bis(2-carboxyethyl)-5(6)- carboxyfluorescein (BCECF). The resting pHi was 7.21 +/- 0.03 (n = 40 bladders, 489 cells) in pH 7.8 bathing solutions, indicating that H+ is not passively distributed across the plasma membrane and is extruded against its electrochemical gradient. Whereas exposure to hypercapnia (5% CO2 saturation) reversibly decreased pHi, mucosally added 20 mM NH4+ reversibly increased pHi. Recovery from the NH4+ effect was slow and lacked an acid-load pHi undershoot; this is interpreted as suggesting significant NH4+ permeability. Recovery from hypercapnic acidosis was blocked by mucosally added amiloride, indicating that apical Na(+)-H+ exchange is involved in pHi regulation. Addition of 0.5 mM NH4+ to the basolateral side when the mucosal side was bathed in mock urine (2 mM NaCl) significantly increased undirectional mucosal-to-serosal Na+ flux, and the increase was blocked by mucosally added amiloride. We conclude that an apically located Na(+)-H+ exchange is important in pHi regulation and may also accept NH4+ as the counterion for Na+.
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PMID:Intracellular pH regulation in trout urinary bladder epithelium: Na(+)-H+(NH4+) exchange. 165 43

Patients with cardiopulmonary insufficiency undergoing laparoscopic surgery with carbon dioxide (CO2) pneumoperitoneum may retain CO2 resulting in clinically significant respiratory acidosis. A canine model of pulmonary emphysema induced by papain inhalation was utilized to evaluate the respiratory effects of both CO2 and helium pneumoperitoneum. Prior to papain inhalation and 5 and 8 weeks after initial treatment under general anesthesia, mechanical ventilation was adjusted to maintain the end-tidal CO2 (ETCO2) at 40 mm Hg during baseline and pneumoperitoneum physiologic monitoring periods. Utilizing an analysis of variance, hemodynamic and respiratory physiologic parameters were compared. In this canine model, all dogs demonstrated consistent hypercarbia during CO2 pneumoperitoneum prior to papain treatments, but CO2 retention was significantly increased in the emphysematous state. The occurrence of hypercarbia during CO2 pneumoperitoneum may be underestimated by ETCO2 monitoring as was revealed by an increased PaCO2 (arterial carbon dioxide pressure)-ETCO2 gradient with an increasing time interval between papain exposure and period of physiologic monitoring. Irrespective of the pulmonary condition of the dog, helium pneumoperitoneum did not produce any hypercarbic or acidic changes when compared with the concomitant baseline period of dogs prior to the induction of pneumoperitoneum, thus suggesting that helium pneumoperitoneum may be a reasonable alternative in patients at risk for CO2 retention.
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PMID:Hypercarbia during carbon dioxide pneumoperitoneum. 173 68

Exposure of rainbow trout to environmental hyperoxia (PIO2 approximately 530 Torr) resulted in an extracellular respiratory acidosis which was fully compensated by 72 h; return to normoxia (PIO2 approximately 145 Torr) at this time induced a metabolic alkalosis which was corrected by 24 h. Intracellular pHi ([14C]DMO method), fluid volumes [3H]PEG-4000 method), and electrolytes were monitored. Environmental hypercapnia (PICO2 approximately 6.5 Torr) was employed to confirm that intracellular responses were specific to respiratory acidosis. Gill pHi did not change during respiratory acidosis despite a very low non-HCO3- buffer capacity, but gill ICFV decreased markedly. A large loss of gill intracellular [Cl-]i in excess of [Na+]i, combined with a substantial gain in [K+]i, contributed to gill pHi regulation by raising branchial [SID]i. In weakly buffered brain tissue, active adjustment of pHi started within 3 h, but two well buffered tissues, RBC and white muscle, exhibited compounding metabolic acidoses during the first 12-24 h. The muscle response was associated with small increases in ICFV and [Cl-]i, and a large decrease in [K+]i which reduced muscle [SID]i. We hypothesize that this initial export of K+ and basic equivalents served to regulate pH in more critical compartments (e.g. gills, brain) at the expense of muscle acidosis. By 48 h, pHi restoration in all tissues was complete, in advance of pHe regulation (72 h). Return to normoxia at 72 h elevated muscle, brain, and gill pHi, but there was no evidence of a comparable 'altruistic' role of muscle during this metabolic alkalosis. Regulation of pHi was complete by 24 h recovery, accompanied by partial or complete restoration of intracellular ions and fluid volumes.
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PMID:Intracellular acid-base responses to environmental hyperoxia and normoxic recovery in rainbow trout. 175 56

This prospective study evaluates the extent and temporal course of the cardiorespiratory effects of CO2 during laparoscopic cholecystectomy in otherwise healthy patients. Sixteen patients (M:F = 3:13, average age = 40.2 +/- 14.1 years) were monitored with capnography, transesophageal cardiac output, continuous blood pressure, heart rate, and pulse oximetry. Arterial blood gases were obtained immediately before insufflation of the abdomen with CO2 and before desufflation. Average operative time was 137 +/- 13 minutes. Patients were paralyzed and mechanically ventilated. Minute ventilation was increased if EtCO2 exceeded 45 mmHg or rose by more than 12 mmHg from baseline. End tidal (EtCO2) and arterial CO2 (PaCO2) increased from 31.4 +/- 0.7 mmHg to 42.1 +/- 1.6 mmHg and 33.3 +/- 0.7 mmHg to 43.7 +/- 1.2 mmHg, respectively, during the course of the procedure. Arterial pH decreased from 7.43 +/- 0.01 to 7.34 +/- 0.01, while bicarbonate concentration remained unchanged. Thirteen of the 16 patients required increased minute ventilation due to hypercarbia detected by capnography. Blood pressure increased from 78 +/- 2 mmHg (mean) at the start to 98 +/- 2 mmHg. This increase was coincidental with the maximal PaCO2. Good agreement was observed between paired EtCO2 and PaCO2 measurements. Laparoscopic cholecystectomy with carbon dioxide insufflation causes significant respiratory acidosis and associated cardiovascular changes in otherwise healthy patients. Careful monitoring and cautious application of this technique in patients with pre-existing cardiopulmonary disorders will be required to prevent acute decompensation.
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PMID:Prospective analysis of cardiopulmonary responses to laparoscopic cholecystectomy. 183 77

Haemodynamic responses to the apnoea test for the diagnosis of brain death were investigated in nine patients with severe head injury or cerebrovascular disease. To prove apnoea, the ventilator was disconnected for ten minutes and oxygen was insufflated to avoid hypoxaemia. No respiratory movement was seen in any patient. Ten minutes after disconnecting the ventilator, PaCO2 was increased to 78 +/- 3 mmHg and pH was reduced to 7.17 +/- 0.02. Adequate oxygenation was maintained in all patients. Cardiac output increased from 4.8 +/- 0.7 to 5.7 +/- 0.8 L.min-1 (P less than 0.05), and mean pulmonary artery pressure increased from 11 +/- 1 to 17 +/- 2 mmHg (P less than 0.01). However, mean arterial pressure, heart rate, pulmonary artery wedge pressure and right atrial pressure did not change. Plasma catecholamines were measured in three patients. Plasma norepinephrine concentrations increased in all three patients but the changes in plasma epinephrine were minimal. These circulatory responses to acute hypercapnia were less than those reported in awake volunteers and in patients during general anaesthesia. However, since plasma norepinephrine concentration increased during the test, some sympathoadrenal response, probably of spinal origin, was present, and may have prevented the direct depressant circulatory effects of acute hypercapnia. In conclusion, the apnoea test did not produce haemodynamic disturbances when respiratory acidosis was limited to a pH 7.17 +/- 0.02 and PaCO2 60-80 mmHg.
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PMID:Haemodynamic changes during the apnoea test for diagnosis of brain death. 190 87


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