Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001127 (respiratory acidosis)
 1,501 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The changes of erythrocyte membrane band 3 protein, blood gases and electrolytes of intraerythrocyte and extra-erythrocyte were investigated in 3 groups: type I respiratory failure (group I, n = 36), type II respiratory failure (group II, n = 33) and control group (CG, n = 50). The distribution of band 3 protein was narrow and the staining intensity of band 3 protein was lower in the electrophotogram of group II. The relative composition of band 3 protein in group II was significantly lower than that in group I and CG (P less than 0.01). The intraerythrocyte HCO3- in group II was significantly higher than that in group I and CG (P less than 0.01), but the extra-erythrocyte Cl- in group II was significantly lower than that in group I and CG (P less than 0.01). These findings suggested that (1) The relative composition reduction of erythrocyte membrane band 3 protein and HCO3-/Cl- exchange restrain may be one of the reasons that aggravated CO2 retention and respiratory acidosis in cor pulmonale patients with type II respiratory failure. (2) Because there was hypochloremia in the most cor pulmonale patients with type II respiratory failure, it was necessary to supply them enough chloride in time, which could not only correct hypochloremia, but also accelerate the rate of HCO3-/Cl- exchange and promote to eliminate CO2.
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PMID:[Erythrocyte membrane band 3 protein and HCO3-/Cl- exchange function in cor pulmonale patients]. 132 60

To investigate the effect of the acid-base imbalance on the gastric mucosal defense mechanism, the intracellular pH of gastric surface epithelial cells were measured with double-barreled H+ selective microelectrodes in the isolated antral mucosa of bullfrog stomach. By knowing the intracellular pH and the PCO2 of the serosal perfusate, the intracellular HCO3- concentration was estimated, and the rate of HCO3- secretion was directly measured with the pH-stat method in mounted preparations on a Ussing's chamber. Both the calculated intracellular HCO3- concentration and the rate of HCO3- secretion were dependent on the exogenous HCO3- supplied from the serosal perfusate. The alkaline tide raised the intracellular HCO3- concentration, thus increasing the mucosal buffering power against acid. Under mild respiratory acidosis, the production of endogenous HCO3- from the serosal CO2 was enhanced, and both the intracellular HCO3- concentration and the rate of HCO3- secretion were increased. As a result, the intracellular pH was maintained at a physiologically optimal level, and the ability of gastric mucosal protection was strengthened by enrichment of cellular bicarbonate supply. It is confirmed in this study that the maintenance of acid-base status in the cell is indispensable in the protection of gastric mucosa against acid invasion.
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PMID:[Intracellular pH of surface epithelial cells and the movement of bicarbonate ions under acid-base imbalance in gastric mucosa]. 140 87

The present study was conducted to examine the roles of hormonal factors in plasma potassium alterations in acute respiratory acidosis. Respiratory acidosis (pH, 7.07-7.10) induced by the inhalation of 10% CO2, 20% O2 and 70% N2 mixed gas caused an increase in the plasma potassium concentration beyond that of the control of 3.44 +/- 0.12 (mean +/- SE) to 4.36 +/- 0.07 mEq/l (p less than 0.01) within 180 min. The plasma norepinephrine concentration was also noted to significantly increase at the same time. Phentolamine (40 micrograms/kg/min i.v.) did not affect the degree of acidosis or acidosis-induced hyperkalemia. No significant changes in the plasma levels of epinephrine, insulin, glucagon, cortisol or aldosterone could be detected. Hormonal factors would thus appear not to be essential to potassium movement from intracellular to extracellular compartments in acute respiratory acidosis.
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PMID:Roles of hormones in plasma potassium alteration in acute respiratory acidosis in dogs. 140 6

Pressure limited ventilation or "lung rest" may prevent further exacerbation of acute lung injury from high airway pressures. A therapeutic goal of an intracorporeal oxygenation and carbon dioxide removal device (IVOX) is reduction of airway pressures. We noted increased IVOX CO2 removal as mixed venous CO2 increased in experimental animals. However, we recognize the limited clinical utility of removing approximately 30% of venous CO2. Therefore, intentional hypoventilation to limit airway pressures (mild permissive hypercapnia) was used in 5 patients with respiratory failure, and again we noted improved CO2 removal with increasing mixed venous CO2 concentrations. Preliminary calculations demonstrate that a CO2 gradient of approximately 70 mm Hg is needed to remove 100 ml CO2/min. The use of more aggressive permissive hypercapnia protocols with IVOX may permit further reduction in airway pressure without problems of severe respiratory acidosis.
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PMID:Intravascular membrane oxygenation and carbon dioxide removal--a new application for permissive hypercapnia? 141 75

Variations of the phosphate concentration in plasma were studied in two groups of 12 patients undergoing cardiac surgery with hypothermic cardiopulmonary bypass (CPB). Management of the acid-base status differed between the groups, according to whether or not carbon dioxide was added to the anesthetic gas mixture during hypothermia ('pH-stat' vs. 'alpha-stat' mode) following correction vs. no correction of pCO2 and pH for body temperature. Phosphate variations throughout the study were mostly within normal limits. From the start to the end of CPB, the mean rise in phosphate levels was 70% in the pH-stat group and 37% in the alpha-stat group (p < 0.001). During 3 hours after CPB, the phosphate values continued to rise by a mean of 25% in the alpha-stat patients, but fell by a mean of 3% in the pH-stat patients (p < 0.001). Such different phosphate patterns during and immediately after CPB may reflect profound metabolic disturbances and may be related to the altering effects of CO2 addition and respiratory acidosis on intracellular metabolic activity and phosphate homeostasis.
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PMID:Effect of acid-base management with or without carbon dioxide on plasma phosphate concentration during and after hypothermic cardiopulmonary bypass. 143 46

We used 31P magnetic resonance spectroscopy to study changes in phosphorus metabolite concentrations in rat skeletal muscle during respiratory acidosis (14 and 20% inspired CO2) and recovery. As intracellular pH fell (from 7.05 to 6.75 after 20 min of 20% CO2), intracellular [P(i)] increased by up to 50% while phosphocreatine concentration decreased by up to 8%. The sum of all intracellular phosphates remained constant. [ADP] decreased by up to 40% in accordance with the creatine kinase equilibrium but the phosphorylation potential [ATP]/([ADP][P(i)]) was preserved as a result of increased [P(i)]. This adjustment may be a mechanism for maintaining mitochondrial ATP synthesis despite low pH. Eventually this increase in cellular [P(i)] could lead to slow efflux of P(i) from the skeletal muscle cell contributing to the hyperphosphataemia of acute respiratory acidosis.
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PMID:Changes in high-energy phosphates in rat skeletal muscle during acute respiratory acidosis. 144 23

Hypercarbia occurs during laparoscopy with carbon dioxide (CO2) insufflation. This may be due to increased ventilatory dead space after expansion of the peritoneal cavity with impairment of diaphragmatic excursion, or to increased absorption of CO2 from the peritoneum. To separate these effects, the authors examined the consequences of different insufflating gases and of diminished tissue perfusion on hypercarbia and dead space during pneumoperitoneum. Helium was chosen as an alternate insufflating gas because it is both inert and minimally absorbed. Eight swine (18 to 20 kg) were anesthetized, paralyzed, and mechanically ventilated at constant minute volume. Pneumoperitoneum with helium was maintained at 15 mm Hg for 45 minutes. After desufflation and stabilization for 1 hour, pneumoperitoneum was repeated with CO2. The sequence was again repeated after hemorrhagic shock to constant mean arterial pressure of 50 mm Hg. Data was analyzed by analysis of variance; significance levels are P < 0.01 unless otherwise listed. Arterial PCO2 increased significantly with CO2 insufflation within 15 minutes in normotensive animals and within 30 minutes during hypotension. Arterial pH decrease with CO2 pneumoperitoneum was significant in both groups at 30 minutes. Mixed venous PCO2 also increased with CO2 pneumoperitoneum within 30 minutes. Hypotension did not alter these changes. No significant changes were seen with helium pneumoperitoneum. Neither helium nor CO2 pneumoperitoneum significantly altered dead space. The authors make the following conclusions: 1) Absorption of CO2 from the abdomen during CO2 pneumoperitoneum produces respiratory acidosis, which is not seen with helium insufflation; 2) Pneumoperitoneum does not significantly increase dead space with either gas; 3) Transperitoneal absorption of CO2 is only partly related to perfusion because significant hypercarbia occurs during hemorrhagic shock.
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PMID:Effectors of hypercarbia during experimental pneumoperitoneum. 145 92

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

Ventilatory and metabolic changes were measured in seven patients undergoing high efficiency hemodialysis using a cuprophane dialyzer and bicarbonate-containing dialysate. At an HCO3 concentration of 35 mEq/liter and a mean in vivo urea clearance of 3.6 ml/kg/min, hypoxemia was not detected during dialysis (PaO2 was 14.00 and 13.60 kPa before and during dialysis). The new findings, related to high efficiency bicarbonate dialysis, include a sustained rise in minute ventilation (VE, 6.1 to 6.8 liter/min, P less than 0.01), an increase in CO2 excretion (VCO2, 194 to 214 ml/min, P less than 0.05), and O2 consumption (VO2, 215 to 246 ml/min, P less than 0.05). The increment in VE and VCO2 was attributed to the high flux rate of bicarbonate while the rise in VO2 is likely the result of metabolic alkalosis. Arterial pH rose from 7.40 to 7.49 mm Hg and serum HCO3 increased from 23.8 to 29.2 mEq/liter, while pCO2 remained normal at 5.07 kPa throughout the study. The acid-base status of the blood changed from that of a metabolic acidosis to that of a respiratory acidosis across the dialyzer where the pH decreased from 7.47 to 7.41 and pCO2 rose from 5.31 to 7.72 kPa. These data indicate that a healthy ventilatory response is needed to excrete the excess CO2 generated during high efficiency bicarbonate hemodialysis. The significance and etiology of the elevated O2 consumption is undetermined.
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PMID:Ventilatory and metabolic changes during high efficiency hemodialysis. 151 87

In pigeons, during shallow nocturnal hypothermia induced by food deprivation, body temperature falls to values between 35 degrees C and 38 degrees C. Body temperature, oxygen consumption, and arterial blood pH and PCO2 were recorded during the entrance into such nocturnal hypothermic periods. In vivo pH was kept constant, while in vivo PCO2 increased slightly during hypothermia. This caused the temperature-corrected value of pH (pH*, measured at 40 degrees C) to fall by -0.014 units/degrees C, and the total CO2-content to rise by 3.2 mM, an increase of 16%. These changes in the acid-base balance represent, in effect, a respiratory acidosis that closely parallels the normal buffer line for pigeons. Q10 values, relating oxygen uptake to body temperature, were higher than 4.0 at the very beginning of the entrance into hypothermia, indicating that the metabolic rate was actively inhibited. However, the present results do not indicate any relationship between the acidosis and the inhibition of the metabolic rate.
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PMID:Oxygen consumption and acid-base balance during shallow hypothermia in the pigeon. 162 38


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