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Results for “ACIDOSIS, RESPIRATORY”

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At least 451 records · Page 25Linked to original sources

PubMed1979

Effect of respiratory acidosis on plasma and CSF free amino acids.

Acid-base data and levels of selected cerebrospinal fluid (CSF) free amino acids were analyzed in a series of 8 patients in acute respiratory failure. In these patients, there were increased CSF concentrations of methionine, phenylalanine, tyrosine, histidine, alpha-amino-N-butyric acid, glutamic acid, glutamine, glycine, alanine, and ammonia, while arginine decreased. Phenylalanine, tryosine, and alanine were correlated with CSF PCO2; and alpha-amino-N-butyric acid to the buffer capacity of CO2 and pH. The data suggest the hypothesis that there are two metabolic phases for ammonia removal from brain tissue, that could explain some of these pathhophysiological conditions.

Acidosis, Respiratory↗

PubMedDate not supplied

Laparoscopic surgery with carbon dioxide insufflation causes respiratory acidosis.

This study analyzes the changes in cardiopulmonary parameters of patients undergoing laparoscopic cholecystectomy. Six healthy females with normal preoperative cardiopulmonary status were selected for laparoscopic surgery using the same criteria as for traditional cholecystectomy. Respiratory and cardiovascular parameters were collected and compared prior to peritoneal insufflation and just before desufflation. Patients experienced significant elevations of arterial and end-tidal CO2, accompanied by decreased pH. Bicarbonate concentration, blood pressure and pulse rate remained constant. Based on these results, and on our laboratory investigations, we have introduced helium as an alternate agent for insufflation, and present the data from the first two patients so managed. No change was observed in EtCO2, PaCO2 or pH in either of these two patients during the course of surgery. We conclude that hypercarbia occurs in those undergoing laparoscopic cholecystectomy with CO2 insufflation. This acidosis requires compensation by increased minute ventilation to prevent decline in pH. In our initial experience, helium did not produce these changes, and therefore merits further investigation as an alternate agent for abdominal insufflation.

Acidosis, Respiratory↗

PubMed1989

Na-HCO3 cotransport and Na-H antiporter in chronic respiratory acidosis and alkalosis.

Renal acidification in renal proximal tubule is thought to be mediated by luminal Na-H antiporter and the HCO3- generated by this antiporter is removed from the cell by a basolateral Na-HCO3 cotransporter. To study the effect of respiratory acid-base disorders on these transport systems, we have measured the Na-HCO3 cotransport in basolateral membranes and Na-H antiporter in luminal membranes in control rabbits, rabbits exposed to 10% CO2 (chronic hypercapnia), and rabbits exposed to 10% O2-90% N2 (chronic hypocapnia). The Vmax of HCO3(-)-dependent 22Na uptake was significantly higher in chronic hypercapnia than controls (2.54 +/- 0.03 vs. 1.18 +/- 0.21 nmol.mg protein-1.3 s-1, P less than 0.001). Likewise, the Vmax of the Na-H antiporter was also increased compared with controls (924.9 +/- 42.1 vs. 549.1 +/- 62.8 fluorescence units (FU).300 micrograms protein-1.min-1). In chronic hypocapnia, the Vmax of Na-HCO3 cotransport was lower than controls (0.72 +/- 0.11 vs. 1.18 +/- 0.21 nmol.mg protein-1.3 s-1, P less than 0.05). There was no difference, however, in the Vmax of the Na-H antiporter between hypocapnia and control (524.2 +/- 24.3 vs. 549.1 +/- 62.8, FU.300 micrograms protein-1.min-1). The Vmaxs of the Na-HCO3 cotransport and of the Na-H antiporter in hypocapnic, control, and hypercapnic rabbits were linearly related (r = 0.81), suggesting a simultaneous adaptation of the two systems in respiratory acid-base disorders.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis, Respiratory↗

PubMed2002

Contribution of respiratory acidosis to diaphragmatic fatigue at exercise.

The factors that may modulate ventilatory muscle fatigue during exercise are controversial. In this study the contribution of acidosis to exercise-induced diaphragmatic fatigue was investigated, using measurements of the twitch mouth pressure response (tw,Pmo) to cervical magnetic stimulation. After learning sessions, 14 healthy subjects performed two cycling tests (at 60% of maximal aerobic power for 16 min), one while breathing spontaneously (mean minute ventilation (V'E) 67.9 L x min(-1)) and the other while hypoventilating voluntarily (mean V'E 53.8 L x min(-1)). Exercise was voluntarily set at a moderate power to avoid a fatiguing effect of exercise per se. As compared with spontaneous breathing (SB), voluntary hypoventilation (VHV) significantly increased mean carbon dioxide tension in arterial blood (Pa,CO2) (51 mmHg versus 41 mmHg) and significantly decreased arterial pH (7.28 versus 7.34). After 10 min of SB test, tw,Pmo was unchanged compared to the baseline value (19.1 versus 18.5 cmH2O) whereas tw,Pmo fell significantly as compared to baseline (17.1 versus 18.5 cmH2O) and to SB (17.1 versus 19.1 cmH2O) after the VHV test. The results of this study suggest that exposure to hypercapnia may impair respiratory muscle function. This impairment could be more clinically relevant in patients with chronic obstructive lung disease.

Acidosis, Respiratory↗

PubMed1976

Intracellular pH of brain: alterations in acute respiratory acidosis and alkalosis.

To evaluate the metabolic adaptations of the brain to acute respiratory acid-base disturbances, a method was developed to measure intracellular pH (pHi) in the brain of dogs under conditions in which arterial pH is rapidly altered. Brain pHi was determined by measuring the distribution of 14C-labeled dimethadione (DMO) in brain relative to cortical CSF. Brain extracellular space (ECS) was evaluated as the 35SO4 = space relative to cortical CSF, and arterial Po2 was maintained at 82-110 mmHg. In normal dogs, brain (cerebral cortex) pHi was 7.05, and after 1 h of hypercapnia (arterial pH = 7.07) it fell to 6.93. However, after 3 h with arterial Pco2 maintained at 85 mmHg brain pHi was normal (7.06), and during this time brain bicarbonate had risen from 11.3 to 24.4 meq/kg H2O. These changes were not prevented by intravenous doses of acetazolamide,

Acid-Base Imbalance↗

PubMed1971