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

The studies were carried out on 48 sheep, 2-6 years old, weighing 33-67 kg. The animals were divided into two groups, 24 sheep each. From these 24, 16 sheep were tested for the plasma electrolytes contents, and 8 were tested for the acid-base balance and the oxygenation level of the arterial blood. Sheep from the first group were given xylasine in the dose of 0.1-10.3 mg/kg od body weight and etomidate (1 mg/kg of body weight). Sheep from the second group were given diazepam in the dose of 0.5 mg/kg of body weight and ketamine (20 mg/kg of body weight). In the first group the surgically effective anaesthesia lasting 15-20 minutes was obtained. During the anaesthesia a respiratory depression together with the decrease of oxygen saturation of the blood was observed. Also, a respiratory insufficiency leading to a respiratory acidosis, hypokalemia, hypocalcemia, hypomagnesemia and hypochloremia of plasma were observed. In the second group of sheep treated with ketamine and diazepam the increased pulse rate, respiratory insufficiency, hypokalemia, hypocalcemia and hypophosphatemia were observed. It has been said that respiratory and blood oxygenation disorders are the result of the forced long lasting position on one side. After treating with diazepam and ketamine bigger changes were observed. Usually all these changes and disorders recessed at the end of the experiment.
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PMID:[Comparative studies of general anesthesia of sheep with ketamine and etomidate]. 326 7

In metabolic alkalosis, a compensatory decrease in alveolar ventilation with hypercapnia has been noted only rarely. We recently managed a patient with gastric outlet obstruction from a duodenal ulcer who survived after arriving in the emergency room comatose with severe hypochloremic metabolic alkalosis, compensatory hypoventilation, and hypercapnia. We know of no report in the English literature of a patient with gastric outlet obstruction having a respiratory acidosis or hypochloremia as severe as that in our patient. Proper understanding of the pathophysiology of primary metabolic alkalosis due to gastric losses is necessary to correct the acid-base abnormalities quickly and to restore normal alveolar ventilation.
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PMID:Marked hypochloremic metabolic alkalosis with severe compensatory hypoventilation. 376 30

The metabolic contributions to chronic acid-base changes were examined in the plasma of arterial blood in patients with chronic obstructive pulmonary disease (COPD) and chronic hypercapnia, by a quantitative physical-chemical analysis. Patients were stratified into three groups: group 1 (Paco2 less than 40 mmHg; 1 mmHg = 133.3 Pa), group 2 (Paco2 between 40 and 50 mmHg), and group 3 (Paco2 higher than 50 mmHg). With the development of hypercapnia (Paco2 from 38.2 +/- 1.6 to 53.8 +/- 0.6 mmHg) and hypoxemia (Pao2 from 73.6 +/- 2.5 to 62.1 +/- 2.1 mmHg), blood pH decreased slightly (from 7.405 +/- 0.007 to 7.372 +/- 0.009). The strong ion difference ([SID]) increased in the hypercapnic group (from 39.7 +/- 1.7 to 46.2 +/- 2.9 mequiv.L-1) parallel to the increase in [HCO3-] (from 23.8 +/- 0.5 to 30.8 +/- 0.8 mequiv.L-1). The change in [SID] was quantitatively similar to the [HCO3-] change, thus reflecting a metabolic compensation of chronic respiratory acidosis. [SID] increase was mainly accounted for by changes in the [Na+]/[Cl-] ratio due to a significant decrease in plasma [Cl-]. Other ions measured as well as the weak acid buffers ([ATOT]) remained constant. From the present results, we suggest the usefulness of the physical chemical approach in the characterization of acid-base disturbances due to chronic hypercapnia when water retention or protein depletion are expected further to hypochloremia, as can be the case in severe COPD patients.
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PMID:A physical-chemical analysis of the acid-base response to chronic obstructive pulmonary disease. 902 82

The study was carried out on healthy Friesian calves (n = 10) aged between 10 and 30 days. Hypochloremia and alkalosis were induced by intravenous administration of furosemide and isotonic sodium bicarbonate. The venous and arterial blood samples were collected repeatedly. 2,3-diphosphoglycerate (2,3-DPG), hemoglobin and plasmatic chloride concentrations were determined. The red blood cell chloride concentration was also calculated. pH, PCO2 and PO2 were measured in arterial and mixed venous blood. The oxygen equilibrium curve (OEC) was measured in standard conditions. The correspondence of the OEC to the arterial and mixed venous compartments was calculated, taking blood temperature, pH and PCO2 values into account. The oxygen exchange fraction (OEF%), corresponding to the degree of blood desaturation between the arterial and mixed venous compartments and the amount of oxygen released at the tissue level by 100 mL of blood (OEF Vol%) were calculated from the arterial and mixed venous OEC, combined with PO2 and hemoglobin concentration. Oxygen delivery (DO2) was calculated using the arterial oxygen content, the cardiac output measured by thermodilution, and the body weight of the animal. The oxygen consumption (VO2) was derived from the cardiac output, OEF Vol% and body weight values. Despite the plasma hypochloremia, the erythrocyte chloride concentration was not influenced by furosemide and sodium bicarbonate infusion. Due to the alkalosis-induced increase in the 2,3-DPG, the standard OEC was shifted to the right, allowing oxygen to dissociate from hemoglobin more rapidly. These changes opposed the increased affinity of hemoglobin for oxygen induced by alkalosis. Moreover, respiratory acidosis, hemoconcentration, and the slight decrease in the partial oxygen pressure in mixed venous blood (Pvo2) tended to improve the OEF Vol% and maintain the oxygen consumption in a physiological range while the cardiac output, and the oxygen delivery were significantly decreased. It may be concluded that, despite reduced oxygen delivery, oxygen consumption is maintained during experimentally induced hypochloremic alkalosis in healthy 10-30 day old calves.
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PMID:Mechanisms controlling the oxygen consumption in experimentally induced hypochloremic alkalosis in calves. 1249 70