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)

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

During acute respiratory acidosis, cardiac contractile pressure first drops but then recovers substantially. We investigated the mechanism of this response in isovolumic perfused ferret hearts. Developed pressure (DP) and its first derivative (dP/dt) were measured before, during, and after hypercapnia induced by equilibrating the perfusate with 15% CO2, rather than the 5% CO2 used in control. Intramyocardial pH (pHi) was measured by phosphorus nuclear magnetic resonance (NMR) spectroscopy. After the onset of hypercapnia (1-2 min), DP and +dP/dt reached minimal mean values of 37 +/- 2 and 39 +/- 3% of control, respectively. This early decline in myocardial contactility was followed by a partial recovery such that DP and +dP/dt had returned to 66 +/- 6 and 62 +/- 4% of control, respectively, by 14 min of hypercapnia. pHi fell from 7.17 +/- 0.01 in control to 6.88 +/- 0.11 after approximately 2 min of hypercapnia. Thereafter, pHi recovered linearly with a mean slope of 0.011 +/- 0.003 pH U/min. Ethylisopropylamiloride (10(-6) M), a blocker of Na(+)-H+ exchange, prevented the recovery of pHi during hypercapnia and attenuated the recovery of contractility by 40%. We conclude that the recovery of contractility during respiratory acidosis at least partially reflects an underlying recovery of pHi mediated by Na(+)-H+ exchange.
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PMID:Recovery of contractility and pHi during respiratory acidosis in ferret hearts: role of Na(+)-H+ exchange. 216 81

The aim of this study was to assess prospectively the variations of serum phosphorus concentration (P) after onset of mechanical ventilation (MV) in patients with chronic obstructive pulmonary disease (COPD) and acute respiratory acidosis. In 14 COPD patients, we measured P, PaCO2, and pH, immediately before MV (H0), then one hour (H1), 4 (H4), 7 (H7), 12 (H12), and 24 h (H24) after starting MV. P at H0 was in or above the normal range in ten patients and below normal range in four patients. P decreased significantly (p less than .001) after MV at H1, H4, H7, H12, and H24. Hypophosphatemia was present in all patients after MV, but was severe (p less than .3 mmol/L) in only two patients. There was a significant correlation (r = .56 p less than .01) between the decrease of P and the increase of pH after MV. Hypophosphatemia was a constant and early finding after institution of MV in COPD patients and was presumably related to an intracellular shift of P secondary to the correction of respiratory acidosis.
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PMID:Hypophosphatemia induced by mechanical ventilation in patients with chronic obstructive pulmonary disease. 279 90

Prolonged metabolic acidosis is associated with depressed phosphate (Pi) uptake by the brush-border membrane (BBM) of the proximal tubule. To examine if changes in systemic pH underlie this inhibition, we measured Pi transport by renal cortical BBM from thyroparathyroidectomized rats with respiratory or metabolic acidosis of 1 or 3 h, respectively, and in appropriate controls. Also, Pi transport was measured in BBM prepared using tissue slices from nonacidotic rats that were preincubated for 20 or 45 min at either pH 6.9 (HCO3 = 10 mM, CO2 = 10%) or 7.4 (HCO3 = 10 mM, CO2 = 2.5%). Despite comparable acidemia (pH 7.06 +/- 0.05 with respiratory acidosis and 7.10 +/- 0.03 with metabolic acidosis), Na-dependent Pi uptake at 5 s incubation was reduced by 15.2 +/- 3.5% with respiratory acidosis compared with paired controls. It was not altered with metabolic acidosis. Vmax in respiratory acidosis (1.2 nmol X mg protein-1 X 5 s-1) was less than in controls (1.6); Kt was similar in both groups. 22Na transport and Na-dependent glucose transport were unchanged. Plasma phosphorus (P) increased from 8.75 +/- 0.35 mg/dl to 12.42 +/- 1.9 with respiratory acidosis. Therefore BBM vesicles transport was measured in controls after plasma P was raised. Under these conditions, Pi transport was similar to that with respiratory acidosis. Also Pi transport by BBM was unchanged when tissue slices were preincubated in vitro at high CO2 concentrations for 20 or 45 min. Thus respiratory acidosis specifically inhibits Na-dependent Pi transport by decreasing the number or rate of the BBM Pi carrier.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of acute acidemia on phosphate uptake by renal proximal tubular brush-border membranes. 377 85

Although metabolic acidosis produces calciuric, phosphaturic, and magnesiuric effects, the consequences of chronic respiratory acidosis are unclear. To examine the role of systemic pH on renal divalent metabolism, 4-day balance studies were performed in rats with both metabolic acidosis induced by adding 1.5% NH4Cl to the drinking water, and respiratory acidosis produced by exposure to 10% atmospheric CO2 in an environmental chamber, and in controls pair-fed with each group. By the fourth day, blood pH had decreased to an identical degree with both chronic metabolic and respiratory acidosis and averaged 7.28. As anticipated, chronic metabolic acidosis resulted in significant calciuria, magnesiuria, and phosphaturia. However, despite the similar decrement in blood pH, calcium, phosphorus, and magnesium excretion was similar to that in the pair-fed controls with chronic respiratory acidosis. These findings indicate that a low systemic pH, per se, does not account for the modifications in urinary divalent ion handling that accompany chronic metabolic acidosis. However, additional observations suggest that differences in the intracellular pH of the proximal tubular epithelium may be an important regulatory variable.
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PMID:Renal excretion of divalent ions in response to chronic acidosis: evidence that systemic pH is not the controlling variable. 379 12

The diseases which are commonly complicated by hypercapnic respiratory failure also compromise the respiratory muscles in several ways. Increased work of breathing, mechanical disadvantage, neuromuscular disease, impaired nutritional status, shock, hypoxemia, acidosis, and deficiency of potassium, magnesium, and inorganic phosphorus are the major non-neurologic factors which contribute to respiratory muscle fatigue and failure. Respiratory muscle fatigue has two components. High frequency fatigue occurs rapidly with intense contractile efforts but is usually not severe. It also recovers rapidly with rest. Low frequency fatigue develops more slowly but is severe and requires hours for recovery. Since the spontaneous rate of neural stimulation is predominantly in the low frequency range, this component of fatigue is of particular clinical importance. Fatigue of the inspiratory muscles leads to acute respiratory acidosis, but before carbon dioxide retention occurs, it can be recognized from characteristic symptoms and signs. These include dyspnea which responds to mechanical ventilation, rapid shallow breathing, and asynchronous movements of the chest and abdomen. Inspiratory muscle fatigue must be treated by putting these muscles to rest, by mechanically supporting ventilation. In addition, underlying metabolic nutritional and circulatory abnormalities must be corrected and infection treated. Aminophylline and isoproterenol can restore inspiratory muscle contractility, but controlled clinical trials remain to be done regarding their application in acute and chronic respiratory failure. Inspiratory muscle training improves strength and endurance in patients with obstructive lung disease, cystic fibrosis, and spinal cord injury, but does not always improve physical exercise performance. Again, more work is needed to develop the indications for inspiratory muscle training and to determine the optimum type and duration of the training regimen.
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PMID:Respiratory muscle failure. 634 27

The study was aimed at informing about the results of metabolic trials in large cattle stocks for the period from 1977 to 1980, particularly in view of the dynamics of changes in different metabolic parameters in each year season. The histogram method of statistical evaluation was used. Attention is drawn to the prevailing risk factors in each season and it is possible to investigate the general trend of the rise of new metabolic disorders, or suppression of older ones, in large cattle stocks. The risk metabolic factors of each season can be derived from the results. The summer season is characterized by the tendency to metabolic and respiratory acidosis, by the highest elimination of calcium combined with potassium stress, and by a lack of sodium ions. In the autumn the animals show a more pronounced form of metabolic and respiratory acidosis, not always sufficiently compensated; the liver is overloaded, there is a tendency to hypocalcaemia, and ketosis occurs more frequently, often very pronounced. In winter the acid-base balance of blood improved, acidosis is compensated more intensively by the renal route, calcium is increasingly eliminated in the urine, the overload on liver function is at its maximum, and ketosis occurs most frequently. The spring findings included increased elimination of calcium with the urine, the lowest Ca X P product over the whole year (this is in a high correlation with the higher activities of the ALP enzyme). the highest load of nitrogen compounds and worsened haemogenesis. It can be stated that the mentioned results represent some improvement in the metabolic profile as compared with earlier studies. The situation in enzyme activities can be regarded as a factor of deterioration: high activities of alkaline phosphatase documenting a tension in the metabolism of calcium and phosphorus, and increasing occurrence of chronical overloading of liver function, particularly in winter.
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PMID:[Changes in metabolic indicators in cattle by season of the year]. 681 64

Sixty pigs were used for the study. The animals were divided into 5 groups, 12 pigs in each. The following substances were administered intravenously in the individual groups: I -- 20 ml of physiological solution NaCl (placebo, II -- chloral hydrate (10% solution), III -- Nembutal, IV -- Eunarcon, V -- Brevinarcon (10% solution). Blood was collected from the anterior vena cava after 1 hour and after 1, 3 and 7 days since the moment of administration of physiological saline (group I), or since the appearance of general anaesthesia (groups II-V). Determinations in blood serum concerned: Na, K and Ca -- with the use of a flame photometer, Mg -- by the method of Lange, Cl -- by the method of Schales and Schales, inorganic phosphorus -- by the Fiske-Subbarow method. The results were analysed statistically by determining the mean, the standard deviation and the significance of variations according to the t Student test (risk of error -- 5%). The results obtained in groups II-V were compared with the corresponding results from group I. It was found that chloral hydrate, Nembutal, Eunarcon and Brevinarcon, used to produce general anaesthesia in healthy pigs (not operated upon) produce a decrease in the sodium and potassium content, an increase in the magnesium and inorganic phosphorus content, and slight changes in the calcium and chlorine content. The greatest and most prolonged deviations were found after chloral hydrate and Nembutal the slightest after Brevinarcon. Eunarcon produced short-lived changes, but greater than after Brevinarcon. These changes in the level of electrolytes in serum should be attributed to disturbances of respiration (respiratory acidosis), and to decreased activity of muscles during anaesthesia in pigs.
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PMID:[Blood serum electrolyte content in pigs during general anesthesia induced by administration of chloral hydrate, nembutal, eunarcon and brevinarcon]. 720 71

The metabolic and respiratory changes of 21 patients with heat stroke were studied. Admission arterial blood gas levels were measured, and serum bicarbonate, lactate, calcium, phosphorus, and anion gap determinations were performed. Seven patients had a metabolic acidosis (pH 7.20 +/- 0.04, PCO2 32 +/- 2 mm Hg, and bicarbonate 12 +/- 1 mEq/L), seven a combined metabolic acidosis and respiratory alkalosis (pH 7.39 +/- 0.01, PCO2 25 +/- 1 mm Hg, and bicarbonate 15 +/- 1 mEq/L), four a respiratory alkalosis (pH 7.45 +/- 0.01, PCO2 30 +/- 1 mm Hg, and bicarbonate 20 +/- 1 mEq/L), one a metabolic and respiratory acidosis (pH 7.13, PCO2 52 mm Hg, and bicarbonate 17 mEq/L), and one a respiratory acidosis (pH 7.30, PCO2 56 MM Hg, and bicarbonate 27 mEq/L). The 15 patients with a metabolic acidosis had a pH of 7.28 +/- 0.03, PCO2 of 30 +/- 2 mm Hg, bicarbonate level of 14 +/- 1 mEq/L, lactate concentration of 6.5 +/- 1.0 mEq/L, and an anion gap of 26 +/- 4 mEq/L. Nine patients were hypocalcemic (7.8 +/- 0.3 mg/dL), and five patients were hypophosphatemic (2.0 +/- 0.2 mg/dL). The predominant metabolic change in heat stroke is a metabolic acidosis secondary to increased lactate content and/or a respiratory alkalosis. Hypocalcemia is common and hypophosphatemia is not infrequent.
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PMID:The metabolic and respiratory alterations of heat stroke. 739 91

Phosphorus plays an essential role in cellular metabolism, especially in the oxidative phosphorylation process and in the synthesis of 2-3 DPG and membrane phospholipids. Moreover phosphorus is necessary as a buffer, mainly when the organism's principal buffer, the H2CO3/HCO3- system, is working at maximal rate. The authors describe a case of severe hypophosphatemia in a ICU patient with a mixed disorder of the acid-base balance. C.P., a woman, aged 71, obese (IBW 145%), at admission in ICU showed increasing dyspnea, hypoxemia and acidosis. Besides alkaline drugs a Venturi mask with FiO2 = 0.3 alternated to CPAP cycles (7 cm H2O) with facial mask applied. Bading on CVP, MAP and ABG results, a pharmacologic therapy with enoximone, furosemide, bronchodilators, mucolytics, antacids, antibiotics and inotropics was performed. TPN with only essential amino acids was performed, in order to activate lipolysis and ketogenesis; but the ABG showed over again mixed disorder of acid-base balance (metabolic and chronic respiratory acidosis), only partially leading to ketogenesis. The reduction of the hematic HCO3-, without changes of PaCO2, was justified by the blood lactic acid of 6.2 mmol/L. And what about blood lactic acid increase? During patient hospitalization, the hematic phosphorus had decreased to, 0.8 mg/dl. Diuretic therapy together with acidosis tamponage, and reduced phosphorus feed had been responsible of severe hypo-phosphatemia. Therapy adjustments brought the phosphatemia to normal values and to a substantial improvement of clinical conditions.
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PMID:[Severe hypophosphatemia in intensive care]. 761 39


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