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Query: UMLS:C0001127 (respiratory acidosis)
 1,501 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects on hemoglobin oxygen transport of acute respiratory acidosis have been studied in dogs inhaling a gaseous mixture with 12% CO2 (O2 21%) for two to five hours. In a first series of experiments, it was shown that the shape of the oxyhemoglobin dissociation curve (ODC) was not modified by severe acidosis (pH congruent to 7) lasting for two and a half hours. The Hill number (N equals 2.6) did not change significantly. The aim of the second experimental series was to stuey the Bohr effect and the hemoglobin oxygen affinity (P50). The control value for the respiratory Bohr coefficient (B) was --0.54; neither after two hours (--0.52), nor after five hours of hypercapnia (--0.55) was it significantly modified. The P50 expressed at arterial pH was much increased in acidosis (congruent to 45 torr); when expressed at standard p/ 7.4, it was slightly but significantly decreased (congruent to 1 torr) at the fifth hour. At the same time there was a decrease (p smaller than 0.05) in the erythrocyte 2,3-DPG approaching 15 p. cent; on the other hand the ATP concentration did not change significantly. No significant individual correlation was found between P50(7.4), 2,3-DPG and mean hemoglobin corpuscular concentration. These results suggest that during severe respiratory acidosis neither a change in the shape of ODC, nor a change in Bohr effect do affect the hemoglobin oxygen transport. The main characteristic remains the decrease in oxygen affinity of hemoglobin, due to the erythrocyte [H+] increase induced by hypercapnia ; this phenomenon is observed as long as the 2,3-DPG decrease stays moderate.
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PMID:[Hemoglobin oxygen transport during experimental acute hypercapnia (author's transl)]. 23 80

When the crab Carcinus maenas respires in hypercapnic water, a respiratory acidosis occurs, which is progressively compensated by a rise of the blood bicarbonate concentration. The CO2 partial pressure in the blood increases in proportion to the change in ambient CO2 partial pressure. Therefore, the regulation of the acid-base status depends mainly on non-respiratory adjustments of the blood bicarbonate concentrations.
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PMID:[Effect of hypercapnia on the acid base states of the blood in the crab Carcinus maenas (L.) (Crustacea-Decapoda)]. 23 96

The inotropic effect of 1.25 times 10(-6)M acetylstrophanthidin (ACS) and the influx and efflux of labeled potassium (42K+) were studied in the arterially perfused rabbit interventricular septum under control conditions and during respiratory acidosis. An increase in the CO2 content of the gas mixture with which the modified Ringer's solution was equilibrated from 5 to 30% reduced the perfusate pH from 7.37 to 6.66. The increment in developed tension in the presence of ACS was 3.0 +/- 0.2 g (n equals 10) under control conditions, but it was greater, 7.1 +/- 0.9 g (N equals 9) during acidosis (P less than less than 0.001). The net K+ loss due to an increase in K+ efflux was 1.8 +/- 0.2 mmoles/kg wet weight in control experiments but only 0.1 +/- 0.1 mmoles/kg net weight under acidotic conitions (P less than less than 0.001); in seven of nine experiments in respiratory acidosis, no increase in K+ efflux occurred despite a marked positive inotropy. In three septums, K+ influx was reduced by ACS during respiratory acidosis. These results demonstrate that during acidosis ACS inhibits sodium-potassium adenosinetriphosphatase (Na+-K+ ATPase) and causes an inotropic effect but does not increase K+ efflux. K+ efflux cannot be linked to calcium (Ca2+) influx or regarded as the controlling factor of glycoside-induced inotropy. The results give further support to the proposal that digitalis-induced inotropy is secondary to an enhancement of a Na+-Ca2+ exchange system.
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PMID:Glycoside inotropy in the absence of an increase in potassium efflux in the rabbit heart. 23 98

The effect of norepinephrine (NE) on the intracellular hydrogen ion concentration [H+]i of isolated rat hearts perfused with a modified Krebs-Henseleit solution (SHS) was determined. The [H+]i was calculated with the [14C]-dimethyloxazolidinedione method. Respiratory or metabolic acidosis was produced by equilibrating the KHS with 20% C02 or decreasing the [HC03-] of the KHS, respectively. Three types of experiments were carried out: 1) beta blockade--MJ 1999 (Sotalol) was added to the KHS; 2) control--no pharmacological treatment; and 3) NE-norepinephrine was added to the KHS. The effective CO2 buffer values (delta[HC03-]i/deltapHi) during respiratory acidosis were: beta blockade, 11; control, 35; and NE, 84. The production of metabolic acidosis resulted in the following [H+]i changes: beta blockade, 52 mM; control, 60 nM; and NE 7 nM. These results suggest that NE markedly attenuates the changes in [H+]i accompanying respiratory and metabolic acidosis and may account in part for previous observations that the effective C02 buffer value of cardiac muscle in vivo is greater than that in vitro.
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PMID:Effect of norepinephrine on myocardial intracellular hydrogen ion concentration. 24 Feb 82

Serum gastrin concentration and basal acid secretion were studied in normal subjects under the influence of respiratory acidosis induced by CO2 rebreathing. During the intragastric instillation of 100 ml/h 0.5 M bicarbonate a significant increase of gastrinaemia from 133 to 158 pg/ml (p less than 0.01) occurred in ten subjects during respiratory acidosis (pCO2 62 torr, pH 7.25). Under the intragastric instillation of 100 ml/h 0.1 N HCl the rise of gastrin concentration in response to CO2 rebreathing (pCO2 68 torr, pH 7.20) was not significant. The relationship between the decrease of pH and the increase of the gastrin concentration was shifted in the direction of a greater systemic acidosis compared to the results performed in the presence of a neutral intragastric pH. 50 mug/kg propranolol intravenously produced a decrease of gastrin concentrations from 145 to 127 pg/ml (p less than 0.01) and a total suppression of hypergastrinaemia in response to CO2 rebreathing, suggesting activation of beta-cell receptors in respiratory acidosis. The infusion of phentolamine in a dose of 0.6 to 1.8 mg/min. resulted in a rise of gastrin concentration from 140 to 165 pg/ml (p less than 0.01) which was not further elevated during respiratory acidosis. The basal acid secretion showed a significant rise in response to CO2 rebreathing, which was abolished by the administration of propranolol.
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PMID:The effect of propranolol and phentolamine on serum gastrin concentration in response to respiratory acidosis in normal man. 24 51

Two carbonic anhydrase inhibitors, acetazolamide and benzolamide, are capable of increasing the toxicity of sodium salicylate in mice. Beginning at about 2 mg/kg, each of the inhibitors, in combination with a fixed (400 mg/kg) dose of salicylate, generates a dose-mortality curve that reaches a plateau at about 60% deaths at 6 to 8 mg/kg. This effect can be duplicated by 8 to 10% inspired CO2. It appears that the respiratory acidosis secondary to the inhibition of red cell carbonic anhydrase is responsible for the increased toxicity; earlier work by others shows that acidosis increases the concentration of salicylate in the brain. In the treatment of salicylate poisoning by carbonic anhydrase inhibitors, the goal is to alkalinize the urine and increase the excretion of salicylate. With the newer inhibitor, benzolamide, it is possible to dissociate the respiratory acidosis from the renal effect. Maximal alkalinization of the urine is possible with a dose (about 1 mg/kg) below that which generates a respiratory acidosis. With this dose, there is no increase in the early toxicity of salicylate.
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PMID:CO2 retention as a basis for increased toxicity of salicylate with acetazolamide: avoidance of increased toxicity with benzolamide. 24 36

The pre-ejection period (PEP) of the fetal cardiac cycle was studied on 22 chronically instrumented pregnant ewes. The PEP was measured from the onset of the Q wave on fetal electrocardiogram to the onset of the upstroke on the fetal arterial blood pressure curve. Lengthening of the PEP was observed in association with an increase in gestational age, fetal body weight, fetal brow-rump length, and fetal heart weight. Consequently, the PEP values were calculated to those at fetal heart weight of 10 grams. The PEPc (calculated) was prolonged by acidosis but no significant relationship was found between the PEPc and arterial blood pO2. An increase in coronary blood flow was associated with a shortening of the PEPc in the fetuses under normal physiologic conditions. Fetal hypoxemia and respiratory acidosis created by administration of 10 per cent O2 and 20 per cent CO2 with 20 per cent O2 to the mother increased fetal coronary flow and was in general associated with a prolonged pre-ejection period.
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PMID:Pre-ejection period of cardiac cycles in fetal lamb. 44 90

Pulmonary function, acid-base balance, renal electrolyte excretion, hematology, biorhythms and psychomotor test results were studied in six men during 30 days of exposure to a PICO2 of 14 torr (FICO2 = 0.02) with pre- and postexposure periods on air. Alveolar and arterial PCO2 increased and remained constant throughout the CO2 exposure (delta PACO2 = delta PACO2 = 2.5 torr); the rise in expiratory minute volume (delta VE = 60%) was related to the increased tidal volume. Oxygen uptake and carbon dioxide output increased about 10% because of the ventilatory work overload. Physiological dead space increased 8% without an alveolar-arterial PCO2 difference. Respiratory acidosis was mild (delta pH approximately or equal to 0.01) and the renal response was slight. There was no variation in plasma electrolytes, except a slight decrease in potassium. Red blood cell count decreased, showing a confinement effect. Adaptation to exercise was slightly impaired. Results of electrobiological and psychomotor tests and biorhythm evaluations showed no variation; application of these findings to CO2 exposure limits is discussed.
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PMID:Effects on man of 30-day exposure to a PICO2 of 14 torr (2 %): application to exposure limits. 50 32

An electron microscope study of the left ventricular myocardium from rat acclimatized to chronic hypercapnia was done in order to complete the preceding work concerning general effects of respiratory acidosis. After 15 and 30 days of the acclimatation to 8% CO2 no lesions of the myocardium could be found. The results of the morphometric analysis indicated, however, discrete modifications of heart ultrastructure similar to those found before in hypoxic and failing hearts: namely a decrease of mitochondrial mean diameter and a non significant decrease of mitochondrial fractional volume. The latter was accompanied by a significant decrease of myofibrillar mass. The presence of cellular oedema seems to be suggested by an increase of fractional volume of the cytosol. The mechanism of these changes is not easy to explain. Further work will be necessary to make a choice between two possibilities: (1) depressed contractility related to some direct effect of high pCO2 and (2) tissue hypoxia secondary to local effects of the former.
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PMID:[The rat ventricular myocardium in chronic hypercapnia. Electron microscopic study]. 77 46

Buffer mechanism of cerebrospinal fluid (CSF) against acute hypercapnia was studied in eighteen dogs. The dynamic response of CSF to a stepwise change of CO2 concentration in inspired gas (room air -- 6% CO2 -- 12% CO2) was observed in eleven dogs, maintaining each condition for two hours. The changes in CSF acidity were less than that in arterial blood, while increases of bicarbonate ion concentration [HCO3-] in CSF were more prominent. Apparent buffer values, delta[HCO3-]/deltapH, were calculated from the results in different levels of CO2 breathing : they were 22.7 slykes from room air to 6% CO2 (step 1), and 39.7 slykes from 6% to 12% CO2 (step 2). Similar experiments were performed in seven dogs, suppressing carbonic anhydrase activity by systemic administration of acetazolamide. Apparent buffer values of CSF were 14.4 slykes in step 1 and 16.0 slykes in step 2. From the result we conclude : 1) that the activity of buffer mechanism of CSF in respiratory acidosis is PCO2 dependent and becomes stronger when PCO2 of CSF increases ; 2) for the explanation of this characteristic buffer mechanism of CSF, participation of carbonic anhydrase is suggested for transport mechanism of bicarbonate ion into CSF.
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PMID:The apparent buffer value of cerebrospinal fluid in acute hypercapnia. 82 71


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