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 effects of acute metabolic and respiratory acidosis and acute metabolic alkalosis on magnesium excretion and on fractional magnesium delivery to the end-accessible proximal tubule of the superficial nephron and the end-descending limb of the juxtamedullary nephron were examined by micropuncture in anesthetized thyroparathyroid-intact rats. Compared with normal control rats, acute metabolic acidosis (HCl infusion) did not produce any significant change. Acute respiratory acidosis (15% CO2 in inspired air) significantly increased the absolute but not the fractional excretion of magnesium and did not alter fractional delivery of magnesium to the end-accessible superficial proximal tubule or juxtamedullary end-descending limb. Acute metabolic alkalosis (NaHCO3 infusion) significantly reduced absolute and fractional magnesium excretion and fractional magnesium delivery to the end-descending limb of the juxtamedullary nephron but did not affect fractional magnesium delivery to the end-accessible proximal tubule of the superficial nephron. Tubule fluid-to-ultrafilterable magnesium ratio was a function of tubule fluid-to-plasma inulin ratio in the end-descending limb when all groups were combined. These results suggest that although acute metabolic or respiratory acidosis has no significant effect, acute metabolic alkalosis enhances magnesium reabsorption in the juxtamedullary proximal nephron--possibly in the pars recta.
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PMID:Effects of acute acid-base disturbances on renal tubule reabsorption of magnesium in the rat. 711 19

Shifts of Na+, K+, Cl- and HCO3- between the cells and extracellular fluid of nephrectomized mammals in acute response to hypercapnia and to HCl or KCl infusion are simulated in steady state models involving just intracellular buffering and a simply defined interdependence of ionic gradients. Such models integrate diverse kinds of data and suggest new interpretations. In respiratory acidosis K+, HCO3- and water leave some cells and move both to where chemical buffering is least (ECF and other cells) and to cells that regulate pH particularly well by active transport. Buffering by erythrocytes is important, but the effects of distinguishing erythrocytes from other cells in a model is mainly just to emphasize Cl- movements. Effects of departures from the mammalian norm of body composition are explored.
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PMID:The role of intracellular buffers in acid-base disturbances: mathematical modelling. 736 Oct 19

To elucidate the factors mediating the response of renal ammoniagenesis to acute acidosis, the isolated perfused rat kidney was subjected to acute metabolic and respiratory acidosis with either standard collection or drainage of urine back into the perfusate. Midway during a 90-min perfusion with 0.4 mM glutamine and 5 mM glucose, perfusate pH was decreased to 6.8 by addition of HCl or alteration of the PCO2. Metabolic acidosis increased NH3 production, acidified the urine, and increased urinary NH4 excretion. Respiratory acidosis increased NH3 production to a comparable degree without urine acidification and with a minimal increase in NH4 excretion. When respiratory acidosis preceded perfusion at control PCO2 levels, NH3 production was increased but NH4 excretion was lower than control values. If urine drained back into the perfusate, NH3 production was not altered by either metabolic or respiratory acidosis. Accordingly, acute changes in perfusate pH stimulate renal ammoniagenesis by the isolated perfusate pH stimulate renal ammoniagenesis by the isolated perfused kidney independent of changes in urinary pH and NH4 excretion. This response is inhibited by an unidentified factor excreted in the urine.
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PMID:Stimulation of ammoniagenesis by acute acidosis: evidence for a urinary inhibitor. 743 19

We studied sympathetic nerve activity (SNA) responses, recorded in multifiber preparations of left third thoracic white ramus, to respiratory or isocapnic metabolic acidosis or to CO2 enhancement at constant pH in chloralose-anesthetized paralyzed artificially ventilated cats. Cardiopulmonary, baro-, and peripheral chemoreceptors were denervated by bilaterally cutting vagus and carotid sinus nerves. Acidosis was induced by either decreasing artificial ventilation or infusing HCl (0.5 M i.v.). Both respiratory and isocapnic metabolic acidosis induced a decrease in local extracellular pH, measured directly with pH-sensitive microelectrodes within medulla region containing sympathoexcitatory bulbospinal neurons. The magnitude of changes in medullary pH was independent of the way systemic acidosis was generated. Despite uniformity of changes in local medullary extracellular pH due to systemic respiratory or isocapnic metabolic acidosis, different responses were observed in preganglionic SNA. Isocapnic metabolic acidosis resulted in a slight increase in SNA, averaging 6.4% per 0.05 systemic pH unit decrease. In contrast, respiratory acidosis induced by decreasing artificial ventilation produced a more pronounced increase of SNA, reaching peak changes of approximately 70% compared with control level with normal blood gases, an average increase of 13% per 0.05 systemic pH unit decrease. We conclude that systemic CO2 and H+ concentrations represent different stimuli to sympathetic nervous system. Despite similar changes of local extracellular pH within rostral ventrolateral medulla during systemic acidosis, different responses of SNA suggest other sites or as yet unknown additional effects of CO2 as being responsible for excitation of sympathetic activity.
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PMID:Different effects of respiratory and metabolic acidosis on preganglionic sympathetic nerve activity. 796 Dec 30

Lung carbonic anhydrase (CA) permits rapid pH responses when changes in regional ventilation or perfusion alter airway and alveolar PCO2. These pH changes affect airway and vascular resistances and lung compliance to optimize the balance of regional ventilation (VA) and perfusion (Q) in the lung. To test the hypothesis that these or other CA-dependent mechanisms contribute to VA/Q matching, we administered acetazolamide (25 mg/kg intravenously) to six anesthetized and paralyzed dogs and measured VA/Q relationships before and after CA inhibition by the multiple inert gas elimination technique. Four other groups of dogs were studied to control for possible confounding effects of time under anesthesia and nonselective CA inhibition by acetazolamide: (a) saline placebo as a control for duration of anesthesia, (b) 4% CO2 inhalation to mimic systemic CO2 retention, (c) 1 mg/kg benzolamide (a selective renal CA inhibitor) or 0.5 meq/kg HCl to mimic systemic metabolic acidosis, and (d) 500 mg/kg 4,4'-dinitrostilbene-2,2'-disulfonate (an inhibitor of red cell band 3 protein) to mimic the respiratory acidosis arising from an intracapillary block to rapid mobilization of plasma HCO3- in CO2 exchange. Acetazolamide increased VA/Q mismatch and reduced arterial PO2 measured at equilibrium but these did not occur in the control group. There was no deterioration in VA/Q matching when systemic respiratory acidosis produced either by CO2 inhalation or 4,4'-dinitrostilbene-2,2'-disulfonate or metabolic acidosis (benzolamide or HCl) were imposed to mimic the effects of acetazolamide apart from its inhibition of lung CA. These results support the concept that lung CA subserves VA/Q matching in the normal lung.
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PMID:Effects of carbonic anhydrase inhibition on ventilation-perfusion matching in the dog lung. 834 9

Two recent clinical reports suggested that succinylcholine (SCh) may cause severe hyperkalemia in hemorrhagic, acidotic humans. To investigate this, we anesthetized rabbits with halothane and N2O, and inserted venous and arterial catheters. Control rabbits (Group C, n = 4) remained anesthetized and undisturbed. Hemorrhage/profound acidosis (HPA) was accomplished by withdrawal of 25-30 mL/kg of blood and waiting until pHa approximately 7.05 (Group HPA, n = 5). Hemorrhage/minimal acidosis (HMA) was accomplished by withdrawal of 25-30 mL/kg of blood, but acidosis was minimized by not waiting for it to occur and by administering NaHCO3 0-1.4 mEq/kg (Group HMA, n = 4). In a metabolic acidosis group (n = 4), HCl was infused until pHa approximately 7.05. Respiratory acidosis (n = 4) was accomplished by partial obstruction of the endotracheal tube until PaCO2 approximately 120 mm Hg and pHa approximately 7.05. Potassium levels were determined before the above interventions (baseline), immediately before (pre-SCh), and 1, 3, 5, 7, 10, and 13 min after SCh 1 mg/kg intravenously. In Group C, potassium gradually increased from 3.5 +/- 0.2 mEq/L to 4.8 +/- 0.2 mEq/L 13 min after SCh. In Group HPA, potassium increased from 3.8 +/- 0.3 to 7.0 +/- 1.8 mEq/L after hemorrhage/acidosis and then to 11.4 +/- 1.7 mEq/L at 13 min after SCh. The metabolic acidosis group was significantly different from Group C at 7, 10, and 13 min after SCh (maximum at 13 min, 6.8 +/- 1.2 mEq/L).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Succinylcholine causes profound hyperkalemia in hemorrhagic, acidotic rabbits. 836 59

The purpose of this study was to examine whether initial acidic reperfusion after ischemia followed by stepwise normalization of perfusate pH could improve functional recovery and to assess whether this is associated with a reduction in Ca2+ overload. Isolated rat hearts were subjected to global ischemia for 25 min, followed by 30 min of reperfusion. In the control group (Group C), the perfusate pH was 7.4 throughout reperfusion. In the acidic groups, the perfusate pH was 6.8 for the first 5 min, 7.1 for the second 5 min, and 7.4 for the remainder of reperfusion. Acidic buffer was produced either by adding HCl (metabolic acidosis, Group MA) or by bubbling with gas containing 12 to 24% CO2 (respiratory acidosis, Group RA). The recovery of ventricular function, Ca2+ uptake, and energy metabolites were analyzed. Thirteen of the 15 hearts in Group C, 14 of the 15 in MA and 8 of the 15 in RA recovered regular cardiac rhythm at the end of reperfusion. In these hearts which exhibited normal rhythm, the percent recovery in developed pressure was higher (MA: 73 +/- 8, RA: 68 +/- 6, C: 51 +/- 5%, p < 0.05) and left ventricular end-diastolic pressure was lower (MA: 5.1 +/- 1.4, RA: 5.9 +/- 1.3, C: 14.2 +/- 2.7 mmHg, p < 0.05) in the acidic groups. The improved recovery was associated with a significant reduction in Ca2+ uptake which persisted with the restoration of normal pH. These results demonstrate that early acidic reperfusion enhances contractile recovery and diminishes Ca2+ overload. Moreover, these salutary effects are maintained after stepwise normalization of the perfusate pH to physiological values.
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PMID:Effect of stepwise normalization of perfusate pH on post-ischemic functional recovery and Ca2+ overload in isolated rat hearts. 890 86

We tested the hypothesis that myocardial extracellular acidosis during early reperfusion limits infarct size. The left anterior descending coronary artery was perfused with blood through a bypass tube in dogs. We occluded the bypass tube for 40 (protocol I; n = 24 hearts) and 90 min (protocol II; n = 36 hearts). In protocols I and II, we infused one group of hearts with HCl (60 micrograms.kg-1.min-1) for 60 min after the onset of reperfusion (the metabolic acidosis group), and another group of hearts were ventilated with 3 liters of 70% O2-30% CO2 mixed with room air 10 min before the onset of reperfusion for 70 min (the respiratory acidosis group). pH in the coronary venous blood and myocardial pH during reperfusion in the metabolic and respiratory acidosis groups were lower than those in the control groups. Infarct sizes in the metabolic (16.4 +/- 2.5 and 22.3 +/- 2.5%) and respiratory (16.7 +/- 2.6 and 22.3 +/- 2.5%) acidosis groups in protocols I and II, respectively, were smaller than those in the control groups (33.1 +/- 3.0 and 40.6 +/- 4.1%, respectively). Thus we conclude that temporary acidosis during reperfusion limits infarct size.
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PMID:Temporary acidosis during reperfusion limits myocardial infarct size in dogs. 917 71

Somatolactin is a putative pituitary hormone of the growth hormone/prolactin family in fish. Its function is still unknown. The effects of environmental hypercapnia and hypoxia, acid (HCl) infusion and exhaustive exercise on plasma somatolactin levels were examined in the chronically cannulated rainbow trout to study the possible physiological roles of somatolactin. Respiratory acidosis induced by hypercapnia (2% CO2) did not affect plasma somatolactin level. In contrast, metabolic acidosis induced by acid infusion and exercise increased plasma somatolactin level. Blood pH was depressed to a similar extent by both types of acidosis, whereas plasma [HCO3-] was elevated by respiratory acidosis but reduced by metabolic acidosis. A moderate hypoxia (water PO2 9.3kPa) affected neither acid&shy;base status nor plasma somatolactin level. A more severe hypoxia (water PO2 6.1kPa) resulted in metabolic acidosis accompanied by an apparent rise in plasma somatolactin level, although the difference in somatolactin level from the control value was not statistically significant. Somatolactin immunoneutralization retarded recovery of plasma [HCO3-] following acid infusion. These results indicate that somatolactin is involved in the retention of HCO3- during metabolic acidosis but not in the active accumulation of HCO3- for acid&shy;base compensation of respiratory acidosis in rainbow trout Oncorhynchus mykiss.
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PMID:Possible involvement of somatolactin in the regulation of plasma bicarbonate for the compensation of acidosis in rainbow trout 932 95

In order to evaluate the effect of brain acidosis on neuronal functions as assessed by the in vivo studies, changes of cerebral blood flow (CBF), brain pH ([pH]o) and brain amino acid levels in the same brain region of the two different acidosis model rats were measured under isoflurane anesthesia. Three micro probes to measure CBF, [pH]o and amino acids, respectively, were implanted into the frontal cortex, and these parameters were recorded simultaneously. In the metabolic acidosis rats, the sustained decrease of [pH]o and amino acid levels, particularly Glu, were detected after the treatment with 10 min-i.v. infusion of 1 N HCl, although the significant changes of CBF did not appear because of the respiratory management. In the respiratory acidosis model, however, transient and significant increase of CBF and decrease of Glu and [pH]o were recorded after 10 min-exposure to about 30% CO2 (N2O:O2:CO2 = 2:5:3). The levels of Gly and Gln were reduced after acute exposure to hypercapnia, but these levels recovered to the control level in 20-30 min after hypercapnia exposure. In both animals, the amounts of Tau was gradually reduced after the treatment with 1 N HCl and hypercapnia, and these levels did not return to the control level when other amino acid levels had recovered. These differences of brain amino acid levels in the two different types of acidosis model rats may be related to the brain amino acid metabolic pathway. Thus, during brain acidosis induced by 1 N HCl and hypercapnia, the amount of extracellular Glu in the brain was reduced, and this reduction may contribute to the neuroprotective effects.
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PMID:[Acidosis and neuroprotection in two types of acidosis model rats under isoflurane anesthesia: evaluation of blood flow, pH and amino acid levels in the cortex]. 983 87


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