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[The therapeutic dilemma in respiratory acidosis].
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beta-Adrenergic activity and cardiovascular response to severe respiratory acidosis.
The mechanism responsible for the depressive myocardial effects of severe respiratory acidosis is unclear; however, sympathetic stimulation and catecholamines are known to be involved. The influence of beta-adrenergic receptor activity on the myocardial response to severe respiratory acidosis was studied in 18 anesthetized, mechanically ventilated dogs. Arterial CO2 tension (PaCO2) was raised by increasing the inspired CO2 fraction in O2. In control animals, as PaCO2 increased, heart rate (HR) decreased (PaCO2 approximately 110 mmHg), then returned to control (PaCO2 approximately 220 mmHg), whereas arterial blood pressure (Pa) and cardiac output (Q) remained unchanged from prehypercapnia levels. At PaCO2 greater than 350 mmHg, Pa, HR, and Q decreased and left ventricular function (LVF) curves were depressed. Death occurred at a PaCO2 of 404 +/- 25 mmHg (pH 6.48 +/- 0.02). In a second group of animals, administration of isoproterenol during the increase in PaCO2 did not result in depression of myocardial function, and death did not occur even at a significantly higher PaCO2 (PaCO2 496 +/- 12 mmHg; pH 6.39 +/- 0.02) than in the control group. Administration of propranolol to a third group of animals as PaCO2 increased did not change Pa, HR, and Q; however, LVF curves indicated a more rapid and severe depression of myocardial performance than in control, and death occurred at a significantly lower PaCO2 (PaCO2 220 +/- 25 mmHg; pH 6.65 +/- 0.02). We conclude that beta-adrenergic receptor stimulation can prevent hypercapnic heart failure and that beta-adrenergic receptor activity is involved in the mechanism responsible for this failure.
Effects of respiratory acidosis on HCO3- transport by rabbit collecting tubules.
These studies were performed to determine whether in vitro elevation of bath PCO2 with associated reduction in pH (acute respiratory acidosis) affected bicarbonate transport by isolated perfused rabbit cortical collecting tubules (CCT) and collecting tubules from the outer (OMCTos) and inner (OMCTis) stripes of the outer medulla. When the PCO2 was elevated and pH reduced from approximately 7.4 to 7.0 the rate of total CO2 absorption increased to 252% of that observed at pH 7.4 in CCT, 146% in OMCTos, and 150% in OMCTis. In OMCTis, pretreatment with colchicine inhibited the stimulation of total CO2 absorption associated with respiratory acidosis, whereas lumicolchicine did not. Similar inhibition was observed in the presence of maptam and a low calcium concentration and in the presence of a calmodulin inhibitor. No differences were observed in apical or basolateral membrane morphometry of principal or intercalated cells between control tubules and those subjected to respiratory acidosis. The results indicate that acute respiratory acidosis stimulates acidification by the rabbit distal nephron in vitro through a process(es) that, at least in OMCTis, evidently involves the cell cytoskeleton and changes in cell calcium and calmodulin activities.
[CLINICAL RESULTS OF THE CURRENT THERAPEUTIC TRENDS IN RESPIRATORY ACIDOSIS IN EMPHYSEMATOUS PATIENTS].
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Reactivity of skin and muscular blood vessels to noradrenaline during induced respiratory acidosis in cats.
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Effect of chronic respiratory acidosis on urinary calcium excretion in the dog.
It is currently believed that the two chronic acidemic disorders exert disparate effects on urinary calcium excretion: chronic metabolic acidosis induces consistent hypercalciuria, but no appreciable change or even a decrease in calcium excretion is reported to attend chronic respiratory acidosis. Whereas the effect of metabolic acidosis is well documented, little work has been carried out in chronic hypercapnia. In fact, most of the studies on chronic respiratory acidosis were short in duration, had employed only mild hypercapnia, or had failed to control carefully the prevailing metabolic conditions. We have carried out balance observations in nine dogs exposed to a 10% CO2 atmosphere in an environmental chamber for a period of two weeks. Chronic respiratory acidosis led to a significant increase in urinary calcium excretion from a mean control value of 0.4 +/- 0.1 mmol/day to 0.6 +/- 0.1 mmol/day during both week 1 and 2 of hypercapnia (P less than 0.05). Hypercalciuria occurred even though filtered load of calcium fell. Mean fractional excretion of calcium increased significantly during each week of hypercapnia averaging 0.60 +/- 0.12% during control, 1.05 +/- 0.13% during week 1, and 1.26 +/- 0.17% during week 2 of hypercapnic exposure (P less than 0.05). There were no changes in plasma levels of immunoreactive parathyroid hormone or 1,25-dihydroxyvitamin D3. These findings suggest that chronic respiratory acidosis, just like chronic metabolic acidosis, augments urinary calcium excretion by a direct depressive effect on the tubular reabsorption of calcium.
Recovery of contractility and pHi during respiratory acidosis in ferret hearts: role of Na(+)-H+ exchange.
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.
Early postoperative respiratory acidosis after large intravascular volume infusion of lactated ringer's solution during major spine surgery.
UNLABELLED: In this study, we compared the effects of large intravascular volume infusion of 0.9% saline (NS) or lactated Ringer's (LR) solution on electrolytes and acid base balance during major spine surgery and evaluated the postoperative effects. Thirty patients aged 18-70 yr were included in the study. General anesthesia was induced with 5 mg/kg thiopental and 0.1 mg/kg vecuronium IV. Anesthesia was maintained with oxygen in 70% nitrous oxide and 1.5%-2% sevoflurane. In Group I, the NS solution, and in Group II, the LR solution were infused 20 mL. kg(-1). h(-1) during the operation and 2.5 mL. kg(-1). h(-1), postoperatively. Electrolytes (Na+, K+, Cl-) and arterial blood gases were measured preoperatively, every hour intraoperatively and at the 1st, 2nd, 4th, 6th, and 12th hours postoperatively. In the NS group, pHa, HCO3 and base excess decreased, and Cl- values increased significantly at the 2nd hour and Na+ values increased at the 4th hour intraoperatively (P < 0.001). The values returned to normal ranges at the 12th hour postoperatively. In the LR group, blood gas analysis and electrolyte values did not show any significant difference intraoperatively, but the increase in PaCO2 and the decrease in pHa and serum Na+ was significant at the 1st hour postoperatively. Although intraoperative 20 mL. kg(-1). h(-1) LR infusion does not cause hyperchloremic metabolic acidosis as does NS infusion, it leads to postoperative respiratory acidosis and mild hyponatremia. IMPLICATIONS: The infusion of large-volume lactated Ringer's solution does not cause hyperchloremic metabolic acidosis as does 0.9% saline during major surgery, but leads to postoperative mild hyponatremia and respiratory acidosis.
Effect of acute respiratory acidosis on two populations of intercalated cells in rat cortical collecting duct.
Recent studies suggest the presence of two populations of intercalated cells in the rabbit cortical collecting duct (CCD), one involved with hydrogen ion secretion and another that may play a role in bicarbonate secretion. The purpose of this study was to determine whether two populations of intercalated cells are present in the rat CCD and to establish their response to acute respiratory acidosis. Rats were studied during normal acid-base conditions and after 4-5 h of respiratory acidosis. In all animals light microscopy and transmission and scanning electron microscopy revealed two configurations of intercalated cells, type A with an extensive apical tubulovesicular membrane compartment and prominent surface microprojections and type B with a well-developed vesicular compartment and short sparse surface microprojections. By transmission electron microscopy, studs were present on the cytoplasmic face of the apical plasmalemma and tubulovesicular profiles of A cells. In respiratory acidosis there was a striking increase in apical microprojections and in the surface density of the apical membrane of type A cells similar to the response observed previously in intercalated cells in the outer medullary collecting duct (OMCD) studied under the same physiological conditions. No changes were observed in type B cells. Scanning electron microscopy revealed no change in the relative number of type A and type B cells in respiratory acidosis. We conclude that two distinct populations of intercalated cells exist in the rat CCD: type A, which resembles the intercalated cells in the OMCD, and type B. The response of type A cells to acute respiratory acidosis and the similarity between these cells and intercalated cells in the OMCD, which are believed to secrete hydrogen ion, suggest that the type A cells are involved in hydrogen ion secretion in the CCD.
Net calcium efflux from live bone during chronic metabolic, but not respiratory, acidosis.
In vivo chronic metabolic acidosis induces bone mineral dissolution. Whether the dissolution is due to alterations in physicochemical factors alone, as in acute metabolic acidosis, or requires participation of bone cells is not clear. The effect of chronic respiratory acidosis on bone has also not been established. To determine the effects of chronic metabolic and respiratory acidosis on net calcium flux from bone, we cultured live and dead neonatal mouse calvariae for 99 h in control medium or in medium acidified (pH approximately equal to 7.1) either by lowering the bicarbonate concentration (Met) or by increasing the PCO2 (Resp). We measured net calcium flux (JCa) over 0-48, 48-96, and 96-99 h. Over the first 48 h, there was greater net calcium efflux from live and dead Met than from both Resp groups. All four acidic groups had greater net calcium efflux than controls. Over the last 51 h of the chronic 99 h culture, there was net calcium efflux only from live Met (JCa = 285 +/- 129 nmol.bone-1.3 h-1) and not from any of the other groups (live control, JCa = -183 +/- 24; live Resp, JCa = -110 +/- 22; dead control, JCa = -256 +/- 12; dead Met, JCa = 11 +/- 78; dead Resp, JCa = -27 +/- 47; each P less than 0.02 vs. live Met). There is net calcium efflux from live cultured neonatal mouse calvariae during chronic metabolic, but not respiratory, acidosis. During chronic acidosis, decreased medium bicarbonate, and not just a fall in pH, is necessary to enhance net calcium efflux from live bone.
[The role respiratory acidosis in the development of acute pancreatitis (author's transl)].
The effects of respiratory acidosis on the pancreas were studied in 25 Wistar rats. Ligation of the duct combined wiht respiratory acidosis resulted in the development of acute pancreatitis. In explantation of the results it is suggested that exhaustion of the buffering capacity causes a dramatic fall in pH of the pancreatic juice. The clinical relevance of findings is discussed.
Respiratory acidosis, including the use of intermittent pressure breathing.
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Treatment of respiratory acidosis with N-allylnormorphine (nalline).
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The induction of respiratory acidosis by oxygen breathing.
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Muscle composition in respiratory acidosis.
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