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PubMed2005

Intrapulmonary percussive ventilation in acute exacerbations of COPD patients with mild respiratory acidosis: a randomized controlled trial [ISRCTN17802078].

INTRODUCTION: We hypothesized that the use of intrapulmonary percussive ventilation (IPV), a technique designed to improve mucus clearance, could prove effective in avoiding further deterioration in patients with acute exacerbations of chronic obstructive pulmonary disease (COPD) with mild respiratory acidosis. METHODS: The study was performed in a medical intensive care unit of a university hospital. Thirty-three patients with exacerbations of COPD with a respiratory frequency >or= 25/min, a PaCO2 > 45 Torr and 7.35 <or= pH <or= 7.38 were included in the study. Patients were randomly assigned to receive either standard treatment (control group) or standard treatment plus IPV (IPV group). The IPV group underwent two daily sessions of 30 minutes performed by a chest physiotherapist through a full face mask. The therapy was considered successful when both worsening of the exacerbation and a decrease in pH to under 7.35, which would have required non-invasive ventilation, were avoided. RESULTS: Thirty minutes of IPV led to a significant decrease in respiratory rate, an increase in PaO2 and a decrease in PaCO2 (p < 0.05). Exacerbation worsened in 6 out of 17 patients in the control group versus 0 out of 16 in the IPV group (p < 0.05). The hospital stay was significantly shorter in the IPV group than in the control group (6.8 +/- 1.0 vs. 7.9 +/- 1.3 days, p < 0.05). CONCLUSION: IPV is a safe technique and may prevent further deterioration in patients with acute exacerbations of COPD with mild respiratory acidosis.

Acidosis, Respiratory↗

PubMed1993

Effects of metabolic and respiratory acidosis on bone.

Acidosis had long been thought to influence the bone mineral; however, there was little direct evidence to support this impression. When neonatal mouse calvariae are cultured for 3 hours in medium with a reduced bicarbonate concentration, a model of acute metabolic acidosis, there is net calcium efflux from bone in addition to a net influx of protons into bone lessening the magnitude of the acidosis. The protons appear to exchange for sodium and potassium on the bone surface. In these acute experiments, the calcium efflux appears to be due to mobilization of carbonated apatite through an alteration in the physicochemical driving forces for bone accretion and dissolution. In more chronic cultures (greater than 48 hours) metabolic acidosis induces calcium efflux by stimulating osteoclastic bone resorption and inhibiting osteoblastic bone formation. When calvariae are cultured acutely in medium with an elevated partial pressure of carbon dioxide, a model of respiratory acidosis, there is also calcium efflux, but at the same decrement in pH the magnitude is far less than that observed during metabolic acidosis. There does not appear to be any measurable influx of protons into bone, and during chronic cultures there is no measurable calcium efflux. Thus, acidosis influences the bone mineral; however, for the same decrement in pH there is a marked difference in the response of bone to models of metabolic and respiratory acidosis.

Acidosis↗

PubMed1984

Response of renal NH3 production to chronic respiratory acidosis.

Although chronic metabolic acidosis results in an adaptive increase in the renal capacity to produce NH3, the response to a low pH produced by chronic respiratory acidosis is unknown. Rats were placed in a specially constructed chamber with an ambient CO2 of 10% for 3 days, which increased their PCO2 to 76 +/- 4 mmHg. NH3 production was determined in vitro using both isolated kidneys perfused with 0.5 mM glutamine and cortical tubules incubated with 1 mM glutamine. Conscious rats with chronic respiratory and chronic metabolic acidosis had similar arterial pHs (7.29 +/- 0.01 and 7.31 +/- 0.01), which were significantly lower than controls (7.41 +/- 0.04). NH3 production by kidneys from rats with chronic respiratory acidosis perfused at pH 7.4 did not differ significantly from normal controls (1.13 +/- 0.13 vs. 1.07 +/- 0.17 mumol X min-1 X g-1). By contrast, kidneys from rats with chronic metabolic acidosis produced significantly more NH3 than both these groups (2.73 +/- 0.29 mumol X min-1 X g-1). Cortical tubules from rats with chronic respiratory acidosis also showed no evidence of adaptation in both NH3 (8.8 +/- 0.8 vs. 11.6 +/- 0.8 mumol X min-1 X g-1) and glucose (1.38 +/- 0.08 vs. 1.41 +/- 0.13 mumol X min-1 X g-1) production in comparison with controls, whereas chronic metabolic acidosis stimulated both ammoniagenesis and gluconeogenesis twofold or more. Thus a low systemic pH does not account for the adaptation in the capacity of the kidney to produce either ammonia or glucose.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis↗

PubMed1995

Effect of chronic respiratory acidosis on calcium metabolism in the rat.

Chronic metabolic acidosis typically results in hypercalciuria and negative calcium balance. The impact of chronic respiratory acidosis on calcium metabolism has been less well studied. To address this issue, metabolic balance and static bone histomorphometric data were obtained during a 14-day exposure of rats to 10% CO2 (blood pH 7.33, PaCO2 83 mm Hg) and were compared with pair-fed controls. All rats were fed a 0.8% calcium diet. Urinary calcium excretion (mg/period, mean +/- SEM) was increased during both week 1 and week 2 (16 +/- 3 vs 9 +/- 1 and 16 +/- 2 vs 9 +/- 1, CO2 group vs controls, respectively [p < 0.05]). Net intestinal calcium absorption (intake minus fecal excretion) was increased throughout the period of hypercapnia (week 1, 213 +/- 19 mg vs 135 +/- 15 mg; week 2, 135 +/- 16 mg vs 43 +/- 14 mg; and cumulatively, 344 +/- 27 mg vs 178 +/- 20 mg, CO2 group vs controls [p < 0.01]). As a consequence of the marked increment in intestinal calcium absorption during hypercapnia, mean net calcium balance was more positive than that of controls throughout the study (week 1, 197 +/- 18 mg vs 126 +/- 15 mg; week 2, 120 +/- 15 mg vs 34 +/- 15 mg; and cumulatively, 317 +/- 25 mg vs 159 +/- 20 mg, CO2 group vs controls, respectively [p < 0.01]). There were no significant differences in calcium intake, plasma total calcium, immunoreactive parathyroid hormone, 25-hydroxyvitamin D, or creatinine clearance between the two groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis, Respiratory↗

PubMed1994

pH control in rat skeletal muscle during exercise, recovery from exercise, and acute respiratory acidosis.

We used 31P magnetic resonance spectroscopy to compare the response of rat skeletal muscle to three kinds of proton load. During exercise (tetanic sciatic nerve stimulation), protons from lactic acid were buffered passively and consumed by net hydrolysis of phosphocreatine (PCr). During recovery from exercise, the pH-dependent efflux of protons produced by PCr resynthesis could be partially inhibited by amiloride or 4,4'-diisothiocyanostilbene-2,2'-disulphonate (DIDS), implicating both sodium/proton and bicarbonate/chloride exchange, but was not inhibited by simultaneous respiratory acidosis. In early recovery, up to 30% of proton efflux was mediated by lactate/proton cotransport. During acute respiratory acidosis at rest, the eventual change in muscle pH was consistent with passive buffering and was unaffected by amiloride or DIDS, implying no significant contribution of proton fluxes.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗

PubMed1993

Altered adrenal steroid production in term infants having respiratory acidosis.

Prior studies have provided evidence for reduced fetal adrenal production of dehydroepiandrosterone sulfate and normal or increased production of cortisol in association with pregnancy complications believed to result in fetal stress. In the present study, we sought to determine the status of adrenal steroidogenesis in 36 term infants having respiratory acidosis and to compare acidotic infants to (i) non-acidotic infants matched for pregnancy complications, gestational age, and method and indications for delivery (control infants), and (ii) non-acidotic infants of non-complicated pregnancies who were also matched for gestational age and delivery method (normal infants). Umbilical cord serum levels of dehydroepiandrosterone sulfate were lowest in acidotic infants, intermediate in the condition matched control infants and highest in the non-acidotic infants of normal pregnancies. On the other hand, cortisol levels were highest in acidotic infants, intermediate in control infants and lowest in the normal infants. These data suggest that various pregnancy complications give rise to significant alterations in adrenal steroidogenesis (decreased dehydroepiandrosterone sulfate and increased cortisol). Intrauterine deterioration during labor with resultant respiratory acidosis has an additional effect on fetal adrenal function.

Acidosis, Respiratory↗

PubMed1991

The influence of a respiratory acidosis on the exercise blood lactate response.

The purpose of the present study was to examine the influence of a respiratory acidosis on the blood lactate (La) threshold and specific blood La concentrations measured during a progressive incremental exercise test. Seven males performed three step-incremental exercise tests (20 W.min-1) breathing the following gas mixtures; 21% O2 balance-nitrogen, and 21% O2, 4% CO2 balance-nitrogen or balance-helium. The log-log transformation of La oxygen consumption (VO2) relationship and a 1 mmol.l-1 increase above resting values were used to determine a La threshold. Also, the VO2 corresponding to a La value of 2 (La2) and 4 (La4) mmol.l-1 was determined. Breathing the hypercapnic gas mixtures significantly increased the resting partial pressure of carbon dioxide (PCO2) from 5.6 kPa (42 mm Hg) to 6.1 kPa (46 mm Hg) and decreased pH from 7.395 to 7.366. During the incremental exercise test, PCO2 increased significantly to 7.2 kPa (54 mm Hg) and 6.8 kPa (51 mm Hg) for the hypercapnic gas mixtures with nitrogen and helium, respectively, and pH decreased to 7.194 and 7.208. In contrast, blood PCO2 decreased to 4.9 kPa (37 mm Hg) at the end of the normocapnic exercise test and pH decreased to 7.291. A blood La threshold determined from a log-log transformation [1.20 (0.28) l.min-1] or as an increase of 1 mmol.l-1 [1.84 (0.46) l.min-1] was unaffected by the acid-base alterations. Similarly, the VO2 corresponding to La2 and La4 was not affected by breathing the hypercapnic gas mixtures [2.12 (0.46) l.min-1 and 2.81 (0.52) l.min-1, respectively].(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis, Respiratory↗

PubMed1985

Influence of respiratory acidosis or alkalosis on pressor responses mediated by alpha 1- and alpha 2-adrenoceptors in pithed normotensive rats.

The effect of respiratory acidosis and alkalosis on the vasoconstriction to alpha 1- and alpha 2-adrenoceptor stimulation was studied in pithed normotensive rats. The selective alpha 1-adrenoceptor agonists (-)amidephrine, cirazoline, (+/-)erythro methoxamine, (-)phenylephrine, Sgd 101/75 and St 587 were used, as well as the selective alpha 2-adrenoceptor agonists B-HT 920, B-HT 933, DP-6,7-ADTN, M-7 and UK 14,304. The non-selective alpha-adrenoceptor agonists xylazine, noradrenaline and adrenaline were included as well. The latter two were also studied under selective doses of the antagonists rauwolscine and prazosin, thus yielding the respective alpha 1- and alpha 2-adrenoceptor components of the vasoconstriction to these agonists. The effect of acid-base balance disturbances on presynaptically released noradrenaline elicited by electrical stimulation of preganglionic nerves was studied as well. Dose response curves for the agonists were generated under various conditions of ventilation, yielding either alkalotic, normal or acidotic values of arterial blood pH. Pressor responses to all agonists were maximally affected by changes in acid-base status at the low doses of the agonists. Acidosis was found to inhibit increases in diastolic pressure mediated by the alpha 1-as well as the alpha 2-adrenoceptor agonists studied, although not to the same extent. Alkalosis exerted either an obvious potentiation or did not significantly influence alpha 1-adrenoceptor mediated pressor responses. On the basis of acid-base sensitivity the following groups of agonists were distinguished: Cirazoline, phenylephrine, methoxyamine, electrically released noradrenaline from presynaptic sites, of which pressor responses are obviously potentiated and attenuated by alkalosis and acidosis, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗

PubMed1981

Effect of acute hypoxemia and respiratory acidosis on the fetal heart rate in monkeys.

The fetal heart rate (FHR) response to acute nonacidemic hypoxemia and to acute respiratory acidosis was studied in unanesthetized pregnant monkeys by means of chronically implanted catheters and electrodes. Average FHR and short- and long-term FHR variability were analyzed separately. The FHR response to either hypoxemia or hypercapnia consisted of slowing and increased variability. The slowing was more consistent with hypercapnia than with hypoxemia. Long-term FHR variability increased with both test stresses. The increase in short-term FHR variability was much greater in response to hypoxemia than to hypercapnia. Both the FHR slowing and the increases in variability in response to the test stresses were reduced by prior administration of atropine to the fetus.

Acidosis, Respiratory↗

PubMed1991

Rat kidney band 3 mRNA modulation in chronic respiratory acidosis.

Recent evidence indicates the existence of a protein related to the erythroid chloride-bicarbonate exchanger (band 3 protein) in the basolateral aspect of type A intercalated cells of the distal nephron. To probe the possible participation of this transporter in the renal adaptation to chronic hypercapnia, we examined the steady-state abundance of band 3 mRNA in the kidney during respiratory acidosis of variable duration. Total RNA was isolated from renal cortex and medulla of rats maintained in a 10% CO2 atmosphere for 2 or 5 days and from contemporaneous controls. The RNA was analyzed by Northern blot assay using cDNA probes for band 3 and beta-actin genes. Using a 3' cDNA probe encoding the membrane-associated domain of band 3 protein that is involved in anion exchange, we found a two- to threefold increase in steady-state mRNA levels (whether or not correction for the beta-actin signals was applied) in renal cortex and medulla at 5 days of hypercapnia. Similar, but less definitive, increases were observed at the 2-day time point. Using a 5' cDNA probe encoding an erythroid-protein segment absent from the kidney band 3 major transcript, we detected meager hybridization in renal tissue and no measurable variation during hypercapnia. Use of splenic RNA as a positive control for the 5' probe disclosed marked reduction of band 3 mRNA levels in hypercapnia, indicating organ specificity of band 3 gene expression. We conclude that steady-state levels of kidney band 3 mRNA increase in chronic respiratory acidosis as a result of transcriptional or posttranscriptional regulatory mechanisms. This adaptation might be involved in the augmentation of renal acidification characteristic of chronic hypercapnia.

Acidosis, Respiratory↗

PubMed1993

Ionic composition of cisternal CSF in acute respiratory acidosis: lack of effect of large dose bumetanide.

Sodium/chloride cotransport carrier is known to be involved in transepithelial fluid absorption and secretion in various tissues. Recent studies indicate that Na,K,2Cl cotransport carrier also exists in the choroid plexus cells and inhibition of the carrier alters ionic composition of the choroidal tissue. In this study, we report the effects of large dose intravenous bumetanide, a potent inhibitor of Na,K,2Cl carrier, on cisternal CSF ionic composition in acute respiratory acidosis in pentobarbital-anesthetized mechanically ventilated dogs. Renal pedicles were ligated to prevent bumetanide-induced diuresis. The experimental group (Group II, n = 7) received 50 mg/kg of bumetanide intravenously and Group I (the control group, n = 7) received the vehicle. Analysis of serum and choroidal plexus tissue revealed bumetanide concentration of approximately 10(-5) mol/L in Group II. During 5 h of acute respiratory acidosis in both groups, the mean PaCO2 increased approximately 25 mm Hg, with comparable changes in CSF PCO2. In both groups, CSF [HCO3-] and [H+] increased approximately 3 mEq/L and 20 nEq/L, respectively. Furthermore, changes in CSF [Na+], [K+], [Ca2+], [Mg2+], [Cl-], and [Na(+)-Cl-] were also similar and were not significantly different from each other. These data show that bumetanide, at the dose that inhibits NaCl cotransport carrier, does not significantly affect ionic composition of cisternal CSF.

Acid-Base Equilibrium↗

PubMed1994

Acute respiratory acidosis: large-dose furosemide and cerebrospinal fluid ions.

NaCl cotransport carrier is known to be involved in transepithelial fluid absorption and secretion in various tissues. Recent studies indicate that Na-K-2Cl cotransport carrier also exists in the choroid plexus cells and that inhibition of the carrier decreases cerebrospinal fluid (CSF) production. In this study, we used large-dose intravenous furosemide, an inhibitor of Na-K-2Cl carrier, to determine the effects on cisternal CSF ionic composition in acute respiratory acidosis. In pentobarbital-anesthetized mechanically ventilated dogs, renal pedicles were ligated to prevent furosemide-induced diuresis. The experimental group (group II, n = 7) received 400 mg/kg of furosemide intravenously, and group I (control group, n = 7) received the vehicle. In group II, serial serum and CSF furosemide concentrations were approximately 10(-3) and 10(-5) mol/l, respectively. During 5 h of acute respiratory acidosis in both groups, the mean arterial PCO2 increased approximately 25 Torr, with comparable changes in CSF PCO2. In both groups, CSF [HCO3-] and [H+] rose approximately 3 meq/l and 20 neq/l, respectively. Changes in CSF [Na+], [K+], [Cl-], and [Na(+)-Cl-] were also similar and were not significantly different from each other when the two groups were compared. These data show that furosemide at the dose that inhibits NaCl cotransport carrier does not significantly alter ionic composition of cisternal CSF.

Acid-Base Equilibrium↗

PubMed1988

Division of the pattern-evoked retinal response by respiratory acidosis.

Analysis in the frequency domain divided the pattern-evoked retinal response (PERR) of the cat into two analog components. A mild respiratory acidosis was produced by raising the end-tidal CO2 from 4-6% to 12-14%. The onset of the acidosis (without hypoxia) was highly correlated with marked decreases in the low-frequency PERR component and in the b-wave of the flash-elicited ERG. The high-frequency PERR component was unchanged relative to the labile low-frequency component (p less than 0.01). The literature has established a firm link between local pH and Müller cell function. These data tend to confirm the hypothesis that the cat's PERR to some grating stimuli of less than 100% contrast may contain separable components of different cellular origin(s).

Acidosis, Respiratory↗

PubMed1994

Greater inhibition of in vitro bone mineralization with metabolic than respiratory acidosis.

At a similar decrement in pH, acidosis produced by lowering the concentration of medium bicarbonate (metabolic acidosis) induces greater net calcium efflux from cultured neonatal mouse calvariae than acidosis produced by increasing the partial pressure of carbon dioxide (respiratory acidosis). This differential effect is due, at least in part, to enhanced cell-mediated bone mineral resorption during metabolic acidosis. To determine the effect of acidosis on osteoblastic bone formation we utilized primary cultures of neonatal mouse calvarial cells which produce calcified nodules in culture. Cells were plated at 4.5 x 10(4) cells/35 mm dish and incubated until confluent (day 9). Nodule formation was then induced by addition of beta-glycerophosphate and ascorbic acid and the cultures were randomly divided and then cultured in control (Ctl, N = 18) medium or in medium simulating metabolic (Met, N = 17) or respiratory (Resp, N = 19) acidosis. Medium was changed and calcium (Ca) measured every 48 hours until day 23. The mean initial medium pH of all Resp cultures (7.186 +/- 0.002) was lower than Met (7.243 +/- 0.006, P < 0.01), which was lower than Ctl (7.502 +/- 0.002, p < 0.01), yet the number of discrete nodules formed in Met (22 +/- 4 nodules/cm2) was lower than Resp (43 +2- 7, P < 0.01), and both were lower than Ctl (88 +/- 6, P < 0.01 vs. both Met and Resp).(ABSTRACT TRUNCATED AT 250 WORDS)

3T3 Cells↗

PubMed1979

Influence of respiratory acidosis and alkalosis on volume of distribution of theophylline in dogs.

The volume of distribution of theophylline at nomal pH, and following induction of respiratory acidosis and alkalosis, was studied in four dogs in a three-way crossover design. Although serum half-lives of theophylline varied widely, and acidemia prolonged the time required for distribution equilibration, the volumes of distribution were almost identical for each of the three experimental conditions assuming one compartment pharmacokinetics apply.

Acidosis, Respiratory↗

PubMed1991

Alteration in surface ion composition of cultured bone during metabolic, but not respiratory, acidosis.

Acidosis produced by a fall in [HCO3-] (metabolic acidosis, Met) produces greater Ca efflux from cultured bone than that produced by a rise in PCO2 (respiratory acidosis, Resp). To compare the effects of Met and Resp on bone surface ion composition we measured the surface abundance of 40Ca, 23Na, and 39K in cultured bone with a scanning ion microprobe utilizing secondary-ion mass spectrometry. Neonatal mouse calvariae were incubated for 24 h in medium simulating either Met (pH = 7.193 +/- 0.034, [HCO3-] = 15.1 +/- 1.4 meq/l), Resp (pH = 7.153 +/- 0.014, PCO2 = 85.4 +/- 1.2 mmHg) or normal physiological (Ctl; pH = 7.484 +/- 0.009, [HCO3-] = 29.7 +/- 0.7, PCO2 = 39.6 +/- 0.3) conditions. The surface of Ctl at 2-nm depth is rich in Na and K relative to Ca (Na/Ca = 25.6, K/Ca = 12.0, ratios of counts/s of secondary ions). Compared with Ctl, Met produced a sharp fall in both Na/Ca (6.5, P less than 0.01) and K/Ca (4.6, P less than 0.01), whereas Resp did not alter Na/Ca (23.8) or K/Ca (15.0). Ca efflux was greater in Met (873 +/- 54 nmol.bone-1.24 h-1) than in Resp (546 +/- 71 nmol.bone-1.24 h-1, P less than 0.01), which was greater than that in Ctl (315 +/- 49 nmol.bone-1.24 h-1, P less than 0.01 vs. Met and vs. Resp).(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis↗

PubMed1985

Correction of respiratory acidosis and transient hypomagnesemia.

Four elderly patients with established chronic obstructive airways disease were admitted with a days' to weeks' history of increasing dyspnea. Acute respiratory acidosis was diagnosed and mechanical ventilation instituted. A few hours after initiation of treatment, arterial pH was normal in all patients, but serum magnesium concentrations decreased over the next 1-3 days. Thereafter, a spontaneous normalization was seen. It is suggested that the transient hypomagnesemia is due to correction of the acidosis per se.

Acidosis, Respiratory↗

PubMed1975

The effects of respiratory acidosis on plasma renin activity in the dog.

The effects of arterial PCO2 on plasma activity was studied in chloralose anesthetized dogs undergoing carefully controlled respiratory acidosis. Plasma renin activity, measured by radioimmunoassay, was enhanced (P less than 0.001) during inhalation of CO2 despite insignificant changes in renal blood flow and arterial pressure. Although underlying mechanism remained to be investigated, activation of sympathetic nervous system and intrarenal effects of CO2 seemed to be involved in this enchancement.

Acidosis, Respiratory↗