Metabolic Acidosis Improves Airway Conductance in Patients with Asthma
The objective was to investigate whether acute metabolic acidosis could cause bronchodilation in patients with asthma. Twelve patients with asthma (8 females, mean age 39 (± SD 12) years, forced expiratory volume in 1 second [FEV1] 93 [±9] % predicted, PC20 1.9 (±1.0) mg/mL) participated in a double...
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| Veröffentlicht in: | The Journal of asthma Jg. 46; H. 7; S. 656 - 658 |
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| Sprache: | Englisch |
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England
Informa UK Ltd
01.01.2009
Taylor & Francis |
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| ISSN: | 0277-0903, 1532-4303, 1532-4303 |
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| Abstract | The objective was to investigate whether acute metabolic acidosis could cause bronchodilation in patients with asthma. Twelve patients with asthma (8 females, mean age 39 (± SD 12) years, forced expiratory volume in 1 second [FEV1] 93 [±9] % predicted, PC20 1.9 (±1.0) mg/mL) participated in a double-blind, placebo-controlled trial. Subjects ingested calculated amounts of ammonium chloride to induce acidosis or saline as placebo, in random order, each on a separate day. Airway resistance (Raw), specific airway conductance (sGaw), FEV1, and PEF were measured as primary variables. To evaluate the consequences of alterations in bronchial contractility on the airway responsiveness, the histamine provocation test (PC20) was measured as secondary variable.
The intervention resulted in a mean (SD) decrease in base excess from -0.5 (±1.4) to -3.9 (±1.1) mmol/L (p < 0.01) and a decrease in pH from 7.41 (±0.02) to 7.36 (±0.02) (p < 0.01). This caused a statistically significant increase in sGaw from 1.15 (±0.16) to 1.26 (±0.13) 1/kPa.s) (p < 0.05). Tendencies towards increase were found in PEF (7.79 (±2.2) versus 8.09 (±1.9) (NS, p = 0.10) and in FEV1 (2.98 (±0.9) versus 3.06 (±0.9) (NS, p = 0.15). PC20 did not change significantly.
It was concluded that acute metabolic acidosis has a modest bronchodilating effect in patients with asthma. |
|---|---|
| AbstractList | The objective was to investigate whether acute metabolic acidosis could cause bronchodilation in patients with asthma. Twelve patients with asthma (8 females, mean age 39 (+/- SD 12) years, forced expiratory volume in 1 second [FEV(1)] 93 [+/-9] % predicted, PC(20) 1.9 (+/-1.0) mg/mL) participated in a double-blind, placebo-controlled trial. Subjects ingested calculated amounts of ammonium chloride to induce acidosis or saline as placebo, in random order, each on a separate day. Airway resistance (R(aw)), specific airway conductance (sG(aw)), FEV(1), and PEF were measured as primary variables. To evaluate the consequences of alterations in bronchial contractility on the airway responsiveness, the histamine provocation test (PC(20)) was measured as secondary variable. The intervention resulted in a mean (SD) decrease in base excess from -0.5 (+/-1.4) to -3.9 (+/-1.1) mmol/L (p < 0.01) and a decrease in pH from 7.41 (+/-0.02) to 7.36 (+/-0.02) (p < 0.01). This caused a statistically significant increase in sG(aw) from 1.15 (+/-0.16) to 1.26 (+/-0.13) 1/kPa.s) (p < 0.05). Tendencies towards increase were found in PEF (7.79 (+/-2.2) versus 8.09 (+/-1.9) (NS, p = 0.10) and in FEV(1) (2.98 (+/-0.9) versus 3.06 (+/-0.9) (NS, p = 0.15). PC(20) did not change significantly. It was concluded that acute metabolic acidosis has a modest bronchodilating effect in patients with asthma.The objective was to investigate whether acute metabolic acidosis could cause bronchodilation in patients with asthma. Twelve patients with asthma (8 females, mean age 39 (+/- SD 12) years, forced expiratory volume in 1 second [FEV(1)] 93 [+/-9] % predicted, PC(20) 1.9 (+/-1.0) mg/mL) participated in a double-blind, placebo-controlled trial. Subjects ingested calculated amounts of ammonium chloride to induce acidosis or saline as placebo, in random order, each on a separate day. Airway resistance (R(aw)), specific airway conductance (sG(aw)), FEV(1), and PEF were measured as primary variables. To evaluate the consequences of alterations in bronchial contractility on the airway responsiveness, the histamine provocation test (PC(20)) was measured as secondary variable. The intervention resulted in a mean (SD) decrease in base excess from -0.5 (+/-1.4) to -3.9 (+/-1.1) mmol/L (p < 0.01) and a decrease in pH from 7.41 (+/-0.02) to 7.36 (+/-0.02) (p < 0.01). This caused a statistically significant increase in sG(aw) from 1.15 (+/-0.16) to 1.26 (+/-0.13) 1/kPa.s) (p < 0.05). Tendencies towards increase were found in PEF (7.79 (+/-2.2) versus 8.09 (+/-1.9) (NS, p = 0.10) and in FEV(1) (2.98 (+/-0.9) versus 3.06 (+/-0.9) (NS, p = 0.15). PC(20) did not change significantly. It was concluded that acute metabolic acidosis has a modest bronchodilating effect in patients with asthma. The objective was to investigate whether acute metabolic acidosis could cause bronchodilation in patients with asthma. Twelve patients with asthma (8 females, mean age 39 (± SD 12) years, forced expiratory volume in 1 second [FEV1] 93 [±9] % predicted, PC20 1.9 (±1.0) mg/mL) participated in a double-blind, placebo-controlled trial. Subjects ingested calculated amounts of ammonium chloride to induce acidosis or saline as placebo, in random order, each on a separate day. Airway resistance (Raw), specific airway conductance (sGaw), FEV1, and PEF were measured as primary variables. To evaluate the consequences of alterations in bronchial contractility on the airway responsiveness, the histamine provocation test (PC20) was measured as secondary variable. The intervention resulted in a mean (SD) decrease in base excess from -0.5 (±1.4) to -3.9 (±1.1) mmol/L (p < 0.01) and a decrease in pH from 7.41 (±0.02) to 7.36 (±0.02) (p < 0.01). This caused a statistically significant increase in sGaw from 1.15 (±0.16) to 1.26 (±0.13) 1/kPa.s) (p < 0.05). Tendencies towards increase were found in PEF (7.79 (±2.2) versus 8.09 (±1.9) (NS, p = 0.10) and in FEV1 (2.98 (±0.9) versus 3.06 (±0.9) (NS, p = 0.15). PC20 did not change significantly. It was concluded that acute metabolic acidosis has a modest bronchodilating effect in patients with asthma. The objective was to investigate whether acute metabolic acidosis could cause bronchodilation in patients with asthma. Twelve patients with asthma (8 females, mean age 39 (± SD 12) years, forced expiratory volume in 1 second [FEV 1 ] 93 [±9] % predicted, PC 20 1.9 (±1.0) mg/mL) participated in a double-blind, placebo-controlled trial. Subjects ingested calculated amounts of ammonium chloride to induce acidosis or saline as placebo, in random order, each on a separate day. Airway resistance (R aw ), specific airway conductance (sG aw ), FEV 1 , and PEF were measured as primary variables. To evaluate the consequences of alterations in bronchial contractility on the airway responsiveness, the histamine provocation test (PC 20 ) was measured as secondary variable. The intervention resulted in a mean (SD) decrease in base excess from -0.5 (±1.4) to -3.9 (±1.1) mmol/L (p < 0.01) and a decrease in pH from 7.41 (±0.02) to 7.36 (±0.02) (p < 0.01). This caused a statistically significant increase in sG aw from 1.15 (±0.16) to 1.26 (±0.13) 1/kPa.s) (p < 0.05). Tendencies towards increase were found in PEF (7.79 (±2.2) versus 8.09 (±1.9) (NS, p = 0.10) and in FEV 1 (2.98 (±0.9) versus 3.06 (±0.9) (NS, p = 0.15). PC 20 did not change significantly. It was concluded that acute metabolic acidosis has a modest bronchodilating effect in patients with asthma. The objective was to investigate whether acute metabolic acidosis could cause bronchodilation in patients with asthma. Twelve patients with asthma (8 females, mean age 39 (+/- SD 12) years, forced expiratory volume in 1 second [FEV(1)] 93 [+/-9] % predicted, PC(20) 1.9 (+/-1.0) mg/mL) participated in a double-blind, placebo-controlled trial. Subjects ingested calculated amounts of ammonium chloride to induce acidosis or saline as placebo, in random order, each on a separate day. Airway resistance (R(aw)), specific airway conductance (sG(aw)), FEV(1), and PEF were measured as primary variables. To evaluate the consequences of alterations in bronchial contractility on the airway responsiveness, the histamine provocation test (PC(20)) was measured as secondary variable. The intervention resulted in a mean (SD) decrease in base excess from -0.5 (+/-1.4) to -3.9 (+/-1.1) mmol/L (p < 0.01) and a decrease in pH from 7.41 (+/-0.02) to 7.36 (+/-0.02) (p < 0.01). This caused a statistically significant increase in sG(aw) from 1.15 (+/-0.16) to 1.26 (+/-0.13) 1/kPa.s) (p < 0.05). Tendencies towards increase were found in PEF (7.79 (+/-2.2) versus 8.09 (+/-1.9) (NS, p = 0.10) and in FEV(1) (2.98 (+/-0.9) versus 3.06 (+/-0.9) (NS, p = 0.15). PC(20) did not change significantly. It was concluded that acute metabolic acidosis has a modest bronchodilating effect in patients with asthma. |
| Author | Van Den Elshout, F. J.J. Brijker, F. Bosch, F. H. Folgering, H. Th.M. Heijdra, Y. F. |
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| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/19728200$$D View this record in MEDLINE/PubMed |
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| SubjectTerms | Acidosis - chemically induced Administration, Oral Adult Airway Resistance - drug effects Airway Resistance - physiology Ammonium Chloride - administration & dosage Ammonium Chloride - pharmacology Ammonium Chloride - therapeutic use asthma Asthma - drug therapy Asthma - physiopathology Bronchial Hyperreactivity - drug therapy Bronchial Hyperreactivity - physiopathology bronchodilation Double-Blind Method Female Forced Expiratory Volume - drug effects Forced Expiratory Volume - physiology Humans Hydrogen-Ion Concentration - drug effects In Vitro Techniques Male metabolic acidosis Middle Aged Peak Expiratory Flow Rate - drug effects Peak Expiratory Flow Rate - physiology specific airway conductance Treatment Outcome |
| Title | Metabolic Acidosis Improves Airway Conductance in Patients with Asthma |
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