Ineffectiveness of beta-adrenergic blockers on ventilatory response to carbon dioxide

Ahmad, Dildar; Hamilton, John T. G.; Carruthers, S. George

doi:10.1038/clpt.1982.162

Cited by 5 publications

(2 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…With rebreathing techniques, however, controversial results have been reported concerning C 0 2 sensi tivity after propranolol [5,6,8,21,22,28,29,36,37] and several other (3-adrenergic blocking drugs [6,21,22,37]. From these results it is unclear whether (3-blockade af fects the ventilatory response or the C 0 2-dependent central drive.…”

Section: Introductioncontrasting

confidence: 45%

“…The measurement of ventilatory re sponse to carbon dioxide is well estab lished as a method of assessing the action of drugs on ventilatory drive [36], Pro pranolol and several other (3-adrenergic blocking drugs have been shown to have a significant influence on the CO; respon siveness [5,8,28,36], while other investi gators did not find any changes following beta-blockade [6,21,22,29,37], In all of these studies, the (modified) Read Method [31] was used and measurements were evaluated in terms of slope and intercept values [32], Unlike previous investigators, we mea sured both FIco; and PaCo; instead of PAco,. Thus, during room air breathing, the effects of bupranolol on ventilation must be interpreted with respect to PaCO; as the dependent variable.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Differential Effects of Beta-Adrenergic Blockade on P<sub>0.1</sub> and Mean Inspiratory Flow

Chowanetz¹,

Balk²,

Jany³

1988

Respiration

View full text Add to dashboard Cite

To quantitatively examine and compare the effects of β-adrenergic blockade on ventilation, we studied 20 healthy volunteers during inhalation of room air and at steady state CO₂ (2.0, 4.4, 6.0%) following a single oral dose of bupranolol (vs. placebo). During room air breathing, minute ventilation (V_E) and mean inspiratory flow (V_τ/Tι) were significantly reduced after β-blockade with a concomitant increase in blood Pa_CO2 (p < 0.01). The timing factor Tι/T_tot and mouth occlusion pressure P_0.1 remained unchanged. These differences were, as shown from calculated effective alveolar ventilation, mainly attributed to a decrease in physiological dead space ventilation following β-blockade. With a stepwise increase in FI_CO2, the difference in Pa_CO2 between placebo and bupranolol tended to approach zero, whereas V_E and V_τ/Tι remained significantly lower during β-blockade (P < 0.05). In contrast, no difference existed in P_0.1 between bupranolol and placebo. We suggest that (1) respiratory drive assessed by P_0.1 is unaffected by β-blockade and (2) mean inspiratory flow depends also on CO₂ elimination characteristics, which are influenced by β-blockade

show abstract

Section: Introductioncontrasting

confidence: 45%

Section: Discussionmentioning

confidence: 99%

Differential Effects of Beta-Adrenergic Blockade on P<sub>0.1</sub> and Mean Inspiratory Flow

Chowanetz¹,

Balk²,

Jany³

1988

Respiration

View full text Add to dashboard Cite

show abstract

Influence of cardioselectivity and respiratory disease on pulmonary responsiveness to beta-blockade

Clague

Ahmad

Carruthers

1984

Eur J Clin Pharmacol

View full text Add to dashboard Cite

The effects on ventilation of the non-selective beta-blocker propranolol, and the relatively cardioselective beta-blocker, metoprolol, were compared in a randomized single-blind crossover study in 16 patients with asthma, bronchitis and emphysema (American Thoracic Society criteria). Group I had "fixed" airways disease with less than 20% improvement in FEV1 following inhaled salbutamol 5 mg by nebuliser. Group II had "reversible" obstruction, greater than 20% improvement. Bronchodilator therapy was withheld for 24 h with the exception of aerosols which were permitted until 12 h before study. After control observations on each of 2 study days, each patient received cumulative doses of propranolol (maximum 170 mg) and metoprolol (maximum 187.5 mg). Ventilatory function (FEV1, FVC, FEV1%) was assessed at 0, 2, 4, 6 and 8 h. In Group I, 2 patients were unable to complete the study. One patient became dizzy with propranolol 70 mg but tolerated metoprolol 187.5 mg. One patient developed wheeze with propranolol 15 mg but tolerated metoprolol 187.5 mg. Metoprolol was tolerated in all 8 patients with "fixed" disease, although FEV1 was reduced by more than 30% in 1 patient. Three patients in Group II did not complete the study because of wheezing following propranolol 10 mg, metoprolol 37.5 mg; propranolol 17.5 mg, metoprolol 37.5 mg; propranolol 45 mg, tolerated metoprolol 187.5 mg respectively. Wheezing responded in all cases to inhaled isoprenaline. The response to either propranolol or metoprolol was unpredictable in patients with "reversible" disease. When wheezing occurred in this group, it developed following small, potentially subtherapeutic doses of each drug. Although metoprolol was better tolerated, the practical benefit of cardioselectivity in those patients with reversible airways disease was negligible.

show abstract

Alpha-and Beta-Adrenoceptor Antagonists

Foëx

1984

British Journal of Anaesthesia

View full text Add to dashboard Cite

Ineffectiveness of beta-adrenergic blockers on ventilatory response to carbon dioxide

Cited by 5 publications

References 0 publications

Differential Effects of Beta-Adrenergic Blockade on P<sub>0.1</sub> and Mean Inspiratory Flow

Differential Effects of Beta-Adrenergic Blockade on P<sub>0.1</sub> and Mean Inspiratory Flow

Influence of cardioselectivity and respiratory disease on pulmonary responsiveness to beta-blockade

Alpha-and Beta-Adrenoceptor Antagonists

Contact Info

Product

Resources

About