Comparison of Respiratory Effects of Two Cardioselective Beta-Blockers, Celiprolol and Atenolol, in Asthmatics: Results

In: Asthma

8 Oct 2014

Acute Single-Dose Drug Challenge
Following the single-dose challenge with atenolol, the FEVx, FVC and PEF fell progressively during 3 h, and were significantly lower at the end of the 3 h (p<0.01), but improved significantly (p<0.05) to prechallenge levels after treatment with salbutamol inhaler (Fig 2). After celiprolol therapy, the FEVj, FVC and PEF remained unchanged, yet responsiveness to salbutamol was retained. No deterioration in spiro-metric parameters was seen when placebo was given.
The single-dose response following two weeks of maintenance beta-blocker therapy was similar to that seen when placebo was given.
Long-Term Control of Asthma
Day-to-day control of asthma was no different with either atenolol or celiprolol therapy when compared with placebo therapy (Fig 3, Table 3). This was true for cough and asthma symptom scores, mean peak flow measurements taken twice daily and frequency of inhaler use. Seven patients regularly used a bron-chodilator (Table 1). canadian family pharmacy

In this study on a small group of selected patients Adth coexisting hypertension and asthma, a singledose challenge with atenolol, 100 mg, caused bron-choconstriction in most subjects, while the response to single-dose challenge with celiprolol, 400 mg, closely resembled that with placebo. Without the sustained bronchodilator benefit of beta-2 agonists during the preceding 10-h period, the adverse effect of atenolol on FEVi, FVC and PEF was obvious. Following salbutamol inhalation, respiratory parameters improved to prechallenge levels (p<0.05), suggesting that atenolol, 100 mg, is sufficiently cardio-selective to preserve a clinical bronchial responsiveness to beta-2 agonists.
Similarly, after celiprolol, bronchial responsiveness to the salbutamol was retained. The fact that further bronchodilation could be achieved by salbutamol suggests that any intrinsic sympathomimetic activity on the bronchial tree is minor compared with salbutamol. Pruss et al have suggested that the bronchodilatory effect of celiprolol is not due to beta-2 ISA, since it is unaffected by pretreatment with propranolol in the cat model. Other beta-blockers possessing ISA, such as oxprenolol, acebutolol and pindolol, have not shown bronchosparing properties in single-dose studies. Celiprolol did not cause any bradycardia, which may be explained by its peripheral vasodilatory properties, although beta-1 agonist effects cannot be excluded.

Figure 2. Acute single-dose challenge with beta-blocker or placebo.

Figure 2. Acute single-dose challenge with beta-blocker or placebo.

Figure 3. Effects of celiprolol and atenolol during chronic therapy on morning and evening PEF (means ± SEM). Differences between placebo, celiprolol and atenolol were not significant.

Figure 3. Effects of celiprolol and atenolol during chronic therapy on morning and evening PEF (means ± SEM). Differences between placebo, celiprolol and atenolol were not significant.

Table 3—Effects of Celiprolol and Atenolol During Chronic Therapy on Symptoms and Inhaler Use in Asthmatic Subjects During Chronic Therapy

Day Night
Asthma scores
Placebo 1.9 ±0.16 1.5 ±0.13
Celiprolol 1.9 ±0.12 1.6±0.13
Atenolol 1.9±0.16 1.7±0.20
Cough scores
Placebo 1.9±0.18 1.7±0.18
Celiprolol 1.7 ±0.10 1.7±0.16
Atenolol 1.8 ±0.16 1.9 ±0.24
Inhaler use
Placebo 1.7±0.69 0.7 ±0.33
Celiprolol 1.7±0.66 1.3 ±0.63
Atenolol 1.6±0.77 1.2 ±0.59

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