Metabolic and cardiovascular side effects of the beta 2‐adrenoceptor agonists salbutamol and rimiterol.

Phillips, Pat; Vedig, AE; Jones, Peter; Chapman, M. G.; Collins, Michael D.; Jb, Edwards; Smeaton, TC; Duncan, B M

doi:10.1111/j.1365-2125.1980.tb05844.x

Cited by 84 publications

(46 citation statements)

References 35 publications

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“…There are a small number of reports of elevated lactate levels with intravenous salbutamol [1,2], with intravenous and nebulised salbutamol combined [3,4], and with inhaled salbutamol alone [5,6]. We were unable to find evidence of why only some patients develop hyperlactaemia, or the specific dose of salbutamol required to produce this unusual phenomenon.…”

contrasting

confidence: 44%

“…We were unable to find evidence of why only some patients develop hyperlactaemia, or the specific dose of salbutamol required to produce this unusual phenomenon. Both Massara and colleagues [1] and Phillips and colleagues [2] used 'therapeutic' infusions of intravenous salbutamol and observed a rise in lactate levels. Rodrigo and Rodrigo studied 18 patients with acute severe asthma [5].…”

mentioning

confidence: 99%

“…Both the use of volatile agent and the AnaConDa have been described for ICU sedation [2,3] but in the light of the practicalities, familiarity, efficacy, cost and safety of intravenous sedation regimes in the ICU, we wanted to be able to justify volatile use. Suffice to say the only valid alternative we have come up with so far was its use for postoperative sedation following cardiac surgery.…”

mentioning

confidence: 99%

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Hyperlactaemia due to nebulised salbutamol

Jee¹,

Brownlow²

2007

Anaesthesia

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confidence: 44%

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confidence: 99%

mentioning

confidence: 99%

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Hyperlactaemia due to nebulised salbutamol

Jee¹,

Brownlow²

2007

Anaesthesia

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“…In the present studies both H-I 42 and atenolol competitively blocked an isoprenaline tachycardia with the effect of 400 mg H-I 42 being less than atenolol. The isoprenaline induced increase in blood glucose, serum insulin, serum potassium (Leitch etal., 1976) and serum lactate (Phillips et al, 1980) are all 02-adrenoceptor mediated responses. There was no difference in the change of these metabolic parameters after any of the treatments.…”

Section: Discussionmentioning

confidence: 94%

The assessment in man of the beta‐adrenoceptor blocking activity and cardioselectivity of H‐I 42 BS, a long acting beta‐adrenoceptor blocking drug.

Pringle

Deering

Scott

et al. 1987

Brit J Clinical Pharma

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Ireland1 The pharmacokinetic and pharmacodynamic effects of the ,3-adrenoceptor antagonist H-I 42 BS were examined in healthy subjects. 2 In an open dose ranging study, H-I 42 BS 50, 100, 200 and 400 mg were given as single oral doses to four subjects. H-I 42 BS 400 mg caused maximum reduction in exercise heart rate (20.4 ± 1.0% -mean ± s.d.) at 4 h and still reduced exercise heart rate at 96 h (18.4 ± 7.2%). 3 Seven subjects received in double-blind, randomised order, single oral doses of H-I 42 BS 50, 100 and 200 mg, atenolol 50 and 100 mg and placebo. H-I 42 BS 400 mg was given in a single blind manner as the last dose of the study. Both H-I 42 BS and atenolol reduced supine and standing heart rate and systolic blood pressure (P < 0.05) although atenolol had the more marked effect. The maximum percent reduction of exercise heart rate after H-I 42 BS 50 mg was 10.9 ± 7.1%, after 100 mg was 18.7 ± 5.8%, after 200 mg was 20.6 + 6.4% and after 400 mg was 21.9 ± 8.2%. H-I 42 BS 400 mg still caused 11.0 ± 3.5% reduction at 168 h. Atenolol 50 mg caused maximum percent reduction of exercise heart rate of 26.0 ± 6.0% but did not reduce exercise heart rate after 24 h. 4 The mean peak plasma concentrations for all doses of H-I 42 BS occurred at 5.1 ± 1.5 h. The plasma elimination half-life was 47.6 ± 8.1 h. There was a linear correlation between the dose and AUCO-o (r = 0.97). 5 The cardioselectivity of H-I 42 BS and atenolol was compared. Six subjects received in double-blind random order H-I 42 BS 100 and 400 mg, atenolol 50 mg and placebo. After each dose, graded infusions of isoprenaline were given until the heart rate increased by 50 beats min-1 . Dose-response curves for heart rate, diastolic blood pressure, forearm blood flow and finger tremor were constructed. 6 There was no difference in the dose-response curves for forearm blood flow or finger tremor after H-I 42 BS400 mg or atenolol 50 mg. Atenolol 50 mg caused more attenuation (P < 0.01) of the diastolic blood pressure response. 7 These results indicate that H-I 42 BS is a cardioselective ,B-adrenoceptor antagonist with a long duration of action in man.

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“…Salbutamol has been shown to increase supine heart rate in previous studies (Leitch et al, 1976;Philips et al, 1980;Kennedy & Simpson, 1969) and the specific 32-adrenoceptor antagonist, ICI 118,551 (Bilski et al, 1983) has been shown to abolish this increase in heart rate (McCaffrey et al, 1986) indicating that it is mediated by the 12-adrenoceptor. However the mechanism of the rise in heart rate is unclear and may be partly reflex, secondary to peripheral vasodilation or due to direct stimulation of P2-adrenoceptors in the heart (Stiles et al, 1983) or stimulation of presynaptic 132-adrenoceptors facilitating noradrenaline release at the sympathetic nerve endings (Stjarne & Brundin, 1976).…”

Section: Discussionmentioning

confidence: 99%

An assessment of the partial agonist activity of Ro 31‐1118, flusoxolol and pindolol in man.

McCaffrey

Riddell

Shanks

1987

Brit J Clinical Pharma

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1. The effects of single oral doses of three beta‐adrenoceptor partial agonists (Ro 31‐1118, flusoxolol and pindolol), two beta‐adrenoceptor antagonists (propranolol and atenolol), two beta‐adrenoceptor agonists (salbutamol and prenalterol) and placebo on sleeping heart rate, quality of sleep, supine heart rate, exercise heart rate, blood pressure, forearm blood flow and finger tremor were studied in eight healthy male volunteers. 2. Sleeping heart rate was increased by Ro 31‐ 1118, flusoxolol, pindolol, salbutamol and prenalterol and decreased by propranolol and atenolol. 3. None of the drugs studied affected quality of sleep. 4. Supine heart rate was increased by flusoxolol, prenalterol and salbutamol, unaffected by Ro 31‐1118 and pindolol and reduced by propranolol and atenolol. 5. Exercise heart rate was reduced by both beta‐adrenoceptor antagonists and the three partial agonists and unaffected by salbutamol and prenalterol. 6. Systolic blood pressure was increased by Ro 31‐1118, flusoxolol, salbutamol and prenalterol, unaffected by pindolol and reduced by propranolol and atenolol. Diastolic blood pressure was reduced by salbutamol and prenalterol. 7. Forearm blood flow was increased by Ro 31‐1118, salbutamol and prenalterol, unchanged by pindolol and flusoxolol and decreased by atenolol and propranolol. 8. Finger tremor was increased by Ro 31‐1118, flusoxolol, pindolol, salbutamol, and prenalterol. 9. beta‐adrenoceptor partial agonists have different effects on the cardiovascular system and finger tremor to beta‐adrenoceptor antagonists. 10. While Ro 31‐ 1118 and flusoxolol are antagonists mainly at the beta 1‐adrenoceptor they have agonist activity at both beta 1‐ and beta 2 adrenoceptors. 11. While pindolol is a non‐selective antagonist its agonist activity is mainly at the beta 2‐adrenoceptor.

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Metabolic and cardiovascular side effects of the beta 2‐adrenoceptor agonists salbutamol and rimiterol.

Cited by 84 publications

References 35 publications

Hyperlactaemia due to nebulised salbutamol

Hyperlactaemia due to nebulised salbutamol

The assessment in man of the beta‐adrenoceptor blocking activity and cardioselectivity of H‐I 42 BS, a long acting beta‐adrenoceptor blocking drug.

An assessment of the partial agonist activity of Ro 31‐1118, flusoxolol and pindolol in man.

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