outlawtas2 said:
Doc, do you know of any heart studies done with albuterol? I'm under the impression it's fairly new, so I dunno if anything's been done yet.
Most studies showing cardiac problems were on patients who already had heart problems and the albuterol made them worse (big suprise). I did find this though, again like with the clen studies all done on rats:
Arch Toxicol. 1994;68(4):213-6.
A review of the toxicology of salbutamol (albuterol).Libretto SE.
Pathology and Toxicology Division, Glaxo Group Research Ltd., Ware, Hertfordshire, United Kingdom.
This paper reviews the published toxicology of salbutamol. Salbutamol is a relatively selective beta 2-adrenoreceptor stimulant with rapid, potent bronchodilator activity and only minor inotropic or chronotropic effects. It was not found to be mutagenic. LD50 values and other acute studies indicated low toxicity. Findings published for repeat dose studies were mainly uneventful. Tachycardia and flushing of the skin were observed in dogs. There were several findings peculiar to the rat--growth of the salivary gland, enlargement of the Harderian gland, an increase in colloid in the pituitary, and mesovarian leiomyomas.
Increases in heart weights associated with inflammation, hypertrophy of muscle fibres, focal myocardial necrosis and fibrosis were seen in rats. Malformation, in the form of cleft palate, was reported in mice but not in rats or rabbits. These treatment related effects reported for salbutamol are not compound-related but rather are class-related. They are an expression of pharmacological activity brought about by the excessive beta stimulant action of high dosage with the drug.
PMID: 8067892 [PubMed - indexed for MEDLINE]
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Here's one on muscle hypertrophy:
Br J Pharmacol. 2006 Mar;147(6):587-95.
Systemic administration of beta2-adrenoceptor agonists, formoterol and salmeterol, elicit skeletal muscle hypertrophy in rats at micromolar doses.Ryall JG, Sillence MN, Lynch GS.
Basic and Clinical Myology Laboratory, Department of Physiology, The University of Melbourne, Grattan Street, Victoria 3010, Australia.
beta(2)-Adrenoceptor agonists provide a potential therapy for muscle wasting and weakness, but their use may be limited by adverse effects on the heart, mediated in part, by beta(1)-adrenoceptor activation. Two beta(2)-agonists, formoterol and salmeterol, are approved for treating asthma and have an extended duration of action and increased safety, associated with greater beta(2)-adrenoceptor selectivity. The pharmacological profiles of formoterol and salmeterol and their effects on skeletal and cardiac muscle mass were investigated in 12-week-old, male F344 rats. Formoterol and salmeterol were each administered via daily i.p. injection at one of seven doses (ranging from 1 to 2,000 microg kg(-1) day(-1)), for 4 weeks. Rats were anaesthetised and the EDL and soleus muscles and the heart were excised and weighed. Dose-response curves were constructed based on skeletal and cardiac muscle hypertrophy. Formoterol was more potent than salmeterol, with a significantly lower ED(50) in EDL muscles (1 and 130 microg kg(-1) day(-1), P <0.05), whereas salmeterol had greater intrinsic activity than formoterol in both EDL and soleus muscles (12% greater hypertrophy than formoterol). The drugs had similar potency and intrinsic activity in the heart, with a smaller leftward shift for formoterol than seen in skeletal muscle. A dose of 25 microg kg(-1) day(-1) of formoterol elicited greater EDL and soleus hypertrophy than salmeterol, but resulted in similar beta-adrenoceptor downregulation.
These results show that doses as low as 1 microg kg(-1) day(-1) of formoterol can elicit significant muscle hypertrophy with minimal cardiac hypertrophy and provide important information regarding the potential therapeutic use of formoterol and salmeterol for muscle wasting.
PMID: 16432501 [PubMed - indexed for MEDLINE]