Case Description—3 Quarter Horse racehorses were examined for suspected clenbuterol overdose 12 to 24 hours after administration by mouth of a compounded clenbuterol product.
Clinical Findings—All horses developed sinus tachycardia, muscle tremors, hyperhidrosis, and colic. Abnormalities on serum biochemical analysis included hyperglycemia, azotemia, and high creatine kinase activity. The presence of clenbuterol in the serum of all 3 horses and in the product administered was confirmed and quantified by use of liquid chromatography-electrospray tandem mass spectrometry.
Treatment and Outcome—Propranolol (0.01 mg/kg [0.005 mg/lb], IV) was administered to all 3 horses for antagonism of β-adrenergic effects and caused a transient decrease in heart rate in all patients. All horses also received crystalloid fluids IV and other supportive treatment measures. Two horses were euthanatized (2 and 4 days after admission) because of complications. One horse recovered and was discharged 4 days after admission to the hospital. In the 2 nonsurviving horses, skeletal and cardiac muscle necrosis was evident at necropsy, and tissue clenbuterol concentrations were highest in the liver.
Clinical Relevance—Clenbuterol is a β2-adrenergic receptor agonist licensed for veterinary use as a bronchodilator. At doses ≥ 10 2μg/kg (4.5 μg/lb), in excess of those normally prescribed, β-adrenergic stimulation by clenbuterol may cause sustained tachycardia, muscle tremors, hyperglycemia, and cardiac and skeletal muscle necrosis. Laminitis, acute renal failure, rhabdomyolysis, and cardiomyopathy were fatal complications associated with clenbuterol overdose in 2 horses in the present report. At the dose administered, propranolol was effective for short-term control of sinus tachycardia, but it did not alleviate all clinical signs in patients in the present report. These cases demonstrated the risks associated with the use of nonprescribed compounded medications for which the ingredients may be unknown.
Objective—To determine the effects of clenbuterol, at a dosage of up to 3.2 μg/kg for 14 days, PO, on skeletal and cardiac muscle in healthy horses undergoing treadmill exercise.
Animals—12 healthy horses from 3 to 10 years old.
Procedures—Horses were randomly assigned to a control group (n = 6) or clenbuterol group (6) and received either saline (0.9% NaCl) solution or clenbuterol, PO, every 12 hours for 14 days. Horses were subjected to submaximal treadmill exercise daily during treatment. Muscle biopsy specimens were collected before and after treatment for determination of apoptosis. Echocardiographic measurements, serum clenbuterol and cardiac troponin I concentrations, and serum activities of creatine kinase and aspartate aminotransferase were measured before, during, and after treatment. Jugular venous blood samples were collected every 3 days during treatment. Echocardiography was repeated every 7 days after beginning treatment. Response variables were compared between treatment groups and across time periods.
Results—No significant effect of clenbuterol or exercise on response variables was found between treatment and control groups at any time point or within groups over time.
Conclusions and Clinical Relevance—Results did not reveal any adverse effects of treatment with an approved dose of clenbuterol on equine cardiac or skeletal muscle in the small number of horses tested.
Objective—To determine whether the basis for recurrent
exertional rhabdomyolysis (RER) in Thoroughbreds
lies in an alteration in the activation and regulation
of the myofibrillar contractile apparatus by ionized
Animals—4 Thoroughbred mares with RER and 4
clinically normal (control) Thoroughbreds.
Procedure—Single chemically-skinned type-I (slowtwitch)
and type-II (fast-twitch) muscle fibers were
obtained from punch biopsy specimens, mounted to
a force transducer, and the tensions that developed in
response to a series of calcium concentrations were
measured. In addition, myofibril preparations were
isolated from muscle biopsy specimens and the maximal
myofibrillar ATPase activity, as well as its sensitivity
to ionized calcium, were measured.
Results—Equine type-I muscle fibers were more
readily activated by calcium than were type-II muscle
fibers. However, there was no difference between
the type-II fibers of RER-affected and control horses
in terms of calcium sensitivity of force production.
There was also no difference between muscle
myofibril preparations from RER-affected and control
horses in calcium sensitivity of myofibrillar ATPase
Conclusion and Clinical Relevance—An alteration
in myofibrillar calcium sensitivity is not a basis for
pathologic contracture development in muscles from
RER-affected horses. Recurrent exertional rhabdomyolysis
in Thoroughbreds may represent a novel heritable
defect in the regulation of muscle excitation-contraction
coupling or myoplasmic calcium concentration.
(Am J Vet Res 2001;62:1647–1652)