Australian veterinary journal · 2004
An assessment of the safety of copper heptonate for parenteral therapy in sheep.
Клиническое исследованиеСтатьяРандомизированное исследованиеПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Judson G J, Babidge P J
Аннотация
OBJECTIVE: To investigate any adverse effects of an intramuscular injection (i.m.) of copper heptonate (CuHep) in sheep.
PROCEDURE: Merino wethers about 9 months old were retained in pens and given 1 or 2 mg Cu/kg body weight as CuHep or no Cu treatment. Sheep were weighed and samples of blood for haematology, Cu and enzyme assay and tissues for Cu and Fe assay were collected before and at intervals over 21 days after treatment.
RESULTS: CuHep was removed from the injection site within 7 days of treatment and most of it was retained in the liver. Wethers had adequate liver Cu reserves before treatment and the higher dosage of CuHep raised liver Cu to values associated with Cu toxicity. No clinical signs of Cu toxicity were evident. Transient increases in plasma activity of the liver enzyme glutamate dehydrogenase suggested mild liver necrosis due to CuHep, but there was no histopathological evidence of liver necrosis 7 days after treatment.
CONCLUSIONS: I.m. injection of Cu as CuHep appears to be readily transferred to the liver. No significant necrosis is caused at the injection site.
PROCEDURE: Merino wethers about 9 months old were retained in pens and given 1 or 2 mg Cu/kg body weight as CuHep or no Cu treatment. Sheep were weighed and samples of blood for haematology, Cu and enzyme assay and tissues for Cu and Fe assay were collected before and at intervals over 21 days after treatment.
RESULTS: CuHep was removed from the injection site within 7 days of treatment and most of it was retained in the liver. Wethers had adequate liver Cu reserves before treatment and the higher dosage of CuHep raised liver Cu to values associated with Cu toxicity. No clinical signs of Cu toxicity were evident. Transient increases in plasma activity of the liver enzyme glutamate dehydrogenase suggested mild liver necrosis due to CuHep, but there was no histopathological evidence of liver necrosis 7 days after treatment.
CONCLUSIONS: I.m. injection of Cu as CuHep appears to be readily transferred to the liver. No significant necrosis is caused at the injection site.