Abstract
In1948Nelson andFitzhugh fedsmalldosesof chloroquine toratsoveraperiod oftwoyears and showedthattheydeveloped skeletal muscle lesions. Thisappears tohavebeenforgotten for15years until Whisnant, Espinosa, Kierland, andLambert(1963) published their biopsy findings onfourpatients who haddeveloped muscle weakness whiletaking 2501,000 mg.ofchloroquine adayforseveral months toseven years. Theseshowedmuscle damage with vacuolar myopathy. Muscle necrosis isnotacommonlyreported side effect ofdrugs, andinviewofthe fact thatchloroquine isnowbeing usedasamalaria prophylactic, itwasdecided totryandinvestigate the modeofproduction ofchloroquine myopathy. MATERIAL AND METHODS Tenrabbits ofmixedbreed weighing 1-2kg.weregiven 25mg.ofchloroquine phosphate perkilogram ofbody weight daily. Insixanimals this wasgiven intablet form bymouthandinfourbyintramuscular injection. The numberofdoses given toeachanimal ranged fromseven to42. Thecerebrum, cerebellum, spinal cord, posterior root ganglia, peripheral nerve, heart, kidney, liver, lung, and skeletal musclewereexamined inparaffin sections. Themuscles examined weretheerector spinae, quadriceps femoris, gluteus maximus, tibialis anterior, soleus and triceps brachii. Peripheral nerveswerestained with osmiumtetroxide, teased andexamined undera lowpowermicroscope. Silver impregnations weredoneonthe terminal innervation inthemuscle bySchofield's method. Theskeletal muscle wasalsoexamined histochemically using techniques forphosphorylase (Takeuchi andKuriaki, 1955), succinic dehydrogenase withmenadione (WattenbergandLeong,1960), andacidphosphatase (Holt, 1959).
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