Injured mitochondria are then unable to maintain homeostasis, resulting in cell death or segmental necrosis (4)

Injured mitochondria are then unable to maintain homeostasis, resulting in cell death or segmental necrosis (4). the calf was in lateral recumbency and appeared comatose. VU6005649 The extremities were cool and dehydration was about 5%. The sucking reflex was diminished. The body temperature could not be registered with an electronic digital thermometer ( 32C), the heart rate was 124 beats/min, and the respiratory rate 36 breaths/min. Total serum protein was 61 g/L (reference range, 57 to 81 g/L) and the blood glucose 2.7 mmol/L (reference range, 2.5 to 4.2 mmol/L). The calf was warmed with heating lamps and warm water bags placed between its legs and around the abdomen. A bolus of 20 mL of 50% dextrose was given, IV, and followed by a total of 6 L of warm lactated Ringer’s answer made up of 1.4% dextrose over the next 24 h. The calf’s heat increased gradually; next day, the vital signs were normal and she was able to maintain sternal recumbency. However, she did not attempt to stand, even if assisted. The sucking reflex was poor, so she was tube fed milk, 10% of body weight, for the first 48 h. Congenital nutritional muscular dystrophy was suspected. After 48 h, the calf’s condition became stable, but she was still unable to stand. A venous blood sample was submitted for measurement of creatine kinase (CK), aspartate aminotransferase (AST), and vitamin E and selenium. The urine was grossly normal, but GLUR3 on analysis with the use of a urine reagent strip (Chemstrip 9; Roche Diagnostics, Laval, Quebec), it was found to contain blood, hemoglobin, or myoglobin. The markedly high levels of serum CK and AST, and the low serum levels of vitamin E and selenium (Tables 1 and 2) were suggestive of nutritional muscular dystrophy, which would explain the weakness, stiff gait, and the presence of blood (presumably myoglobin) in the urine. The poor sucking reflex may have been due to possible involvement of VU6005649 the tongue muscles. After 272 IU of vitamin E and 6 mg of selenium (Dystosel; Pfizer Canada, Kirkland, Qubec; Selenium [as sodium selenite], 3 mg/mL; and vitamin E [dl-alpha tocopherol acetate] 136 IU/mL), had been given SC on day 2, the serum muscle enzymes were monitored over 5 successive days. The decrease in total protein to 48 g/L after hydration suggested either over hydration or failure of passive transfer of immunoglobulins because of failure to suck after birth. Mature cow’s blood (800 mL) was transfused, IV, VU6005649 into the calf. A trimethoprim and sulfadoxine combination (Trivetrine; Schering-Plough Animal Health, Pointe-Clair, Quebec), 120 mg and 600 mg, respectively, was given, IV, daily for 5 d to prevent contamination and septicemia, which could have occurred in association with the failure of passive transfer of immunoglobulins. The sucking reflex improved 48 h after presentation, but the calf was still given the same amount of milk (10% of body weight) by a nursing bottle. About 72 h after presentation, the calf stood without help but had a stiff gait. Over the next 3 d, the calf continued to improve and was given another dose of 272 IU of vitamin E and 6 mg of selenium, SC. It developed diarrhea that resolved with supportive therapy. The CK and AST levels continued to decrease and become normal (Table 1). Serum levels of vitamin E and selenium also became normal (Table 2). The calf had no difficulty in standing, walking, or running, but it was kept in the clinic to monitor the clinical response and observe the muscle enzymes. Nine days after presentation, the calf was discharged from the clinic. Two months later, the owner reported that this calf was normal and thrifty. Table 1. Open in a separate window Table 2. Open in a separate windows Nutritional muscular dystrophy (NMD) or white muscle disease is caused by a deficiency of vitamin E, selenium, or both 1). Dietary polyunsaturated fatty acids, unaccustomed exercise, and rapid growth are considered as precipitating factors (1,4). It occurs in all farm animal species, especially rapidly growing calves, lambs, kids, and foals (1). Both vitamin E and selenium are important in the protection of cellular membranes from free radicals, which cause peroxidation of the membrane lipids (4). Vitamin E is an antioxidant that decreases hydroperoxide formation and acts at the extracellular or intracellular level to scavenge free radicals (1,4). Selenium is an important biochemical component of the enzyme glutathione peroxidase, an.