Serum creatine kinase response to exercise during dexamethasone-induced insulin resistance in Quarter Horses with polysaccharide storage myopathy

OBJECTIVE: To determine effects of dexamethasone on insulin sensitivity, serum creatine kinase (CK) activity 4 hours after exercise, and muscle glycogen concentration in Quarter Horses with polysaccharide storage myopathy (PSSM). ANIMALS: 4 adult Quarter Horses with PSSM. PROCEDURE: A 2 x 2 crossover design was used with dexamethasone (0.08 mg/kg) or saline (0.9% NaCl) solution administered IV every 48 hours. Horses were exercised on a treadmill daily for 3 wk/treatment with a 2-week washout period between treatments. Serum CK activity was measured daily 4 hours after exercise. At the end of each treatment period, serum cortisol concentrations were measured, a hyperinsulinemic euglycemic clamp (HEC) technique was performed, and muscle glycogen content was determined. RESULTS: Mean +/- SEM serum cortisol concentration was significantly lower after 48 hours for the dexamethasone treatment (0.38 +/- 0.08 mg/dL), compared with the saline treatment (4.15 +/- 0.40 mg/dL). Dexamethasone significantly decreased the rate of glucose infusion necessary to maintain euglycemia during the HEC technique, compared with the saline treatment. Muscle glycogen concentrations and mean CK activity after exercise were not altered by dexamethasone treatment, compared with the saline treatment. CONCLUSIONS AND CLINICAL RELEVANCE: Dexamethasone significantly reduced whole-body insulin-stimulated glucose uptake in Quarter Horses with PSSM after a 3-week period but did not diminish serum CK response to exercise or muscle glycogen concentrations in these 4 horses. Therefore, a decrease in glucose uptake for 3 weeks did not appear to alleviate exertional rhabdomyolysis in these horses. It is possible that long-term treatment may yield other results.     

Histochemical changes in skeletal muscles of four male horses with neuromuscular disease

Skeletal muscle biopsy specimens were taken from 4 male horses with neuromuscular disease such as myotonia congenita, chronic myositis, exertional rhabdomyolysis, and shivers. Histologic and histochemical techniques were used to evaluate skeletal muscle morphologic features and fiber-type population, size, and area, as well as muscle enzyme activities (acid phosphatase, alkaline phosphatase, and esterase). A histochemical and histologic profile were described for each muscle biopsy specimen.     

Effects of submaximal exercise on adenine nucleotide concentrations in skeletal muscle fibers of horses with polysaccharide storage myopathy

OBJECTIVE: To determine whether disruption of adenine triphosphate (ATP) regeneration and subsequent adenine nucleotide degradation are potential mechanisms for rhabdomyolysis in horses with polysaccharide storage myopathy (PSSM) performing submaximal exercise. ANIMALS: 7 horses with PSSM and 4 control horses. PROCEDURES: Horses with PSSM performed 2-minute intervals of a walk and trot exercise on a treadmill until muscle cramping developed. Control horses exercised similarly for 20 minutes. Serum creatine kinase (CK) activity was measured 4 hours after exercise. Citrate synthase (CS), 3-OH-acylCoA dehydrogenase, and lactate dehydrogenase activities prior to exercise and glucose-6-phosphate (G-6-P) and lactate concentrations before and after exercise were measured in gluteal muscle specimens. Adenine triphosphate, diphosphate (ADP), monophosphate (AMP), and inosine monophosphate (IMP) concentrations were measured before and after exercise in whole muscle, single muscle fibers, and pooled single muscle fibers. RESULTS: Serum CK activity ranged from 255 to 22,265 U/L in horses with PSSM and 133 to 278 U/L in control horses. Muscle CS activity was lower in horses with PSSM, compared with control horses. Muscle G-6-P lactate, ATP, ADP, and AMP concentrations in whole muscle did not change with exercise in any horses. Concentration of IMP increased with exercise in whole muscle, pooled muscle fibers, and single muscle fibers in horses with PSSM. Large variations in ATP and IMP concentrations were observed within single muscle fibers. CONCLUSIONS AND CLINICAL RELEVANCE: Increased IMP concentration without depletion of ATP in individual muscle fibers of horses with PSSM during submaximal exercise indicates an energy imbalance that may contribute to the development of exercise intolerance and rhabdomyolysis.     

Centronuclear myopathy in a Border collie dog

A two‐year old, male entire Border collie was presented with a one‐year history of exercise‐induced collapsing on the pelvic limbs. Physical examination revealed generalised muscle atrophy. Neurological examination supported a generalised neuromuscular disorder. Electromyography revealed spontaneous electrical activity in almost all muscles. Unfixed and formaldehyde‐fixed biopsy samples were collected from the triceps brachii, longissimus and vastus lateralis muscles. Histopathological, histochemical and ultrastructural examinations of biopsy specimens were consistent with either centronuclear or myotubular myopathy. The dog clinically improved with supportive treatment with L‐carnitine, co‐enzyme Q10 and vitamin B compound. To the authors’ knowledge, this is the first report of centronuclear/myotubular myopathy in a Border collie.     

Myopathy with central cores in a foal

Central core disease is a nonprogressive or slowly progressive congenital myopathy with a variable degree of hypotonia and axial and proximal muscle weakness that is histologically characterized by areas devoid of oxidative enzyme activity, resulting from an absence or low numbers of mitochondria in these regions (central core). A 10-month-old, male, pony foal was examined because of stiff gait, marked contractures of the distal portion of the limbs, flexion deformities of the hooves, and moderate hypotonia that had been present from birth. The foal had increased creatine kinase (282 U/liter; reference interval 10-135 U/liter), lactate dehydrogenase (1,188 U/liter; reference interval 150-450 U/liter), and aspartate transaminase (377 U/liter; reference interval <290 U/liter) activities, suggesting muscle disease. Muscle biopsy was performed. In cytochrome oxidase-, succinate dehydrogenase-, and reduced nicotinamide adenine dinucleotide tetrazolium reductase-reacted sections, the dominant morphologic feature was the absence of oxidative enzyme activity in the cores. By use of immunohistochemical technique with a monoclonal antibody against desmin, the cores were clearly delineated and a desmin network was present within the cores. Ultrastructurally, the core areas were characterized by preserved sarcomeres with irregular Z-lines, with some streaming or zigzag appearance and abnormal sarcoplasmic reticulum profiles and T-tubules. Lack of mitochrondria within central cores was observed. Diagnosis of myopathy with central cores was made.     

A glycogen synthase 1 mutation associated with equine polysaccharide storage myopathy and exertional rhabdomyolysis occurs in a variety of UK breeds

Reasons for performing study: A glycogen synthase (GYS1) mutation has been described in horses with histopathological evidence of polysaccharide storage myopathy (PSSM) in the USA. It is unknown whether the same mutation is present in horses from the UK. Objectives: To determine whether the GYS1 mutation occurs in UK horses with histopathological evidence of PSSM and exertional rhabdomyolysis. Hypothesis: The R309H GYS1 mutation is present in a variety of UK horse breeds and that the mutation is commonly associated with exertional rhabdomyolysis. Methods: DNA was extracted from 47 muscle or blood samples from UK horses with histories of exertional rhabdomyolysis in which muscle biopsy diagnosis had been pursued. The proportions of GYS1 mutation positive cases were compared among histopathologically defined groups. In addition, breeds that carried the GYS1 mutation were identified from a total of 37 grade 2 (amylase‐resistant) PSSM cases. Results: Of 47 horses with exertional rhabdomyolysis in which a muscle biopsy diagnosis was pursued, 10 (21%) carried the GYS1 mutation. The mutation was only found in horses with grade 2 PSSM (i.e. not in horses with normal, idiopathic myopathy or grade 1 PSSM biopsy samples). In total, the GYS1 mutation was found in 24/37 (65%) of grade 2 PSSM cases. A variety of breeds, including Quarter Horse, Appaloosa, Warmblood, Connemara‐cross, Cob, Polo Pony and Thoroughbred cross carried the mutation. Conclusions: The GYS1 mutation is an important cause of exertional rhabdomyolysis of UK horse breeds but does not account for all forms of PSSM. Potential relevance: Genotyping is recommended in cases of exertional rhabdomyolysis, prior to or in combination with, muscle biopsy. However a significant proportion of horses with histopathological evidence of PSSM and/or exertional rhabdomyolysis have different diseases.     

Effect of phenytoin on the clinical signs and in vitro muscle twitch characteristics in horses with chronic intermittent rhabdomyolysis and myotonia

In vitro twitch characteristics of the semimembranosus muscle were evaluated in 9 clinically normal horses, in 15 horses with chronic intermittent rhabdomyolysis (CIR) and in 2 horses with myotonia. Effects of phenytoin on in vitro muscle twitch and clinical signs of CIR and myotonia were evaluated in these same horses. Times to 90% relaxation were prolonged in the horses with CIR (mean +/- SEM, 186 +/- 5.9 ms) and in 2 horses with myotonia (197 and 177 ms) compared with those in clinically normal horses (mean +/- SEM, 146 +/- 2.1 ms). Horses with CIR also had significantly (P less than 0.05) longer times to 50% relaxation, compared with clinically normal horses. In the group of horses with CIR, Standardbreds had significantly (P less than 0.05) longer times to 90% and 50% relaxation, compared with Thoroughbreds. Times to 100% peak tension did not differ among the groups. Administration of phenytoin directly into a muscle preparation bath solution had no effect on muscle twitch properties. After the initial muscle biopsy, phenytoin was administered orally for 7 to 10 days to 4 horses with CIR, 2 myotonic horses, and 2 clinically normal horses before repeat biopsy from the same site in the contralateral semimembranosus muscle. Times to 90% relaxation decreased from 197 and 177 ms to 144 and 126 ms, respectively, in the 2 myotonic horses, from a mean of 192 (+/- 9) ms to 170 (+/- 9) ms in the 4 horses with CIR and remained unchanged (154 and 140 ms before vs 155 and 139 ms after treatment) in the 2 clinically normal horses.(ABSTRACT TRUNCATED AT 250 WORDS)     

Reference Values on Serum Biochemical Parameters of Brazilian Donkey (Equus asinus) Breed

Seventeen serum biochemical variables were determined in 40 donkeys of the Brazilian breed (34 females and 6 males) aged from 3 to 19 years. Mean ± standard deviation (SD) (minimum–maximum) values, obtained by automated analysis, were as follows: glucose, 58.35 ± 10.40 (44.00–90.00) mg/dL; cholesterol, 88.41 ± 9.86 (73.58–124.26) mg/dL; serum protein, 6.82 ± 0.40 (6.00–7.52) g/dL; albumin, 3.13 ± 0.21 (2.65–3.69) g/dL; creatinine, 1.80 ± 0.14 (1.51–2.19) mg/dL; urea, 24.25 ± 5.37 (14.12–34.39) mg/dL; lactate, 20.10 ± 4.58 (12.99–33.47) mg/dL; aspartate aminotransferase (AST), 295.81 ± 62.79 (173.71–466.07) IU/L; creatine kinase (CK), 158.00 ± 76.94 (51.69–440.33) IU/L; γ-glutamil-transferase (GGT), 45.82 ± 13.34 (26.17–86.38) IU/L; lactate dehydrogenase (LDH), 576.02 ± 156.32 (213.53–1162.81) IU/L; alkaline phosphatase (AP), 345.36 ± 65.90 (227.25–490.16) IU/L; calcium (Ca), 8.54 ± 0.18 (8.19–8.90) mg/dL; phosphorus (P), 2.76 ± 0.38 (1.99–3.97) mg/dL; chloride (Cl), 106.05 ± 3.20 (99.00–112.00) mEq/L; sodium (Na), 121.50 ± 4.14 (116.00–132.00) mEq/L; and potassium (K), 3.70 ± 0.42 (2.80–4.40) mEq/L. Comparisons of biochemical ranges obtained for the Brazilian donkey breed with reference ranges for other donkey breeds suggested that most values were similar. Biochemical values determined in the present study serve as reference ranges for donkey populations and can be used for health control and diagnosis of diseases.     

Myotonia in related Chow Chow dogs

A myopathy associated with myotonia was observed in three related Chow Chow dogs. The clinical signs were first noticed at 2 to 3 months of age. They included muscle spasm and stiffness of gait which decreased in severity with exercise. Electromyographic findings and the demonstration of a muscle percussion dimple confirmed the presence of myotonia. Dystrophic changes were observed in muscle biopsies but histochemical techniques did not demonstrate fibre type changes. An inherited aetiology was suspected but not confirmed.     

An epidemiological study of myopathies in Warmblood horses

REASON FOR PERFORMING STUDY: There are few detailed reports describing muscular disorders in Warmblood horses. OBJECTIVES: To determine the types of muscular disorders that occur in Warmblood horses, along with presenting clinical signs, associated risk factors and response to diet and exercise recommendations, and to compare these characteristics between horses diagnosed with polysaccharide storage myopathy (PSSM), those diagnosed with a neuromuscular disorder other than PSSM (non-PSSM) and control horses. METHODS: Subject details, muscle biopsy diagnosis and clinical history were compiled for Warmblood horses identified from records of biopsy submissions to the University of Minnesota Neuromuscular Diagnostic Laboratory. A standardised questionnaire was answered by owners at least 6 months after receiving the muscle biopsy report for an affected and a control horse. RESULTS: Polysaccharide storage myopathy (72/132 horses) was the most common myopathy identified followed by recurrent exertional rhabdomyolysis (RER) (7/132), neurogenic or myogenic atrophy (7/132), and nonspecific myopathic changes (14/132). Thirty-two biopsies were normal. Gait abnormality, 'tying-up', Shivers, muscle fasciculations and atrophy were common presenting clinical signs. Forty-five owners completed questionnaires. There were no differences in sex, age, breed, history or management between control, PSSM and non-PSSM horses. Owners that provided the recommended low starch fat supplemented diet and regular daily exercise reported improvement in clinical signs in 68% (19/28) of horses with a biopsy submission and 71% of horses diagnosed with PSSM (15/21). CONCLUSIONS: Muscle biopsy evaluation was a valuable tool to identify a variety of myopathies in Warmblood breeds including PSSM and RER. These myopathies often presented as gait abnormalities or overt exertional rhabdomyolysis and both a low starch fat supplemented diet and regular exercise appeared to be important in their successful management. POTENTIAL RELEVANCE: Warmbloods are affected by a variety of muscle disorders, which, following muscle biopsy diagnosis can be improved through changes in diet and exercise regimes.     

Semilobar holoprosencephaly in a Morgan horse

A6 1/2‐month‐old Morgan filly was examined because of a history of abnormal behavior, teeth grinding, hypothermia, and electrolyte disturbances when weaned. She was from a breeding farm with several other Morgan horses. The 11‐year‐old dam had been purchased the year before as a proven broodmare, which had several previous foals. Breeding, gestation, and birth of this foal were normal. She was raised with 4 other mares and their offspring on pasture with free access to shelter in an open barn. Supplementary feeding consisted of oats and timothy hay. The owners reported that the foal showed unusual behavior, such as lack of apprehension of people, lack of distress from maternal separation, and a higher activity level than other foals of the same age. The foal extensively chewed the dam's tail and mane, masticated oats slowly with rapid jaw movements without actually swallowing them, and ground her teeth. She frequently nibbled the handler's clothes without biting, ate pebbles, and played with the salt block in the paddock. At 4 1/2 months of age, she was treated for suspected gastroduodenal ulcers and weaned. The referring veterinarian examined her 5 days after weaning because of dull demeanor and excessive teeth grinding. The foal was in thin body condition, hypothermic (37°C, 98.6°F), and tachycardic (60 beats per minute [bpm]) and had decreased borborygmi. Major abnormalities on serum biochemistry were severe hypernatremia (166 mmol/L; reference range 136–144 mmol/L) and hyperchloremia (128 mmol/L; reference range 94–104 mmol/L), azotemia (urea, 11.3 mmol/L; reference range 4.2–8.9 mmol/L), and hyperfibrinogenemia (5.2 g/L, reference range 1.6–2.9 g/L). The only abnormality on the CBC was hemoconcentration (PCV, 0.57 L/L; reference range 0.28–0.44 L/L). The foal was treated with penicillin procaine G^a (20,000 IU/kg [9072 IU/1b] IM q12h) and rifampin^b (5 mg/kg [2.7 mg/1b] PO q8h). The next day the tachycardia worsened (120 bpm) and the foal was estimated to be 5–8% dehydrated. IV fluid therapy with lactated Ringer solution^c (LRS) was initiated, and the antibiotic was changed to ceftiofur^d (2 mg/kg [0.91 mg/1b] IV q12h). The foal and dam were rejoined, and the foal's clinical status improved with resumption of nursing. Serial laboratory testing showed persistent hypernatremia 160 mmol/L) and hyperchloremia (123 mmol/L), azotemia urea 11.3 mmol/L and creatinine 168 umol/L; reference range 80–130 μmol/L), hyperglycemia (8.7 mmol/L; reference range 3.7–6.7 mmol/L), high aspartate aminotranferase activity (662 U/L; reference range 259–595 U/L), and high creatine kinase (CK) activity (1,196 U/L; reference range 108–430 U/L). The foal's condition improved and IV fluids were discontinued. Ceftiofur administration was discontinued and trimethoprim‐sulfamethoxazole^e (25 mg/kg [11.3 mg/1b] PO q12h) was administered for 3 days. During the next month the foal was stable but the abnormal behavior persisted. She was weaned again, and within days marked behavior changes such as circling, throwing the head around compulsively, and severe hind‐end shivering recurred. At examination, the foal was dull, tachycardic (60 bpm), was hypothermic (33.6°C, 92.5°F), had dark red mucous membranes, and was estimated to be 5% dehydrated. Laboratory findings were similar to those of the previous tests except for high fibrinogen (7.1 g/L). The foal was again rejoined with the dam, treated with intramuscular penicillin, and referred     

Four cases of equine polysaccharide storage myopathy in the United Kingdom

This paper describes four cases of equine polysaccharide storage myopathy which were confirmed by histological examination of muscle biopsy specimens. The horses were of mixed breeding, with warmblood and thoroughbred dominating. They all had recurrent episodes of rhabdomyolysis, indicated by clinical signs and increased plasma levels of muscle enzymes. They were managed conservatively and have continued athletic careers despite their disease.     

Histopathological characterization of the skeletal myopathy in rasH2 mice carrying human prototype c-Ha-ras gene

A skeletal myopathy is found in approximately 100% of rasH2 mice. To confirm detailed features of the rasH2 skeletal myopathy, the biceps femoris, diaphragm, triceps brachii, gastrocnemial (types I and II fiber-mixed muscles) and soleus muscle (type I fiber-dominant muscle) obtained from male rasH2 and non-transgenic littermates aged 10-13 and 34 weeks were examined. Variations in the muscle fiber size, early-scattered degeneration/necrosis and regeneration of muscle fibers were detected in 10-13-week-old rasH2 mice. The severity of the above muscular lesions was more prominent in older rasH2 mice. These lesions were noted in the type II myofiber dominant muscles (biceps femoris, triceps brachii and gastrocnemial). NADH-TR stain clearly demonstrated a disorganized intermyofibrillar network and necrotic change in muscle fibers. No specific morphological changes, like rod structure or tubular aggregation seen in some types of myopathy, were noted in Gomori trichrome and NADH-TR stains in the rasH2 mouse like in many types of muscular dystrophy. Electronmicroscopically, occasional muscle fiber degeneration/regeneration, invaded phagocytic cells, indistinct Z-band suggesting excessive contraction and dilatation of the sarcoplasmic reticulum were observed. In summary, the skeletal myopathy occurring in rasH2 mice is consistent with muscular dystrophy characterized morphologically by progressive degeneration and regeneration of myofibers. The myopathy is confined to the type II myofiber predominant muscles and is not associated with any pathognomonic lesions. These characteristics will provide us with a useful model for research in muscular dystrophy of diverse myofibers.     

Myotonic dystrophy-like disease in a dog

A mature female Rhodesian Ridgeback was determined to have a progressive, degenerative myopathy associated with myotonia, dysphagia, and marked muscle wasting. Clinical findings revealed a diffuse muscular disease with percussion dimpling, dysphagia, and creatine kinase elevation. A paroxysmal atrial tachycardia was found. Electromyography revealed a diffuse myopathy with high-frequency bizarre waves, myotonic discharges especially in the masticatory, laryngeal, and pharyngeal muscles. A few positive sharp waves were found in some of the appendicular muscles. Histopathologic and histochemical stains on skeletal muscle biopsy specimens demonstrated moderate fiber-size variation, myofiber architectural changes, muscle-fiber splitting, focal necrosis and phagocytosis, high percentage of internal nuclei, and atrophy of type-2 muscle fibers. A review of myotonic myopathies in the dog is presented. The clinical, electrophysiologic, and histochemical findings are similar to those for myotonic muscular dystrophy in man.     

Hyperthermia and Delayed-Onset Myopathy after Recovery from Anesthesia in a Horse

A 13-year old Thoroughbred cross gelding (528 kg) underwent lameness investigation. Because of his temperament, general anesthesia was required to facilitate ultrasound of the left fore fetlock and intra-articular medication of three joints. Anesthesia was induced with ketamine/diazepam after acepromazine/detomidine premedication. Anesthesia was maintained for 40 minutes with a guaifenesin/detomidine/ketamine intravenous infusion. Recovery from anesthesia was initially uneventful, although of a moderate duration (70 minutes). Once standing, the horse proceeded to box walk in an agitated state and became recumbent on two occasions. The horse was manually restrained, at which time its rectal temperature was 41.8°C. Cooling measures were employed (fans, ice-water enemas, wet rugs, intravenous fluid therapy (IVFT), and topical application of surgical spirit) until rectal temperature reached 38.7°C. IVFT was continued for a further 16 hours. Four days after recovery from anesthesia, bilateral triceps, deltoideus, trapezius, and rhomboideus muscle swelling was observed. Blood creatinine kinase was elevated (24,898 IU/L). Treatment for postanesthetic myopathy was initiated (hot packing of the muscle groups, topical dimethylsulfoxide [DMSO] cream application, and oral phenylbutazone). Myoglobinuria was not observed at any time. Muscle swelling decreased over the following 3 days. The horse was discharged on day 11 and has since returned to work.     

Neonatal Alloimmune Thrombocytopenia in a Quarter Horse Foal

Neonatal alloimmune thrombocytopenia is recognized as a spontaneous disease of human infants, piglets, and possibly mules, but it has not been previously reported in horses. A 1–day-old Quarter Horse foal presented to Michigan State University Large Animal Clinic with severe thrombocytopenia of unknown origin. Immunoglobulins that bound to the foal's platelets were identified in the mare's plasma, serum, and milk by indirect assays. The immunoglobulins were further shown to recognize platelets from the foal's full brother, born 1 year earlier. These findings, coupled with the clinical course of the foal during its period of hospitalization, strongly suggest that neonatal alloimmune thrombocytopenia can spontaneously occur in neonatal horses. This diagnosis should be considered for foals with severe thrombocytopenia when other causes can be excluded, and platelet antibody assays should be used to support this diagnosis.     

Salinomycin poisoning in point-of-lay turkeys

Salinomycin poisoning occurred in a flock of 700 point-of-lay turkeys; 400 birds died over 7 days as a result of consuming feed contaminated with 50 ppm salinomycin. No gross lesions were detected. Histologic evidence of a myopathy was most readily detected in leg muscles of turkeys 5 to 7 d after ingesting salinomycin. Feeding trials were undertaken and individual susceptibility to the drug was found to vary greatly. In affected birds the plasma concentrations of creatine kinase (CK) and aspartate aminotransferase (AST) were found to be in the range of 500,000 to 2,500,000 IU/l and 9000 to 25,000 IU/l, respectively. The marked increase in the plasma activities of these enzymes preceded histological evidence of segmental muscle necrosis.     

Quantitative electromyographic examination in myogenic disorders of 6 horses

Electromyographic needle examination (EMG), including the semiautomatic quantitative analysis of motor unit action potential (MUAP), is an important diagnostic tool for myopathy in humans. The diagnostic possibilities of this technique have not been fully explored in horses; however, recent studies have shown that MUAP analysis can be performed in conscious horses. To determine the diagnostic possibilities of EMG in horses, we compared the EMG results of the subclavian muscle, the triceps, and the lateral vastus muscle in 6 equine patients thought to have myogenic disorders with those in 7 normal control horses. The EMG results were compared with the results of the histopathologic examination of the lateral vastus muscle in patients and controls. Histopathologic examination showed muscle disease in 3 patients. In the patient group, several types of abnormal spontaneous activities were observed (mainly fibrillation potentials and positive sharp waves), and the MUAPs of the patient group had a markedly shorter duration and lower amplitude than those of the control group. In the subclavian muscle, triceps, and lateral vastus muscle of affected horses, the MUAP duration was 5.0 +/- 0.4 (mean +/- SD), 3.9 +/- 0.3, and 4.7 +/- 1.1 milliseconds, respectively. The MUAP amplitude was 217 +/- 55, 150 +/- 74, and 180 +/- 54 microV; the number of phases was 2.4 +/- 0.2, 2.5 +/- 0.3, and 2.3 +/- 0.1; and the number of turns was 2.6 +/- 0.2, 2.4 +/- 0.2, and 2.8 +/- 0.5, respectively. In conclusion, it appears that the EMG may be a more sensitive method than other techniques for examining muscle biopsies for diagnosis of early-stage myopathy in horses.     

High-frequency jet ventilation in a neonatal foal

High-frequency jet ventilation was performed on a premature foal for respiratory difficulty attributable to in utero-acquired pneumonia. The procedure involves delivery of compressed gas through a small-bore cannula at frequencies up to 400 cycles/min. Ventilation settings of drive pressure, frequency, and FIO2 were varied to optimize PaO2 and PaCO2 values. The foal was ventilated with this equipment for 14 hours. Evidence of a favorable response to this method of ventilation was observed in the form of improvement in arterial blood gas values as well as the foal's attitude and degree of respiratory effort. High-frequency jet ventilation appears to be a useful method of ventilation for respiratory disease in neonatal foals; however, there remains no clear-cut advantage over conventional positive-pressure ventilation.     

Acute kidney injury mediated by oxidative stress in Egyptian horses with exertional rhabdomyolysis

The present study was carried out to evaluate the role of oxidative stress in the pathophysiologic process of acute renal failure associated with exertional rhabdomyolysis (ER) in Egyptian horses. ER was tentatively diagnosed in 31 Baladi horses based on case history, physical examination findings and confirmed by elevation of plasma creatine kinase (CK) and urine myoglobin concentrations. According to severity of the condition, the diseased horses were categorized into two main groups; the first group included 18 horses with minimal clinical signs and plasma CK <60 000 IU/L; whereas, the second group included 13 horses with overt clinical signs and plasma CK >100 000 IU/L). It was found that plasma creatol (CTL) was positively correlated (p < 0.01) with plasma malondialdehyde (MDA) (r = 0.775), nitric oxide (NO) (r = 0.768), methyguanididne (MG) (r = 0.995), CK (r = 0.768), urine glucose (r = 0.778), urine protein (r = 0.767), renal failure index (RFI) (r = 0.814) and urine sodium (r = 0.799) and negatively correlated (p < 0.01) with total antioxidant capacity (TAC) (r = −0.795), superoxide dismutase (SOD) (r = −0.815), glutathione peroxidase (GSH-Px) (r = −0.675), Vitamin C (r = −0.830), urine creatinine (r = −0.800), urine/plasma creatinine ratio (r = −0.827) and urine/plasma urea ratio (r = −0.807). The correlation between these biochemical variables might suggest a possible role of oxidative stress in renal injury associated with severe rhabdomyolysis in horses. It is suggested that exaggeration of oxidative stress associated with increased muscle membrane leakage plays a key role in acute kidney injury in Baladi horses with severe rhabdomyolysis.