Biomedical subjects
Publications and source records attributed to S M Reed.
Cervical vertebral malformations are recognized clinically when they result in spinal cord compression causing neurologic deficits. Confirmation of diagnosis is based on radiographic and myelographic evidence of cord compression. Medical therapy is not usually successful. Several successful surgical treatments are described.
Auditory brain stem response testing, using insert earphones, was performed in 10 healthy horses given general anesthesia. The procedure involved clicks of alternating polarity delivered at a rate of 25 clicks/s. Wave forms, including five peaks, were commonly identified. Latencies were measured in milliseconds for waves I through V for all intensities. Latencies of all waves decreased as stimulus intensity increased. For waves I through V, a least-squares regression line was determined for each horse, using all responses between 87-dB sound pressure level (SPL) and 136-dB SPL, inclusive. Slopes were significantly (P less than 0.05) less than zero for waves I through IV, but not for wave V. Peak latencies of each wave averaged at 87-dB SPL for waves I through V were 1.73, 2.6, 3.82, 4.80, and 5.71 ms, respectively; latencies of these five waves at 136-dB SPL were 1.36, 2.2, 3.06, 3.92, and 4.71 ms, respectively. The decrease in latency among the five waves ranged from 0.13 to 0.004 ms/dB. When peak values were below 87-dB SPL, waves became essentially unrecognizable.
Labrador Retrievers with type-II muscle fiber deficiency were examined electrodiagnostically. Electromyographic changes consisted of positive sharp waves, fibrillation potentials, bizarre high-frequency discharges, and, rarely, myotonic-like discharges. Fasciculation potentials were recorded infrequently. Fibrillation potentials and bizarre high-frequency discharges were the most commonly observed electromyographic changes. Bizarre high-frequency discharges were prominent in muscles of the head and neck, proximal muscles of the thoracic limbs, and the thoracolumbar paraspinal musculature. Marked abnormalities were not observed in the motor nerve conduction velocity. Decremental responses of the evoked compound muscle action potential to repetitive nerve stimulation were not observed.
Three horses less than or equal to 3 years old were evaluated because of stunted growth, weight loss, anorexia, depression, and lethargy of at least 1 month's duration. A neonatal foal was examined after its death. In each case, gross and microscopic renal lesions were compatible with bilateral renal hypoplasia (ie, cortical hypoplasia with severe medullary hypoplasia). In young horses with renal failure, bilateral renal hypoplasia should be considered in the differential diagnosis, and may represent a congenital lesion.
Acute renal failure was produced in 5 ponies which had received mercuric chloride (0.25 mg/kg) and potassium dichromate (3 mg/kg) intravenously each day for 5 days. Failure was due to acute nephrosis. This was indicated clinically by daily monitoring of the urine output, and B-mode ultrasonography of both kidneys after administering the fifth dose of the chemical agents. Euthanasia was performed after days 14, 9, 5, 8 and 5 respectively in each of the ponies, and the presence of renal disease confirmed by gross and microscopic post mortem examination. The nature of the kidney lesions observed in each animal was consistent, indicating that the induction of renal disease in this manner was reproducible and represented a means by which the pathophysiologic and biochemical development of equine acute renal failure might be studied.
Serum and urinary biochemical changes were recorded in 5 ponies in which acute tubular nephrosis had been induced over 5 days with mercuric chloride and potassium dichromate. Serum osmolality, the serum concentrations of urea nitrogen, creatinine, sodium, potassium and chloride, and blood pH and blood gases were measured daily for 14 days or until humane euthanasia was performed. Levels of the same substances were quantitated daily in urine. In addition, routine urinalyses and determination of urinary gamma glutamyl transferase (GGT) activity were performed on each sample. Changes in the values of the urinary variables preceded alterations in the serum value of the same substance by at least one day. The first notable abnormality detected was in urinary GGT activities. These changes occurred up to 6 days before the detection of azotemia. It was concluded that acute equine renal injury could be diagnosed earliest with biochemical testing of urine. Measurement of urinary GGT levels represents a means by which proximal tubular disease in equidae could be diagnosed in its developmental stages.
The changes in serum and urinary levels of calcium and phosphorus and serum parathyroid hormone (PTH) were studied during controlled, chemically induced, acute renal disease in 4 ponies. There was an initial rise in daily urinary calcium and hydroxyproline excretion in 2 ponies which may have indicated increased bone resorption. Mild hypercalcemia, hypophosphatemia and elevated C-terminal PTH levels were associated with oliguria. Total daily urinary excretion of calcium and phosphorus decreased as oliguria developed. The levels of C-terminal PTH were increased in all four animals. This appears to have been related to their diminished renal function in that C-terminal fragments of intact PTH (which require functioning kidneys in order to be cleared) were probably being accumulated. Although there was no evidence with regard to an actual increase in PTH secretion, prolongation of intact PTH half-life due to renal tubular damage may have contributed to the development of hypercalcemia.
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.
The medical records and follow-up data for 4 horses with fibrotic myopathy of the semitendinosus muscle treated by semitendinosus tenotomy were reviewed. The gait deficit for each of the 4 horses was typical of fibrotic myopathy. Two of the horses had the gait deficit since birth. The efficacy of semitendinosus tenotomy was compared with the traditional treatment of partial myotenectomy of the affected muscle. The functional results in the 4 horses appeared to be equal to partial myotenectomy in returning the horses to athletic function and, compared with what has been reported, was cosmetically superior.
Two adult horses with progressive neurologic signs were examined clinically and at necropsy. Both horses had signs of progressive ataxia and weakness, clinically diagnosed as spinal cord in origin. Differential diagnoses for cervical spinal ataxia in horses included cervical vertebral malformation, equine degenerative myeloencephalopathy, equine herpes-virus-I myeloencephalopathy, and equine protozoal myeloencephalopathy. Necropsy findings in both horses were similar and consisted of a large hematoma in the fourth ventricle, with upward compression of the cerebellum and downward compression of the pons and rostral portion of the medulla.
This experiment was designed to establish a model for the study of gastrointestinal disturbances as a result of prolonged endotoxin uptake in the horse. The hepatic portal vein of 7 horses was catheterized (through flank incisions) to give chronic hepatic portal infusions of lipopolysaccharide (LPS, endotoxin). Lipopolysaccharide was infused at a rate of 1 microgram/kg of body weight/hr for 24 hours. Two of the horses were infused with saline solution for 12 hours before LPS infusions were given. Lipopolysaccharide was shown to affect behavior and hematologic and coagulation values. The 1st hour was critical for the LPS-infused horses; yet by 4 hours, the horses had apparently become refractory to continued infusion of LPS. During the 1st hour, all horses collapsed without an accompanying hypotension. A decrease in polymorphonuclear leukocytes (neutrophils) was seen during this time and was accompanied by a shortening of the recalcification tests, 1-stage prothrombin time, and activated partial thromboplastin time. There was an increased concentration of circulating fibrinogen/fibrin degradatory products. All of the LPS-infused horses showed signs of hoof discomfort and either stood with the 4 feet together beneath the body or continually shifted their weight from one front foot to the other. Hoof temperature decreased approximately 3 degrees (C) during this time and remained decreased for the duration of the experiment.
Of 10 horses in a heavily overgrazed pasture, 4 died within 1 week. Clinical signs included muscle tremors, ataxia, reluctance to walk, heavy sweating, and myoglobinuria. Serum creatine kinase, aspartate transaminase, and alkaline phosphatase activities were high. Histopathologic findings were nonspecific. On the basis of clinical signs, clinicopathologic findings, nonspecific histopathologic findings, the condition of the pasture, the identification of numerous white snakeroot plants from which trematone was extracted, and evidence that these plants had been heavily browsed, it was believed that the horses died from ingestion of Eupatorium rugosum.
In horses with large bowel disease, those with circulating endotoxins but no evidence of altered hemostasis had a good prognosis for survival. Those with circulating endotoxins and evidence of altered hemostasis (fibrin degradation products) had a poor prognosis. Portal vein infusion of endotoxins over 24 hours caused hoof discomfort, evidenced by shifting of weight and standing with all 4 feet together, and a decreased hoof temperature. Clinical signs appeared within 30 minutes of initiation of infusion and subsided within 4 hours despite continued infusion. Long-term heparin therapy results in rapid depletion of RBC but no detectable bleeding. Heparin therapy should be initiated before colic surgery is begun. Coagulation is monitored with the activated partial thromboplastin time. Heparin should initially be given IV, followed by SC or intrafat injections, and should never be given IM. The anticoagulative effects of heparin can be reversed with protamine sulfate.
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In 13 Smooth Fox Terriers with a congenital form of myasthenia gravis, clinical signs included intermittent, progressive muscle weakness that became more pronounced with exercise; muscle wasting; megaesophagus; and aspiration pneumonia. Neurologic abnormalities were apparent only during periods of weakness and included inability to retract the fore- and hindlimbs from painful stimuli. A decrement of the compound muscle action potential was evident during repetitive supramaximal nerve stimulation. Intravenous injection of a short-acting cholinesterase inhibitor evoked immediate improvement of clinical and electromyographic signs. Intracellular microelectrode studies of a biopsied external intercostal muscle revealed reduced amplitude of miniature end-plate potentials, as occurs in acquired myasthenia gravis. However, in contrast to acquired myasthenia gravis, antibodies directed against acetylcholine receptors were not demonstrable in serum and were not bound to acetylcholine receptors in muscle. Despite lack of complexing with immunoglobulin, the amount of acetylcholine receptor protein in biopsied external intercostal muscles from 9 affected pups was less than 25% of the amount in 5 unaffected littermates. The latter finding accounted for the reduction in amplitude of miniature end-plate potential and the failure of neuromuscular transmission. Treatment with a long-acting cholinesterase inhibitor in 6 cases resulted in temporary improvement in muscle strength.
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This study was designed to test the efficacy of heparin anticoagulant therapy in the horse and its effect on the formed elements of blood. Nine clinically normal, nontraumatized adult horses were subjected to 4 different heparin maintenance regimens (dosages of 320, 240, 160, and 40 U/kg of body weight). Porcine intestinal mucosa heparin (20,000 U/ml) was injected subcutaneously every 12 hours for 96 hours (total 9 times). A loading dose of one-third the maintenance dose was given IV just before the first heparin injection. Three control horses were given an equivalent volume of 0.9% saline solution. The 2 large doses of heparin (320, 240 U/kg) resulted in an extension of the therapeutic range for heparin anticoagulant therapy (1.5 to 2.5 X data base-line prolongation of the activated partial thromboplastin time [APTT]). The 160-U/kg dose maintained the APTT in the therapeutic range, and the 40-U/kg dose had no effect on the APTT. Heparin was shown to exert a profound influence on the RBC mass of the horse. Three of the heparin regimens (320, 240, and 160 U/kg) resulted in a significant decrease in RBC numbers, PCV, and total hemoglobin content. Platelet count also was reduced in the horses when given the 320 and 240 U/kg doses. The observed increase in the mean corpuscular volume was associated with decreasing RBC numbers. Plasma proteins, serum bilirubin, free hemoglobin (plasma), haptoglobin (plasma), and urine and fecal hemoglobin values remained unchanged in all groups. Heparin anticoagulation therapy with the smallest dose (40 U/kg) had no detectable effects on the measured values, nor did the saline solution.
Five Arabian or half-Arabian foals with suspected multiple cardiac anomalies were examined. Various combinations of clinical examination, electrocardiography, angiocardiography, cardiac catheterization, blood gas analysis, radiography, and echocardiography resulted in clinical data that allowed accurate antemortem diagnoses to be made. In 4 cases, the clinical diagnosis was substantiated by postmortem findings. The confirmed diagnoses were: pseudotruncus arteriosus, a combination of patent ductus arteriosus, pulmonic stenosis, and tricuspid stenosis, pentalogy of Fallot, and tricuspid atresia. The surviving horse was believed to have an interventricular septal defect and patent ductus arteriosus, or a persistent truncus arteriosus.