12 results on '"HINTZ, H. F."'
Search Results
2. Custer, selenium and swainsonine.
- Author
-
Hintz HF and Thompson LJ
- Subjects
- Animals, Behavior, Animal, Fabaceae chemistry, Fabaceae poisoning, History, 19th Century, Horses, Humans, Plant Poisoning etiology, Plant Poisoning veterinary, Plants, Medicinal, United States, Warfare, Equidae, Horse Diseases etiology, Lameness, Animal etiology, Selenium poisoning, Swainsonine poisoning
- Abstract
The Battle of Little Bighorn was fought over 100 y ago but many controversies remain. Some feel the defeat of Custer could have been avoided if Benteen and Reno had united with Custer. A slow-moving pack train may have hindered the troops of Benteen and Reno from joining up with Custer. One report indicated the horses and mules in the pack train were lame and behaved crazily. It has been previously suggested that the animals had selenium toxicosis. We propose the lameness could have been caused by selenium, but that the behavioral problems may have been caused by the ingestion of plants containing swainsonine.
- Published
- 2000
3. Dietary control of exertional rhabdomyolysis in horses.
- Author
-
Valentine BA, Hintz HF, Freels KM, Reynolds AJ, and Thompson KN
- Subjects
- Animal Feed, Animals, Aspartate Aminotransferases blood, Creatine Kinase blood, Diet veterinary, Female, Glycogen metabolism, Horse Diseases etiology, Horse Diseases prevention & control, Horses, Male, Muscle, Skeletal metabolism, Muscle, Skeletal pathology, Rhabdomyolysis diet therapy, Rhabdomyolysis prevention & control, Selenium administration & dosage, Vitamin E administration & dosage, Dietary Carbohydrates administration & dosage, Dietary Fats administration & dosage, Horse Diseases diet therapy, Physical Conditioning, Animal adverse effects, Rhabdomyolysis veterinary
- Abstract
Objective: To determine whether feeding a low-carbohydrate, high-fat diet would decrease severity of exercise-induced muscle injury in horses with exertional rhabdomyolysis., Animals: 19 horses with a history of exertional rhabdomyolysis., Design: Case series., Procedure: Specimens of the semitendinosus or semimembranosus muscle were obtained for histologic examination, and serum creatine kinase (CK) and aspartate transaminase (AST) activities 4 hours after exercise were determined. Horses were then fed a low-carbohydrate, high-fat diet, and serum CK and AST activities 4 hours after exercise were reevaluated at approximately monthly intervals for 3 to 6 months., Results: Serum CK and AST activities 4 hours after exercise were high before any change in diet. All 19 horses had evidence of chronic myopathic change and abnormal glycogen accumulation in muscle biopsy specimens; 11 horses also had evidence of complex polysaccharide accumulation. Adaptation to diet change required approximately 3 to 6 months. Sixteen horses did not have any episodes of exertional rhabdomyolysis after 3 to 6 months of diet change, and 3 horses had mild episodes of exertional rhabdomyolysis following either a reduction in dietary fat intake or restriction in exercise. Postexercise serum CK and AST activities 3 to 6 months after the change in diet were significantly less than initial values., Clinical Implications: Results indicated that exertional rhabdomyolysis may be a result of abnormal carbohydrate metabolism in some horses. Feeding a diet with low carbohydrate and high fat content may reduce severity of exercise-induced injury in some horses with exertional rhabdomyolysis.
- Published
- 1998
4. Molds, mycotoxins, and mycotoxicosis.
- Author
-
Hintz HF
- Subjects
- Animals, Encephalomalacia etiology, Ergotism etiology, Horses, Mycotoxicosis etiology, Poaceae, Aflatoxins poisoning, Encephalomalacia veterinary, Ergotism veterinary, Horse Diseases etiology, Mycotoxicosis veterinary
- Abstract
Interest in mycotoxins and mycotoxicosis in humans and animals has greatly increased in recent years. Horses have long been considered very susceptible to molds. The signs, treatment, and prevention of several conditions, such as leukoencephalomalacia, aflatoxicosis, ergotism, fescue toxicity, slobbering disease, ryegrass staggers, and moldy sweet clover disease, are discussed.
- Published
- 1990
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5. Goiter in foals caused by excessive iodine.
- Author
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Driscoll J, Hintz HF, and Schryver HF
- Subjects
- Animals, Female, Goiter chemically induced, Horses, Male, Pregnancy, Goiter veterinary, Horse Diseases chemically induced, Iodine adverse effects
- Published
- 1978
6. Plasma and liver copper values in horses with equine degenerative myeloencephalopathy.
- Author
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Dill SG, Hintz HF, deLahunta A, and Waldron CH
- Subjects
- Animals, Brain Diseases blood, Brain Diseases etiology, Brain Diseases metabolism, Copper blood, Copper deficiency, Horse Diseases blood, Horse Diseases etiology, Horses, Spinal Cord Diseases blood, Spinal Cord Diseases etiology, Spinal Cord Diseases metabolism, Brain Diseases veterinary, Copper metabolism, Horse Diseases metabolism, Liver metabolism, Spinal Cord Diseases veterinary
- Abstract
Equine degenerative myeloencephalopathy (EDM) is a common spinal cord disease in the horse. The etiology of EDM currently is unknown. In other species, there are similarities in the clinical signs and neuropathological changes observed in EDM and in copper deficiency. The objective of this study was to determine if horses affected with EDM had low levels of plasma or liver copper. Plasma copper values were determined in 25 EDM affected horses and 35 normal horses. Liver copper levels were determined on 13 EDM affected horses and 22 normal horses. Plasma and liver copper values were not significantly lower in EDM affected horses than in control horses.
- Published
- 1989
7. Some nutritional aspects of colic in horses.
- Author
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Hintz HF
- Subjects
- Animals, Colic etiology, Colic prevention & control, Edible Grain adverse effects, Female, Horse Diseases prevention & control, Horses, Male, Peptic Ulcer etiology, Peptic Ulcer veterinary, Zea mays adverse effects, Animal Feed adverse effects, Animal Nutritional Physiological Phenomena, Colic veterinary, Diet adverse effects, Horse Diseases etiology
- Abstract
Consistency of exercise and diet are important in colic prevention. Water should be offered before and after feeding. Fast-growing foals suckling heavily lactating mares may overeat grain at weaning. Creep feeding to accustom the foal to eating grain and gradually increasing the grain intake after weaning are helpful in preventing colic in foals. Stallions may overeat grain when taken off pasture in hot weather. Feeding hay initially and grain later helps avoid colic in these stallions. Type-D Clostridium perfringens may cause enterotoxemia in foals. Corn should be fed in moderation. High-Mg diets, ingestion of sand, and pelleted feed have been associated with colic. Endoparasitism is the most important cause of colic in horses.
- Published
- 1984
8. Morphologic and biochemical changes in cartilage of foals treated with dexamethasone.
- Author
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Glade MJ, Krook L, Schryver HF, and Hintz HF
- Subjects
- Animals, Bone Development drug effects, Bone and Bones pathology, Cartilage pathology, Cartilage Diseases pathology, Cartilage, Articular pathology, Horses, Joint Diseases pathology, Osteochondritis pathology, Cartilage drug effects, Cartilage Diseases veterinary, Cartilage, Articular drug effects, Dexamethasone pharmacology, Horse Diseases pathology, Joint Diseases veterinary, Osteochondritis veterinary
- Abstract
Epiphyseal and articular cartilages were examined in pony foals treated with intramuscular injections of either 0.5 mg dexamethasone per 100 kg bodyweight daily for 3, 8 or 11 months, or 5.0 mg per 100 kg for 11 months, and in horse foals treated with 5.0 mg per 100 kg for 20 weeks. The proximal femoral growth plates exhibited increased spatial separation between chondrocyte columns, narrowed zones of disorganized columnar and hypertrophic cartilage, abnormal penetration of hypertrophic cartilage by metaphyseal capillaries, retained cartilage in the spongiosa, distal terminal plate formation, transverse trabeculation, chondronecrosis and metaphyseal osteochondrosis dissecans. Destructive articular lesions were observed after 3 months of treatment with 0.5 mg per 100 kg bodyweight. Joint damage originated either at the joint surface or deep within the cartilage. Signs of surface deterioration included edema, fibrillation, enlargement of lacunae, pitting, shredding and erosions of cartilage. Inactivity of articular cartilage growth centers was common, with failure of epiphyseal capillaries to penetrate the lacunae in the calcified cartilage. Chondronecrosis adjacent to the calcification front was accompanied by cartilage ulceration and fracture. Intracartilaginous cysts and subchondral chondroid cysts were also observed. Healing responses included reparative chondrogenesis (focal cartilage hyperplasia), formation of fibrous or fibrocartilaginous "scars," subchondral osteopetrosis and epiphyseal marrow petrosis. Lactate dehydrogenase specific activities per chondrocyte, 35S uptake per cell and glycosaminoglycan contents of articular cartilages were all reduced 55% by 3 months of treatment. This inhibition of articular chondrocyte metabolism initiated cartilage degeneration. Surface destruction and osteochondrosis dissecans followed continued mechanical stress of compromised cartilage.
- Published
- 1983
9. Enteroliths in horses.
- Author
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Lloyd K, Hintz HF, Wheat JD, and Schryver HF
- Subjects
- Animals, Calculi etiology, Horses, Intestinal Diseases etiology, Calculi veterinary, Horse Diseases etiology, Intestinal Diseases veterinary
- Abstract
Many cases of enteroliths were reported in the nineteenth century but the number greatly decreased in the early twentieth century. However, in recent years the number of cases in certain parts of the United States such as California has greatly increased. The reasons for the increase are obscure. The intake of nitrogen, magnesium and phosphorus (the primary components of enteroliths) from water and food is likely to be a factor. Arabians may be more likely to develop enteroliths than horses of other breeds. A nidus such as a small stone is needed because a nidus has been found in every enterolith that has been examined. Further studies in which the effect of mineral intake and form of the mineral on enterolith formation are needed. Studies of enterolith formation in the past have all been retrospective. Models for the development of enteroliths are needed.
- Published
- 1987
10. Mineral metabolism and immobilization osteopenia in ponies treated with 25-hydroxycholecalciferol.
- Author
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Eagle MT, Koch DB, Whalen JP, Hintz HF, and Krook L
- Subjects
- Animals, Bone Diseases, Metabolic metabolism, Bone Diseases, Metabolic prevention & control, Calcifediol therapeutic use, Female, Forelimb, Horse Diseases prevention & control, Horses, Male, Metatarsus diagnostic imaging, Metatarsus metabolism, Radiography, Bone Diseases, Metabolic veterinary, Calcifediol pharmacology, Horse Diseases metabolism, Immobilization, Minerals metabolism
- Abstract
The left thoracic limb was immobilized in a plaster cast in 6 grade weanling ponies for 6 weeks. Two ponies were injected intramuscularly each day with 2.4 micrograms of 25-hydroxycholecalciferol [25(OH)D3] per kg bodyweight, two with 1.2 micrograms and two received no injections. Immobilization of 25(OH)D3 treatment had no significant effect on mineral metabolism. Immobilization resulted in significantly decreased weight and specific gravity of metacarpus III (MCIII). Histologic examination and triple fluorochrome incorporation showed that the osteopenia was caused by atrophy of osteoblasts with failure of bone apposition. Immobilization caused retardation or cessation of proliferation of cartilage in the epiphyseal plate with thinning or premature closure. Treatment with 25(OH)D3 further reduced apposition and enhanced significantly the osteopenia as shown by quantitative morphometry of microradiographs of the MCIII metaphyses. There was parathyroid gland atrophy and fibrosis in proportion to the level of 25(OH)D3 treatment, which, in absence of hypercalcemia in all ponies, was interpreted to be a direct result of vitamin D treatment. It was concluded that immobilization osteopenia under the present design and duration is caused by failure of bone apposition and that treatment with 25(OH)D3 at dose levels applied is contraindicated.
- Published
- 1982
11. Taxus cuspidata (Japanese yew) poisoning in horses.
- Author
-
Lowe JE, Hintz HF, Schryver HF, and Kingsbury JM
- Subjects
- Animal Feed, Animals, Horses, New York, Horse Diseases etiology, Plant Poisoning veterinary
- Published
- 1970
12. Ammonia intoxication resulting from urea ingestion by ponies.
- Author
-
Hintz HF, Lowe JE, Clifford AJ, and Visek WJ
- Subjects
- Ammonia blood, Animal Feed, Animals, Blood Chemical Analysis, Blood Glucose analysis, Body Fluids analysis, Cecum analysis, Horses, Ketoglutaric Acids blood, Neurologic Manifestations, Poisoning diagnosis, Pyruvates blood, Urea blood, Ammonia poisoning, Horse Diseases, Poisoning veterinary, Urea metabolism, Urease analysis
- Published
- 1970
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