Toxemia of pregnancy in sheep: a clinical, physiological, and pathological study

Ferris, Thomas F.; Herdson, Peter B.; Dunnill, M. S.; Lee, M R

doi:10.1172/jci106129

Cited by 45 publications

(14 citation statements)

References 27 publications

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“…Esta alteração pode ser explicada por observações feitas por Ferris et al (1969) e Marteniuk & Herdt (1988), que encontraram inϐiltração excessiva de gordura no epitélio tubular acarretando modiϐicações estruturais glomerulares, provocando uma degeneração dos rins em ovelhas com a doença, e que podem prejudicar a função renal. Teores elevados de creatinina e de uréia são indicativos de um quadro de insuϐiciência renal, que pode ser severo no estágio terminal e está associado com o prognóstico reservado, como foi observado no grupo das ovelhas que morreram.…”

Section: Discussionunclassified

“…Diferente do observado por Ferris et al (1969), que não encontraram elevações do L-lactato sanguíneo e nem um quadro de acidose metabólica expressiva em ovelhas acometidas com a doença. A condição, veriϐicada nas ovelhas com TP no trabalho, é justiϐicada pela cetonemia, que surge como conseqüência ao processo de oxidação exacerbada dos AGNE, que gera a produção excessiva de corpos cetônicos (acetoacetato, acetona e BHB), e como estes são ânions com características ácidas, elevam o "anion Gap" e reduzem a concentração de HCO3-, CL, Na+ e K+, com isso a acidose metabólica ocorre.…”

Section: Discussionunclassified

“…As ovelhas acometidas, em geral, apresentam alterações como hipercetonemia, cetonúria, hipoglicemia, níveis elevados dos ácidos graxos não esteriϐicados (AGNE) e cortisol, além do comprometimento da função hepática e renal (Ferris et al 1969, Ortolani & Benesi 1989, Bruere & West 1993, Sargison et al 1994, Andrews et al 1996.…”

Section: Introductionunclassified

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Indicadores bioquímicos e hormonais de casos naturais de toxemia da prenhez em ovelhas

Santos¹,

Mendonça

Filho³

et al. 2011

Pesq. Vet. Bras.

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Toxemia da prenhez é considerada um transtorno metabólico de grande impacto econômico na produção de ovinos, porém as particularidades de repercussão sistêmicas deste distúrbio ainda são pouco esclarecedoras. O presente estudo teve por objetivo avaliar o perfil bioquímico e hormonal de 77 ovelhas com diagnóstico clínico de toxemia da penhez e comparar os achados laboratoriais de acordo com a resolução clínica dos animais, alta hospitalar (G1) e aqueles que morreram (G2). A manifestação clinica da doença foi observada no período do pré-parto em 100% dos animais, destes 66,2 % (n=51) receberam alta clínica e 33,8% (n=26) morreram. Dos casos de toxemia da prenhez estudados havia gestação múltipla em 55,8%. Dentre os parâmetros estudados, cortisol, uréia, AST e CK estavam mais elevados no G2 em relação ao G1 com diferenças significativas (P<0,05). Foi encontrado aumento nas concentrações de glicose plasmática, frutosamina, albumina, creatinina, ß-hidroxubutirato, ácido graxo não esterificado e L-lactato, porém não houve diferenças entre os grupos (P>0,05). Não ocorreram alterações nas taxas de colesterol e triglicerídios. Houve redução nos índices da insulina, não havendo diferenças entre G1 e G2 (P>0,05). Todas as ovelhas apresentaram cetonúria e acidúria.

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Section: Discussionunclassified

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Indicadores bioquímicos e hormonais de casos naturais de toxemia da prenhez em ovelhas

Santos¹,

Mendonça

Filho³

et al. 2011

Pesq. Vet. Bras.

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“…Glomerular lesions also have been described in toxemia of pregnancy in ewes [31]. Toxemia was induced in 13 of 20 pregnant ewes by the stress of change of environment and food deprivation late in pregnancy.…”

Section: Glomerulonephritis In Ruminantsmentioning

confidence: 95%

Comparative Pathology of Glomerulonephritis in Animals

Slauson

Lewis

1979

Vet Pathol

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Abstract. Glomerulonephritis constitutes an important category of renal diseases in animals and has been recognized with increasing frequency in the last decade. We report here the comparative morphologic aspects of glomerulonephritis as a naturally occurring disease of animals. We briefly review the immunopathogenesis of glomerulonephritis. The morphology of renal lesions occurring in glomerulonephritis in dogs, cats, cattle, sheep, horses and swine has been reviewed with emphasis on the range and specificity of various glomerular lesions and on the comparison of lesions between various species. A distinction was made between glornerulonephritis as a primary disease entity and glomerulonephritis associated with other disease processes. Primary idiopathic glomerulonephritis occurred in all species but was most commonly recognized as a clinically important disease in dogs and cats. Glomerulonephritis also occurred in association with other diseases such as equine infectious anemia, chronic hog cholera, canine pyometra, dirofilariasis, feline leukemia virus infection and canine systemic lupus erythematosus.Glomerulonephritis is responsible for substantial morbidity and mortality in many species of animals. Although the cause is basically unknown, it is a disease generally thought to result from the interaction of immunologic and inflammatory reactants at a fixed tissue site (the glomeruli) with subsequent loss of structural and functional integrity of the injured tissues. It is not the purpose of this paper to detail the pathogenesis of glomerulonephritis. For a better understanding of the disease as it occurs in animals, however, it will be useful to review briefly what is known about the pathways potentially leading to glomerular injury [25, 61, 71, 73, 77, 82, 831. Two major immunologic mechanisms of glomerular injury have been identified. In one, antibodies react with antigens in the glomerular basement membrane. In the other, antibodies react with nonglomerular antigens in the circulation to form immune complexes that are deposited in the glomerulus. With conventional light microscopy, it is difficult to infer the pathogenetic mechanisms responsible for glomerulonephritis from the histologic lesion. Differentiating these two mechanisms usually requires fluorescence and electron microscopy. Glomerular lesions induced by soluble immune complexes have characteristic discrete, interrupted, focal deposits of host IgG and complement when examined by fluorescence microscopy. In contrast, the fluorescence staining pattern of glomeruli injured by anti-glomerular basement membrane antibody is uniform, smooth and linear. To further implicate anti-glo- 135

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“…However, the ewe, which has been utilized for studies of the uterine circulation, has species differences which makes application of the results to the human uterine circulation difficult. The placental implantation of the ewe is different from the human and, unlike the human, the uterus and placenta of the ewe does not contain renin (3). Since it has been postulated that uterine renin may be involved in regulating uterine blood flow during pregnancy, possibly by increasing prostaglandin E synthesis, this difference may be significant (4).…”

Section: Introductionmentioning

confidence: 98%

The effect of changes in perfusion pressure on uteroplacental blood flow in the pregnant rabbit.

Venuto¹,

Cox²,

Stein³

et al. 1976

J. Clin. Invest.

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A B S T R A C T The effect of perfusion pressure on uteroplacental blood flow was determined in pregnant rabbits utilizing the radioactive microsphere method.Control mean arterial pressure, 93 mm Hg±2.6 SEM, was raised by carotid ligation to 109±4.1 mm Hg and then reduced with antihypertensive drugs to 74+1.3 mm Hg. Over this range of pressure there was no significant change in cardiac output, 605+36, 523+37, and 540±39 ml/min; or uteroplacental blood flow, 30+3.2, 27±5.2, and 29±4.5 ml/min, respectively. When prostaglandin synthesis was inhibited with either indomethacin or meclofenamate (2 mg/kg), uterine vascular resistance was higher but maintenance of uteroplacental flow occurred over a perfusion pressure of 89±6.7-115 +9.3 mm Hg. With more severe hypotension induced with trimethaphan, control arterial pressure fell from 92±2.4 to 39+0.9 mm Hg, cardiac output fell from 514 +17 to 407+22 ml/min (P < 0.025) and uteroplacental blood flow fell from 6.1±0.9 to 2.5±0.9% of cardiac output (P<0.05), which represented an absolute fall from 32.4±5 to 10.6±3 ml/min (P <0.025). There was no significant change in renal blood flow expressed as percentage of cardiac output, 14.9+2 and 13±1.5%, or in absolute flow, 75+77 and 54+7 ml/min with trimethaphan-induced hypotension.These studies indicate that uteroplacental blood flow is maintained relatively constant over a range of perfusion pressure of 60-140 mm Hg in both normal and prostaglandin-inhibited pregnant rabbits. However, with reduction in pressure to 36-42 mm Hg, uteroplacental blood flow falls, expressed as a percentage of cardiac output and in absolute flow.

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Toxemia of pregnancy in sheep: a clinical, physiological, and pathological study

Cited by 45 publications

References 27 publications

Indicadores bioquímicos e hormonais de casos naturais de toxemia da prenhez em ovelhas

Indicadores bioquímicos e hormonais de casos naturais de toxemia da prenhez em ovelhas

Comparative Pathology of Glomerulonephritis in Animals

The effect of changes in perfusion pressure on uteroplacental blood flow in the pregnant rabbit.

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