Parâmetros hematológicos de jumentas gestantes em diferentes períodos / Hematological parameters of pregnant donkeys in different periods

The hematological parameters and total protein concentration in healthy donkeys during pregnancy, under grass handling conditions in tropical weather, were evaluated. Fifth-two Marchador Brasileiro breed healthy donkeys, ranging from 8 to 16 years old, were evaluated, 36 of which were pregnant. The animals were separated in four groups: non pregnant (control), pregnancy from 25 to 110 days (first phase), from 111 to 210 days (second phase), and from 211 to 340 days (third phase). Total protein, erythrocyte, and leukocytes counts; packed cell volume; hemoglobin concentration; hematimetric absolute rates of mean corpuscular volume (MCV); mean corpuscular hemoglobin (MCH); and mean corpuscular hemoglobin concentration (MCHC) were evaluated. Total protein and eosinophils count decreased in the first phase. Red blood cells, hemoglobin concentration, and MCHC increased in the third phase of pregnancy. However, MCV and MCH decreased in the same phase.(AU)

Parâmetros hematológicos de jumentas gestantes em diferentes períodos / Hematological parameters of pregnant donkeys in different periods

The hematological parameters and total protein concentration in healthy donkeys during pregnancy, under grass handling conditions in tropical weather, were evaluated. Fifth-two Marchador Brasileiro breed healthy donkeys, ranging from 8 to 16 years old, were evaluated, 36 of which were pregnant. The animals were separated in four groups: non pregnant (control), pregnancy from 25 to 110 days (first phase), from 111 to 210 days (second phase), and from 211 to 340 days (third phase). Total protein, erythrocyte, and leukocytes counts; packed cell volume; hemoglobin concentration; hematimetric absolute rates of mean corpuscular volume (MCV); mean corpuscular hemoglobin (MCH); and mean corpuscular hemoglobin concentration (MCHC) were evaluated. Total protein and eosinophils count decreased in the first phase. Red blood cells, hemoglobin concentration, and MCHC increased in the third phase of pregnancy. However, MCV and MCH decreased in the same phase.

Influência da heparina sódica na ocorrência de laminite eqüina induzida por sobrecarga de carboidratos / Influence of heparin in occurrence of carbohydrate overload-induced equine laminitis

Avaliou-se a eficiência da infusão intravenosa de heparina sódica (100UI/kg/8h, a partir de 24h após o fornecimento de carboidrato, até completar 48h) no controle da laminite eqüina experimentalmente induzida por sobrecarga de carboidrato (17,6g de amido de milho/kg de peso corpóreo). Foram utilizados 15 eqüinos adultos, distribuídos em três grupos experimentais: GI (grupo-controle); GII (grupo laminite) e GIII (grupo laminite+heparina). Posteriormente ao fornecimento de carboidrato, os animais foram submetidos a exames físicos e laboratoriais durante um período de 48 horas. Ao final do experimento, os animais foram submetidos à eutanásia pela aplicação intravenosa de 5ml de maleato de acepromazina seguida de 1g de tiopental sódico e 1 litro de solução saturada de KCl para a obtenção de amostras de tecidos dos cascos, necessárias ao exame histológico. Os animais de GII e GIII, submetidos à sobrecarga de carboidratos, desenvolveram laminite, exibindo claudicação 12 e 24h após o fornecimento de carboidrato, respectivamente, bem como aumentos da freqüência cardíaca e do tempo de preenchimento capilar. As alterações histológicas, semelhantes em GII e GIII, eram do tipo degenerativo, como adelgaçamento de lâminas epidérmicas, retração, achatamento e deslocamento de lâminas dérmicas, vacuolização epidérmica e desorganização do tecido epidérmico. A infusão da heparina sódica não preveniu ou atenuou a degeneração laminar.(AU)

The efficacy of intravenous heparin administration (100UI/kg/8h, from 24 to 48h after carbohydrate administration) in the control of carbohydrate overload-induced equine laminitis (17.6g of corn starch/kg live weight) was evaluated. Fifteen horses were allocated into three experimental groups: GI (control group), GII (laminitis group), and GIII (laminitis+heparin group). These animals were submitted to physical and laboratorial examination during 48h. After that time, they were euthanized with intravenous administration of 5ml of acepromazine followed by 1g of thiopental sodium and 1 liter of saturated solution of KCl to obtain hoof tissues samples for histological examination. GII and GIII horses developed laminitis, showing lameness 12 and 24h after carbohydrate administration, respectively, as well increased heart rate and capillary refill time. The histological alterations, similar in GII and GIII, were degenerative lesions, as thinness of epidermal lamina, retraction, flattening and dislocation of the dermal lamina, epidermal vacuolization, and disruption of the epidermal tissues. The occurrence of laminar degeneration was not prevented or attenuated with intravenous heparin administration.(AU)

Influência da heparina sódica na ocorrência de laminite eqüina induzida por sobrecarga de carboidratos / Influence of heparin in occurrence of carbohydrate overload-induced equine laminitis

Avaliou-se a eficiência da infusão intravenosa de heparina sódica (100UI/kg/8h, a partir de 24h após o fornecimento de carboidrato, até completar 48h) no controle da laminite eqüina experimentalmente induzida por sobrecarga de carboidrato (17,6g de amido de milho/kg de peso corpóreo). Foram utilizados 15 eqüinos adultos, distribuídos em três grupos experimentais: GI (grupo-controle); GII (grupo laminite) e GIII (grupo laminite+heparina). Posteriormente ao fornecimento de carboidrato, os animais foram submetidos a exames físicos e laboratoriais durante um período de 48 horas. Ao final do experimento, os animais foram submetidos à eutanásia pela aplicação intravenosa de 5ml de maleato de acepromazina seguida de 1g de tiopental sódico e 1 litro de solução saturada de KCl para a obtenção de amostras de tecidos dos cascos, necessárias ao exame histológico. Os animais de GII e GIII, submetidos à sobrecarga de carboidratos, desenvolveram laminite, exibindo claudicação 12 e 24h após o fornecimento de carboidrato, respectivamente, bem como aumentos da freqüência cardíaca e do tempo de preenchimento capilar. As alterações histológicas, semelhantes em GII e GIII, eram do tipo degenerativo, como adelgaçamento de lâminas epidérmicas, retração, achatamento e deslocamento de lâminas dérmicas, vacuolização epidérmica e desorganização do tecido epidérmico. A infusão da heparina sódica não preveniu ou atenuou a degeneração laminar.

The efficacy of intravenous heparin administration (100UI/kg/8h, from 24 to 48h after carbohydrate administration) in the control of carbohydrate overload-induced equine laminitis (17.6g of corn starch/kg live weight) was evaluated. Fifteen horses were allocated into three experimental groups: GI (control group), GII (laminitis group), and GIII (laminitis+heparin group). These animals were submitted to physical and laboratorial examination during 48h. After that time, they were euthanized with intravenous administration of 5ml of acepromazine followed by 1g of thiopental sodium and 1 liter of saturated solution of KCl to obtain hoof tissues samples for histological examination. GII and GIII horses developed laminitis, showing lameness 12 and 24h after carbohydrate administration, respectively, as well increased heart rate and capillary refill time. The histological alterations, similar in GII and GIII, were degenerative lesions, as thinness of epidermal lamina, retraction, flattening and dislocation of the dermal lamina, epidermal vacuolization, and disruption of the epidermal tissues. The occurrence of laminar degeneration was not prevented or attenuated with intravenous heparin administration.

CLINICAL AND LABORATORIAL EVALUATION IN PRODROMAL STAGE OF CARBOHYDRATE OVERLOAD-INDUCED EQUINE LAMINITIS. / ESTUDO CLÍNICO E LABORATORIAL DA FASE PRODRÔMICA DA LAMINITE EQÜINA INDUZIDA POR SOBRECARGA DE CARBOIDRATO.

Laminitis is a complex disorder that is difficult to diagnose before the onset of lameness. Ten horses were allocated into 2 experimental groups: The 5 animals of GI did not undergo carbohydrate overload (control group) whereas the remaining 5 in GII underwent carbohydrate overload (laminitis group). After carbohydrate was provided to the animals, clinical and laboratorial examination were performed over a 48-hour period. The hoof tissues underwent histological assessment at the end of study. The digital pulse increased from 12 hours on, simultaneous to initial signs of lameness, which increased to Obel grade 3 after 24 hours. Change of external maxilar artery pulse was noted to 24 hours; at the same time an increase of the capillary refill time was seen. It was verified that heart rate and internal temperature increased 36 hours after overfeeding. Eosinopenia occurred 12 hours after carbohydrate overload. The packet cell volume changed after 36 hours, concomitantly with neutrophilia. Mild leucocytosis occurred during the experiment. The changes of the plasma total protein and fibrinogen concentrations and serum aspartate aminotransferase activity were not significant. Although not expected, the serum creatine kynase activity was highest in control group. The serum alkaline phosphatase activity was highest in laminitis group. The major histological changes were degenerative, in

Laminite é um complexo distúrbio metabólico de difícil diagnostico antes do início da claudicação. Foram utilizados dez eqüinos adultos distribuídos em 2 grupos experimentais: GI, 5 animais hígidos (grupo controle) e GII, 5 animais submetidos à dieta com sobrecarga de carboidratos (grupo laminite). Posteriormente ao fornecimento de carboidratos, os animais foram submetidos a exames físicos e laboratorial durante o período de 48 horas. Ao final do experimento procedeu-se a avaliação histológica dos tecidos dos cascos. Notou-se que o pulso digital elevou-se a partir de 12 horas após o início da fase experimental, simultaneamente aos primeiros sinais de claudicação, que evoluíram para grau III 24 horas após. Alteração do pulso da artéria maxilar externa foi notada a partir de 24 horas, coincidindo com o aumento do tempo de preenchimento capilar. Elevações de freqüência cardíaca e da temperatura retal ocorreram 36 a 48 horas após o fornecimento de carboidratos. Notou-se eosinopenia 12 horas após a administração de carboidratos. O volume globular alterou-se a partir de 36 horas, concomitantemente à neutrofilia. Constatou-se discreta leucocitose ao longo da fase experimental. As alterações dos teores plasmáticos de proteína total e de fibrinogênio e a atividade sérica de aspartato aminotransferase não foram significativas. A atividade sérica de creatina quinase foi maior em eqüinos d

Pravastatin reduces myocardial lesions induced by acute inhibition of nitric oxide biosynthesis in normocholesterolemic rats.

Pravastatin is useful in restoring endothelium-dependent relaxation in hypercholesterolemic animals. A single intravenous bolus injection of N(omega)-nitro-L-arginine methyl ester (L-NAME), a non-specific inhibitor of NO synthase, causes myocardial necrosis and reduces coronary flow in rats. Since rats do not develop hypercholesterolemia and atherosclerosis, we have tested the hypothesis that pravastatin protects the heart from myocardial lesions induced by L-NAME in the absence of alterations in cholesterol levels and plaque formation. Male Wistar rats fed standard chow were divided into four groups: CONTROL (n=14) - rats that received tap water alone for 18 days; L-NAME (n=14) -- rats that received L-NAME (15 mg/kg, i.v.) on the 14th day of the study; PRAVASTATIN (n=11) -- rats that received pravastatin (6 mg/kg/day) in their drinking water for 18 days; PRAVASTATIN+L-NAME (n=12) -- rats that received pravastatin (6 mg/kg/day) and L-NAME (15 mg/kg, i.v.) as indicated in the preceding groups. At the end of 18 days, the rats were sacrificed and the hearts removed for stereological analysis by light microscopy. Plasma nitrate/nitrite and thromboxane B(2) concentrations were determined immediately before and after L-NAME administration. Pravastatin prevented the ischemic lesions induced by the acute inhibition of NO biosynthesis (the area of myocardial lesions in the L-NAME group was greater than in the Pravastatin+L-NAME group: 101.6 microm(2) vs. 1.2 microm(2), respectively; P<0.0001) and markedly increased the plasma nitrate/nitrate concentrations, even before L-NAME administration. There were no significant changes in the plasma thromboxane B(2) concentrations.

Endothelin-1 attenuates bradykinin-induced hypotension in rats.

Endothelin-1 has vasoconstrictor and mitogenic properties and may contribute to the pathogenesis of hypertension by enhancing vasoconstrictor mechanisms. In this study, we investigated the ability of endothelin-1 decrease the hypotensive effects of the vasodilator bradykinin in anesthetized rats. We also studied the effects a two-week oral pre-treatment with losartan (10 mg/kg/day) or enalapril (25 mg/kg/day) on endothelin-1-induced changes in the hypotensive responses to bradykinin. Bradykinin (0.4, 1.6, 6.4, and 25 mcg/kg, i.v.) induced dose-dependent hypotensive responses which were attenuated (P<0.05) by endothelin-1 (2 mcg/kg, i.v.). This effect of endothelin-1 was abolished by the mixed endothelin receptor antagonist N-Acetyl-alpha-[10,11-Dihydro-5H-dibenzo[a, d]cycloheptadien-5-yl]-D-Gly-Leu-Asp-Ile-Ile-Trp (PD145065, 1 mg/kg, i.v.). Endothelin-1 also decreased (P<0.05) the responses to bradykinin in rats pre-treated with losartan, but had no effect in rats pre-treated with enalapril. These results suggest that endothelin-1 may contribute to the development of hypertension by decreasing the responses to bradykinin through a mechanism not involving angiotensin AT(1) receptors, although the inhibition of angiotensin converting enzyme blunted the effect of endothelin-1.

Endothelin ET(A) receptor antagonism attenuates the pressor effects of nicotine in rats.

The increased endothelin-1 levels observed after smoking may result from nicotine-stimulated endothelin-1 production by endothelial cells. In this study, we investigated the effects of selective endothelin ET(A) receptors antagonist Cycle D-a-aspartyl-L-prolyl-D-isoleucyl-D-tryptophyl (JKC 301) and of endothelin ET(B) receptors antagonist N-cis-2, 6-dimethylpiperidino-carbonyl-L-gamma-methyl-leucyl-D-L-m ethoxycarbonyl-tryptophanyl-norleucine (BQ 788) on the changes in mean arterial pressure, heart rate, and plasma thromboxane B(2) (the stable product of thromboxane A(2)) levels caused by increasing doses of nicotine (0.6, 2, 6, and 20 micromol/kg) in anesthetised rats. Nicotine (0.6, 2, and 6 micromol/kg) significantly increased the mean arterial pressure in control and BQ 788-pretreated rats, while only a nicotine dose of 2 micromol/kg) increased the mean arterial pressure in JKC 301-pretreated animals. There were no differences in the nicotine-induced changes in heart rate or in the increases in thromboxane B(2) levels among the groups treated with saline, JKC 301 and BQ 788. These results demonstrate that whereas the antagonism of endothelin ET(A) receptors attenuated the increase in blood pressure after nicotine injections, endothelin ET(B) receptor antagonism had no such effect. In addition, the antagonism of endothelin ET(A) or ET(B) receptors did not affect thromboxane A(2) production after nicotine administration. These findings suggest that endothelin-1 may have a role in the acute effects of nicotine.