Avaliação clínica, laboratorial e anatomopatológica do sistema urinário de ovinos confinados com ou sem suplementação de cloreto de amônio / Clinical, laboratory and anatomopathological evaluation of the urinary system of feedlot sheep with or without ammonium chloride supplementation

A acidificação urinária com cloreto de amônio (CA) é um método preventivo eficiente em urolitíase obstrutiva em ovinos. Os objetivos deste estudo com ovinos confinados, que receberam dieta concentrada com elevado teor proteico, foram: verificar o efeito da dieta sobre a formação de urólitos e o desenvolvimento da doença; analisar as características macroscópicas e histopatológicas do sistema urinário; relacionar os achados clínicos, laboratoriais e necroscópicos com a presença de urólitos. Utilizaram-se 60 ovinos machos: grupo CA (n=40), 400 mg/kg CA/dia, tratados via oral, por 42 dias consecutivos; grupo-controle (n=20), não tratado. Determinaram-se sete momentos de colheita de amostras com intervalos de sete dias, no total de 56 dias de confinamento. Encontraram-se microcálculos na pelve renal em cinco animais de ambos os grupos. As lesões renais microscópicas mais relevantes foram congestão vascular e necrose tubular. Concluiu-se que a dieta rica em concentrado provocou lesão renal em ambos os grupos, embora sem alterar a função renal, o que foi comprovado em testes pela ureia e creatinina séricas. O cloreto de amônio fornecido ao grupo CA não impediu a calculogênese, mas reduziu sua prevalência em relação ao grupo-controle. Os ovinos do grupo-controle tiveram maior comprometimento renal, pela alta incidência de cristalúria e pela necrose tubular, induzidas pelo consumo da dieta rica em grãos.

The urinary acidification with ammonium chloride (AC) is an efficient preventive method for urolithiasis in sheep. The objectives of this study with feedlot sheep receiving concentrated diet with high protein content were (1) to verify the effect of diet on urolith formation and development of the disease, (2) to analyze the macroscopic and histopathological characteristics of the urinary system, and (3) to relate the clinical, laboratory and necropsy findings with the presence of uroliths. Sixty male sheep were used: AC group (n=40), 400mg/kg AC/day, orally treated for 42 consecutive days, and control group (n=20), untreated. Seven times were determined for sampling with a seven-day interval, totaling 56 days of feedlot. Small uroliths were found in the renal pelvis of five sheep in both groups. The most relevant microscopic renal lesions were vascular congestion and tubular necrosis. It was concluded that the highly concentrated diet caused renal injury in both groups, without changing the renal function, what was proven by laboratory tests of urea and creatinine. Ammonium chloride provided to the CA group did not prevent urolith formation, but reduced its prevalence in comparison with the control group. Sheep of the control group had increased kidney damage, which resulted in higher incidence of crystalluria and tubular necrosis induced by the consumption of a diet rich in grains.

Pulmonary vascular remodeling in congenital heart disease: Enhanced expression of heat shock proteins.

In congenital heart disease (CHD), mechanical wall stress by increased pulmonary artery pressure and pulmonary blood flow is believed to play a pivotal role in the pathogenesis of pulmonary plexogenic arteriopathy (PPA). The pathogenesis of this disease that involves significant pulmonary arterial remodelling, is, however, largely unknown. In the systemic circulation, upregulation of HSP-70 and HSP-27 in the arterial wall occurs in response to acute hypertension, whereas HSP-60 and increased titres of anti-HSP-60 antibodies are associated with atherosclerotic vessel disease. We looked for the involvement of HSPs in the stress response of pulmonary endothelial and vascular smooth muscle cells in different abnormal hemodynamic conditions in patients with CHDs. We analyzed the expression pattern of HSP-27, HSP-70 and HSP-60 in lung biopsies of 38 patients with CHD, using immunohistochemistry. These included 4 individuals with an essentially normal pulmonary circulation, who served as controls. Immunoreactivity against HSP-27 and also against HSP-70 was present in the pulmonary endothelium and vascular smooth muscle cells of patients and controls in a similar pattern. In contrast, expression of HSP-60 was absent in pulmonary arteries of both patients and controls. In patients with advanced PPA, cells within plexiform lesions showed strong staining for HSP-27 and HSP-70, but were again negative for HSP-60. The intensity of immunoreactivity against HSP-70 correlated inversely with medial thickness of pre-acinar arteries (r = -0.32; p = 0.04). Expression of HSP-27 and HSP-70 did not correlate with hemodynamic parameters, although immunoreactivity against HSP27 tended to be increased in cases with high pulmonary artery pressure (r = 0.37; p = 0.16) and was highest in patients with flow-associated pulmonary hypertension (p<0.01). HSP-27 and HSP-70, but not HSP-60 are engaged in the stress response of cells of small pulmonary arteries in pulmonary plexogenic arteriopathy. HSP-27 and HSP-70 are increasingly expressed in the advanced proliferative lesions of this disease.