Efeito da hiperprolactinemia induzida pela metoclopramida na glândula lacrimal: estudo experimental

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Abstract

OBJETIVO: avaliar as alterações morfológicas promovidas pela hiperprolactinemia induzida pela metoclopramida na glândula lacrimal de camundongas durante a fase de proestro e gestação. MÉTODOS: 40 camundongas adultas foram divididas em dois grupos: CTR1 (controle) e MET1 (tratadas com metoclopramida). Após 50 dias, metade dos animais de cada grupo foram sacrificados por decapitação. Os restantes foram acasalados, constituindo os grupos controle prenhe (CTR2) e metoclopramida prenhe (MET2), que foram sacrificadas no 6º dia de gestação. O sangue foi coletado e submetido à dosagem hormonal dos níveis de estradiol e de progesterona por quimioluminescência. Em seguida as glândulas lacrimais foram removidas, fixadas em formol a 10% e processadas segundo metodologia histológica para inclusão em parafina, sendo as lâminas coradas pelo HE. A análise morfométrica foi realizada com o programa AxionVision (Carl Zeiss), medindo-se os volumes celulares e nucleares das células acinares. RESULTADOS: os volumes nuclear e celular das glândulas lacrimais dos grupos experimentais MET1 (152,2±8,7; 6,3±1,6 µm³) e MET2 (278,3±7,9; 27,5±0,9 µm³) mostraram-se reduzidos em relação aos grupos controles CTR1 (204,2±7,4; 21,9±1,3 µm³) e CTR2 (329,4±2,2; 35,5±2,0 µm³). Houve redução dos níveis hormonais de estrogênio e de progesterona nos animais que receberam metoclopramida em comparação com os respectivos controles (CTR1: estradiol = 156,6±42,2 pg/ml; progesterona = 39,4±5,1 ng/ml; MET1: estradiol = 108,0±33,1 pg/ml; progesterona = 28,0±6,4 ng/ml; CTR2: estradiol = 354,0±56,0 pg/ml; progesterona = 251,0±56,0 ng/ml; MET2: estradiol = 293,0±43,0 pg/ml, progesterona = 184,0±33,0 ng/ml). CONCLUSÃO: a hiperprolactinemia induzida pela metoclopramida produziu sinais de diminuição na atividade das células da glândula lacrimal tanto em camundongas prenhes quanto não prenhes. Este efeito está possivelmente relacionado com a redução da produção hormonal de estrogênio e progesterona.

Translated abstract

PURPOSE: to evaluate the morphological changes in murine lacrimal glands by metoclopramide-induced hyperprolactinemia during the proestrus phase or pregnancy. METHODS: forty adult mice were divided into two groups: CTR1 (control) and MET1 (treated with metoclopramide). After fifty days, half of the mice were sacrificed. The remaining animals were mated, and then labeled as pregnant controls (CTR2). Part of these animals were treated with metoclopramide and constituted the metoclopramide-treated pregnant (MET2) group. The CTR2 and MET2 groups were sacrificed on the 6th day of pregnancy. The blood was collected for determination of the hormonal levels of estradiol and progesterone by a chemoluminescent method. The lacrimal glands were then removed, fixed in 10% formaldehyde and stained with HE. The morphometric analysis was performed using the Axion Vision program (Carl Zeiss) to measure acinar nuclear and cellular volumes. RESULTS: the nuclear and cellular volumes of the lacrimal glands in the MET1-(152.2±8.7; 6.3±1.6 µm³) and MET2-(278.3±7.9; 27.5±0.9 µm³) treated groups were lower than those in CTR1 (204.2±7.4; 21.9±1.3 µm³) and CTR2 (329.4±2.2; 35.5±2.0 µm³), respectively. There was a significant hormonal level reduction in the animals that received metoclopramide compared to controls (CTR1: estradiol = 156.6±42.2 pg/ml; progesterone = 39.4±5.1 ng/ml; MET1: estradiol = 108.0±33.1 pg/ml; progesterone = 28.0±6.4 ng/ml; CTR2: estradiol = 354.0±56.0 pg/ml; progesterone = 251.0±56.0 ng/ml; MET2: estradiol = 293.0±43.0 pg/ml, progesterone = 184.0±33.0 ng/ml). CONCLUSION: metoclopramide-induced hyperprolactinemia produced morphological signs of reduction of cellular activity in lacrimal glands during the proestrus phase and pregnancy. It is hypothesized that this effect might be related to the hyperprolactinemia-induced decrease in the hormonal production of estrogen and progesterone.

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Most cited references 16

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The harderian gland: a tercentennial review.

Karl A P Payne (1994)

The harderian gland was first described in 1694 by Johann Jacob Harder (1656-1711). It occurs in most terrestrial vertebrates and is located within the orbit where, in some species, it is the largest structure. It may be compound tubular or compound tubuloalveolar, and its secretory duct is usually morphologically distinct only after leaving the substance of the gland to open on the surface of the nictitating membrane. The tubules of the gland are formed of a single layer of columnar epithelial cells surrounded by myoepithelial cells. The chief product(s) of the gland varies between different groups of vertebrates, and epithelial cells possess granules or vacuoles whose contents may be mucous, serous or lipid. In rodents, the gland synthesises lipids, porphyrins and indoles. In the case of lipid vacuoles, the gland is unusual in releasing these by an exocytotic mechanism. It is unclear whether the gland can act both as an exocrine and endocrine organ. There is control of gland structure and synthesis through a variety of humoral agents, including gonadal, thyroid and pituitary hormones; in addition there is a rich autonomic innervation and many neuropeptides have been identified. The proposed functions of the gland are remarkably diverse and include the gland being (1) a source of 'saliva', (2) a site of immune response, (3) a photoprotective organ, (4) part of a retinal-pineal axis, (5) a source of pheromones, (6) a source of thermoregulatory lipids, (7) a site of osmoregulation, and (8) a source of growth factors. The gland is discussed in terms of its embryology and phylogeny, and in relation to ecological variables. Several goals of future research are identified.