Structure In Adult Rats Research Articles

The effect of hyperhomocysteinemia on the patterns of electron microscopic changes in the liver of adult rats

One of the important tasks of modern science is to find biochemical markers that would be able to reflect the risks of development and the nature of the course of various diseases, as well as to predict their possible consequences. In recent years, a significant number of compounds that can affect the biochemical profile of the organism have been identified. Homocysteine – a product of methionine metabolism, belongs to one of these markers, and the effects of its influece on the structure and function of various organs are being actively studied by modern researchers. The aim of the study is to find the patterns of electron microscopic changes in the liver structure of adult rats with hyperhomocysteinemia. The experimental study was performed on 22 white nonlinear mature male rats, which were divided into a control group and an experimental group. A model of persistent hyperhomocysteinemia was created by administering to rats of experimental group thiolactone homocysteine at a dose of 200 mg/kg body weight intragastrically for 60 days. The study of ultrastructural changes in the liver of rats was performed using an electron microscope PEM-125K. In adult rats with experimental hyperhomocysteinemia at the ultrastructural level, dystrophic and destructive changes in hepatocytes, endotheliocytes in the walls of sinusoids and Kupffer cells were found. These changes were more pronounced than in young rats with experimental hyperhomocysteinemia. Revealed structural changes in decompensation (depletion) of mitochondria – fewer number of cristae and enlightened matrix. In contrast to young rats, adult rats with hyperhomocysteinemia in the perisinusoidal spaces showed elongated Ito cells, a significant proportion of the cytoplasm is occupied by the Golgi complex and granular endoplasmic reticulum tanks, indicating protein synthesis for export. In Ito cells, the content of fat droplets, which are located on opposite poles of cells, is reduced. This morphological picture manifests the transformation of Ito cells into fibroblasts.

The effect of bee pollen on femoral bone structure in adult rats

The effect of bee pollen on femoral bone structure in adult rats

Abstract 70: Eplerenone Increases Dilation and the Diameter of Cerebral Penetrating Arterioles in Rats with Sustained Hypertension

Hypertension is linked to dementia in humans, as well as remodeling and dysfunction in large cerebral arteries. The effects of hypertension on cerebral microvessels, such as penetrating arterioles (PenA), are still unknown. These arterioles are the bottlenecks bridging the pial circulation to the deep parenchymal microcirculation, and they are vital for neurovascular coupling and functional hyperemia. Mineralocorticoid receptor (MR) antagonism reverses hypertension-induced changes in large cerebral arteries. Thus, we hypothesized that MR antagonism will improve PenA dilation and structure in adult rats with sustained hypertension. Twelve-week-old male stroke-prone spontaneously hypertensive rats (SHRSP) were treated with the MR antagonist eplerenone (EPL, 100mg/kg/day) or placebo for 6 weeks. PenA function and structure were studied by pressure myography. Data are means±SEM at 60mmHg intralumenal pressure, placebo vs EPL. Myogenic tone generation was not different between groups (%myogenic tone: 40.3±2.3 vs 41.3±2.0). PenA diameter after tone was higher in EPL (42.47±1.5 vs 49.21±2.4μm, p=0.02, t-test). Dilation of PenA to nifedipine (calcium channel blocker) was improved after EPL treatment, as evidenced by an increase in diameter change (10μM nifedipine: 13.44±1.94 vs 18.44±2.39μm, p<0.01, Two-way ANOVA) and PenA diameter (10μM nifedipine: 58.01±2.28 vs 68.58±3.74μm, p<0.01, Two-way ANOVA). PenA passive structure was improved in SHRSP+EPL, as evidenced by an increase in PenA diameter (65.67±1.17 vs 81.00±5.11, p<0.01, Two-way ANOVA) and lumen diameter (55.17±1.8 vs 73.00±5.00, p<0.01, Two-way ANOVA), and a reduction in the wall-to-lumen ratio (0.10±0.01 vs 0.07±0.01, p<0.01, Two-way ANOVA). PenA stiffness was increased after EPL (β-coefficient: 10.91±0.93 vs 14.84±1.83, p=0.03, t-test), but distensibility was unchanged (24.45±3.20 vs 21.88±2.68). These data suggest that MR antagonism improves the structure of cerebral arterioles and their responsiveness to calcium channel blockade in adult rats with sustained hypertension. These improvements have the potential to reduce the risk of developing vascular cognitive impairments and dementia in chronically hypertensive subjects.

Intrauterine growth restriction coupled with hyperglycemia: effects on cardiac structure in adult rats

Intrauterine growth restriction (IUGR) has been linked to heart disease in adulthood. Hence the IUGR heart is likely to be vulnerable to diabetic heart disease. The aim of this study was to examine the effect of induction of type 1 diabetes on myocardial collagen deposition and cardiac function in adult rats with a history of IUGR, after controlling blood glucose levels. IUGR was induced by protein restriction in the pregnant female rat. When the offspring were 24 wk of age, diabetes was induced in male IUGR and non-IUGR rats by means of streptozotocin; insulin injections were used to maintain blood glucose levels at a mild (7-10 mmol/l; n = 8 per group) or moderate level (10-15 mmol/l; n = 8 per group). Echocardiography and cardiac morphology analyses were carried out when the rats were 32 wk of age. IUGR offspring exhibited cardiac hypertrophy at 32 wk, including a thicker posterior wall and increased interstitial fibrosis in the left ventricle. Hyperglycemia led to an increase in heart size and myocardial fibrosis. The response to hyperglycemia was not different between IUGR and non-IUGR rats; however, cardiac fibrosis was greatest when diabetes was present along with a history of IUGR. In general, maintaining blood glucose levels at a mildly hyperglycemic level attenuated the adverse effects of hyperglycemia but did not reverse the fibrosis. Exacerbated fibrosis in hyperglycemic hearts of IUGR offspring may lead to long-term cardiac dysfunction.

The Effects of Maternal Deprivation on the Hippocampal Structure in Adult Rats

To examine the ultrastructural effects of maternal deprivation during developmental periods of limbic-hypothalamo-pituitary-adrenal system on hippocampal dendritic structures in adult rats. The experiments were carried out with male and female Wistar rats in our department. The rats were mated and, after birth, the pups were divided into four groups. The first group (control group) pups remained undisturbed with their dam until postweaning day 22. Maternal deprived groups were separated from their dams for 24 hours at postnatal day 4, 9 and 18. The subjects were provided with food and water ad libitum until 3-months-of-age. At the third month, the rats were transcardially perfused, samples were taken from CA1 and CA3 regions of the hippocampus. Tissues were prepared for electron microscopy. When the data were analyzed, there were no differences between male and female rats in both ultrastructure and semiquantitative analysis of axodendritic synapses. The ultrastructure of Group 1 was seen as normal while in the second Group some neurons nuclear envelope made deep invagination into the nucleus. Additionally, axodendritic synapses were found normal. In Group 3, micrographs and axodendritic synapses were showed normal structure. However, in Group 4 in some neurons invaginations were seen similar to Group 2. Axodendritic synapses were found to be normal. These experiments establish that MD in rats produces slight ultrastructural changes and decreases the number of synapses in CA1 and CA3 subregions of the hippocampus.

Neurotrophic activity of extracts from distal stumps of pre-degenerated peripheral rat nerves varies according to molecular mass spectrum

Objective: We investigated neurotrophic activity of extracts from pre-degenerated and non-pre-degenerated peripheral nerves (complete extracts and extracts with fractions of narrower range of molecular weight) on the injured hippocampus.Methods: The experiment was carried out on male Wistar C rats. The complete extracts or fractions with different ranges of molecular weight were introduced to the site of injury with the autologous connective tissue chambers. We examined DiI-labeled hippocampal cell and AChE-positive nerve endings to assess the regeneration intensity.Results: The highest number of labeled hippocampal cells was observed in the group treated with fraction of molecular weight 10–100 kDa (72.5 ± 13.7) obtained from pre-degenerated nerves. We observed the presence of AChE-positive fibers inside all examined chambers.Discussion: These results demonstrate that suitable modification of CNS environments by introducing the protein fractions obtained from peripheral nerves can initiate the regeneration of the damaged hippocampal structure in adult rats. Moreover, it is possible to intensify their neurotrophic effect by former pre-degeneration of peripheral nerves and extraction from the entire extract proteins of molecular weight of 10–100 kDa.

Mercury-induced alterations in rat kidneys and testes in vivo

In this study effects of mercury administration on the kidney and testicular structure of adult rats were evaluated. Rats received mercury (HgCl2) in single intraperitoneal dose 20 mg HgCl2 (group A), 10 mg HgCl2 (group B) and 5 mg HgCl2 (group C) per kilogram of body weight and were killed after 48 hours following mercury administration. After the preparation of histological samples the results were compared with control group (K). In kidney decreased diameters of glomeruli and renal corpuscles, damaged tubules with affected quality of tubular cells and infiltration of interstitium were detected. Quantitative analysis demonstrated increased relative volume of tubules and renal corpuscles. Also the number of nuclei and glomeruli was increased in all experimental groups. The diameter of glomeruli and renal corpuscles was decreased. In testis undulation of basal membrane, dilatation of blood vessels in interstitium and occurrence of empty spaces in germinal epithelium were observed. Decreased relative volume of germinal epithelium, increased relative volume of interstitium and increased apoptosis occurrence suggest damaged interstitium and revealed occurrence of edemas. The relative volume of seminiferous tubules showed higher luminization. The number of nuclei was decreased in all experimental groups what is in positive relation with occurrence of empty spaces. Also other evaluated criteria demonstrated significant differences between control group and experimental groups. This study reports a negative effect of mercury on the structure and function of kidney and testes.

Methylprednisolone causes matrix metalloproteinase-dependent emphysema in adult rats.

Previous investigations have shown that corticosteroids affect the development and maturation of the developing lung in utero and in neonatal animals. Systemic corticosteroids are routinely used for the treatment of acute exacerbations of chronic obstructive pulmonary disease, and inhaled corticosteroids are more frequently being prescribed for the long-term treatment of patients with chronic obstructive pulmonary disease. Because corticosteroids can affect matrix metalloproteinases and because the concept of protease/antiprotease imbalance is an important concept regarding the pathogenesis of emphysema, we examined the effects of chronic steroid treatment on lung structure in adult rats. Rats treated with 2 mg/kg of methylprednisolone daily for 1, 2, or 4 weeks had an increased mean linear intercept and a decrease of the surface-volume ratio when compared with age-matched control animals, and the animals showed increased matrix metalloproteinase-9 activity in their lungs on zymography. Rats treated concomitantly with methylprednisolone and a broad-spectrum matrix metalloproteinase inhibitor (GM6001) did not develop emphysema. We conclude that systemic treatment of adult rats with the antiinflammatory steroid methylprednisolone increases the activity of matrix metalloproteinases in the lung and causes emphysema.