Preliminary evaluation of neuroendocrine cells in the respiratory tract in rats with experimental uremia

The goal of this study was to investigate the influence of experimetally induced chronic renal failure on endocrine cells in the respiratory tract in rats. After 30 days of uremia, the fragments of rat lungs were collected. Paraffin sections were stained using H+E, silver impregnation and immunohistochemistry with specific antibodies against calcitonin (CT), synaptophysin (SY), somatostatin (ST), and neuron-specific enolase (NSE). A large number of endocrine cells with a strong calcitonin immunoreactivity were observed in the respiratory tract of rats with experimental uremia, as compared with the control group. Other immunoreactions were weakened.     

Gastric endocrine cells in rats with uremia and after thyroparathyroidectomy

The decrease in active kidney parenchyma amount causes disorders in hormone secretion processes and their inactivation failure. Experimental thyroparathyroidectomy is connected with an abrupt reduction in endocrine cells and hormones produced by them, which can be a stimulating factor as far as the increase and intensity of endocrine gastric cells activity is concerned. The aim of the study was the histomorphological and immunohistochemical evaluation of these cells in the gastric pylorus. Thyroparathyroidectomy was performed in rats 30 days after nephrectomy. Fragments of gastric pylorus were collected 14 days after the operation. Paraffin sections were stained with H+E and silver method. Immunohistochemical reactions were conducted using antibodies against calcitonin gene-related peptide (CGRP), somatostatin (ST), synaptophysin (SPh), neuron-specific enolase (NSE), and chromogranin (CgA). The results showed an increase in number of endocrine cells in stomachs of rats in experimental group as compared to controls. Endocrine cells were larger and contained more secretory granules.     

Preliminary evaluation of pancreatic islets in rats with experimental uremia and after thyroparathyroidectomy

Hormonal disorders are the permanent symptoms of renal failure. They concern all known hormones and can be due to quantitative changes of the secretory activity and disturbances of endocrine cell functions. The aim of this study was to establish whether experimental thyroparathyroidectomy in uremic animals causes detectable histomorphological changes in endocrine cells of pancreatic islets. Thyroparathyroidectomy was performed in rats 30 days after nephrectomy. Fragments of pancreatic tissue were collected 14 days after the operation. Paraffin sections were stained with H+E and by silver salt impregnation. Immunohistochemical reactions were conducted using antibodies against calcitoningene-related peptide (CGRP), synaptophysin (SPh), somatostatin (ST), neuron-specific enolase (NSE), and chromogranin (CgA). It was shown that endocrine cells of pancreatic islets in thyroparathyroidectomized rats show intensified immunoreactivity to SPh and ST as compared to the control group of animals. Immunocytochemical reactions for NSE, CgA, and CGRP were negative.     

Preliminary evaluation of gastric endocrine cells in rats with experimental uremia

Chronic renal failure can be the cause of various disturbances in hormonal and electrolyte metabolism, including calcium and phosphate metabolism. The aim of this study was the evaluation of pyloric endocrine cells in Wistar rats with experimental uremia. Fragments of gastric pylorus were collected 30 days after nephrectomy. Paraffin embedded sections were stained with H+E and by silver impregnation. We also performed immunohistochemical reactions with the use of specific antibodies against calcitonin gene-related peptide (CGRP), synaptophysin (SY), somatostatin (ST), and neuronal specific enolase (NSE). The rats with experimental uremia showed an increase in the number of endocrine cells and in intensity of all the examined reactions.     

The effects of experimental uremia in rats on duodenal VIP levels and the interaction of VIP with duodenal epithelial cells

The effects of experimental uremia on the concentration of vasoactive intestinal peptide (VIP) in duodenum as well as on the interaction of this neuropeptide with the corresponding epithelial cells were studied in rats. Duodenal VIP concentration was significantly decreased in uremic rats as compared to control animals. The specific binding of VIP to duodenal epithelial cells increased in rats with uremia due to an increase in the number of VIP receptors rather than a change in the binding affinity or in the extent of VIP degradation. On the other hand, the efficacy but not the potency of VIP upon cyclic AMP generation varied in parallel to that observed at the receptor level.     

The dynamics of morphological changes in the pyloric endocrine cells of rats with uremia

Disturbances in renal homeostatic function lead to changes in endocrine cell secretory activity. The aim of this study was the histomorphological estimation of dependence of gastric APUD system cell morphology and function on the time after subtotal nephrectomy in Wistar rats. Fragments of gastric pylorus were collected 1. 2, 4, and 6 weeks after nephrectomy. Paraffin sections were stained with H+E and by silver impregnation. Immunohistochemical reactions with the use of specific antibodies against calcitonin gene-related peptide (CGRP), synaptophysin (SPh). somatostatin (ST), and neuron-specific enolase (NSE) were also performed. Immunoreactivity of the examined substances in the pyloric mucosa in the first week after nephrectomy was lower than in the control group. However, in the following time intervals, endocrine cells showed stronger immunostaining in comparison with the control rats. The results suggest that chronic renal failure can modulate secretory activity of APUD system cells.     

Upper respiratory tract infection in mouse and rats

Summary Spontaneous aspergilloma in the para-nasal cavities of 2 rats, and a chronic granuloma with grains, caused by Gram-positive cocci in the maxillary sinus of a mouse, are reported.     

Hepatocyte mitochondrion respiratory chain in rats with experimental toxic hepatitis

The purpose of this study was to examine hepatocyte mitochondrion respiratory chain in rats subjected to ethanol and CCl4 administration within 4 weeks to induce an experimental hepatitis. Oxygen consumption was determined as a measure of mitochondrion respiration chain function. The development of liver pathology was accompanied by fat accumulation, fibrosis, triglycerides and lipid peroxidation increase. Respiratory chain characteristics damage was found. Endogenous oxygen consumption by hepatocytes isolated from pathological liver was found 34% higher compared to control. Exogenous malate and pyruvate substrates delivery didn't stimulate cell respiration. Rotenone (the inhibitor of the I complex) decreased 27% oxygen consumption by pathological hepatocytes while dinitrophenol produced 37% cell respiration increase. States 3 (V3) and 4 (V4) mitochondrial respiration with malate + glutamate as substrates were found to be 70 and 56% higher accordingly compared to control level. V3 and Vd (dinitrophenol respiration) for mitochondria from pathological liver didn't differ from control when being tested with malate + glutamate or succinate as substrates. Cytochrome c oxidase activity increased (+ 80%) as compared to control. Administration of hypolipidemic agent simvastatin simultaneously with ethanol and CC14 resulted in decrease liver fat accumulation, fibrosis and peroxidation products. Simvastatin administration caused hepatocyte endogenous respiration decrease while malate + pyruvate, dinitrophenol or rotenone delivery produced oxygen consumption alterations similar to control. However, when isolated mitochondria from liver of simvastatin treated animals being tested the decrease of oxidative phosphorylation coupling for substrates malate + glutamate was found. While simvastatin did not cause changes in cytochrome c oxidase activity. We propose the hypothesis that the NCCR complex in rat mitochondria with experimental toxic hepatitis works extensively on superoxydanion production. Alterations of SCCR, Coenzyme Q-cytochrome c-reductase, cytochrome c oxidase and ATP-synthase activities have an adaptive nature to compensate for impaired NCCR function.     

Preliminary evaluation of endocrine cells in the rat respiratory tract after thyroid and parathyroid gland removal

The complete thyroid and parathyroid gland removal leads to the abrupt reduction of calcitonin, which can be a factor stimulating growth and intensified activity of APUD system cells in the respiratory tract. Thus, neuroendocrine cells in the lungs and trachea in rats after thyroid and parathyroid removal were evaluated. Paraffin specimens of the examined organs were stained with H+E and impregnated with silver. Calcitonin, synaptophysin, somatostatin, and neuronal-specific enolase were detected immunohistochemically by the use of rabbit specific antibodies. Antibodies used in the study immunostained neuroendocrine cells of the examined organs. Rats with removed thyroid and parathyroid glands presented weakened reaction compared to the control group.     

Regional differences in bioavailability of an opioid tetrapeptide in vivo in rats after administration to the respiratory tract

TArPP (Tyr-D-Arg-Phe-Phe-NH(2)), 1-10 micromol/kg, was administered to anesthetized rats by nasal microinfusion, intratracheal microinfusion, intratracheal nebulization, aerosol inhalation, and i.v. bolus and infusion. Plasma concentrations of TArPP and its deamidated metabolite were determined by LC-MS-MS.Regional differences in bioavailability (F), first-pass metabolism, and absorption rate were found for TArPP after delivery to the respiratory tract. Absorption was rapid after both pulmonary and nasal administration (t(max) approximately 10-20 min). After nasal microinfusion, F was 52 +/- 9%. For all the pulmonary groups, F was higher (72-114%). First-pass metabolism of TArPP was lower in the lung than in the nasal cavity. It is evident that the pulmonary route is attractive for successful systemic delivery of small, hydrophilic and enzymatic susceptible peptides.     

Growth of respiratory syncytial virus in primary epithelial cells from the human respiratory tract

Respiratory syncytial virus (RSV) is the most important cause of lower respiratory tract disease in infants and children. To study RSV replication, we have developed an in vitro model of human nasopharyngeal mucosa, human airway epithelium (HAE). RSV grows to moderate titers in HAE, though they are significantly lower than those in a continuous epithelial cell line, HEp-2. In HAE, RSV spreads over time to form focal collections of infected cells causing minimal cytopathic effect. Unlike HEp-2 cells, in which wild-type and live-attenuated vaccine candidate viruses grow equally well, the vaccine candidates exhibit growth in HAE that parallels their level of attenuation in children.     

Antioxidant system activation in rats with experimental cirrhosis after injection of cryopreserved fetal liver cells

The possibility to recover the antioxidant system in rats with experimental liver cirrhosis (LC) after allo- and xenotransplantation of cryopreserved fetal liver cells (FLC) was investigated. It was shown that the content of lipid peroxidation products in the blood serum of animals with LC four weeks after FLC transplantation decreased significantly as compared to control group. Such changes were accompanied by a significant increase of catalase (CAT), glutathione reductase (GR), Se-dependent glutathione peroxidase (GP) activity in the liver and total anti-oxidative activity (AOA) of blood. Obtained results demonstrate that the main direction of FLC effects in animals with LC agree with that we observed previously in other experimental models (partial hepatectomy, chronic alcohol poisoning and hypercholesterolemia). In conclusion, cell therapy may be considered as the universal method for correction of disorders in regulation of free-radical processes in various experimental pathologies.     

PM2.5暴露对Wistar大鼠呼吸道菌群的改变

目的研究暴露于PM_(2.5)环境后Wistar大鼠呼吸道微生态的改变。方法 12只Wistar大鼠随机分为PM_(2.5)暴露组和对照组,每组6只。大鼠饲养1周适应环境,从第2周开始在动式染毒系统暴露仓中暴露染毒,对照组暴露于生理盐水。每天暴露4 h,连续暴露28 d后,收集大鼠气管灌洗液和支气管肺泡灌洗液。采用16S rDNA分析技术对其中所含的菌群种类及丰富度进行高通量测序。结果暴露于PM_(2.5)大鼠的上、下呼吸道菌群结构发生明显改变。经PM_(2.5)暴露后呼吸道中寄居的主要正常菌群厚壁菌门、拟杆菌门、变形菌门、放线菌门的总数较正常对照组都明显降低。结论 PM_(2.5)的暴露能够导致大鼠呼吸道微生态菌群失衡。     

State of liver mitochondrial respiratory chain in rats with experimental toxic hepatitis

Polarographical determination of oxygen concentration has shown that in rats with experimental hepatitis induced by combined ethanol and CCl₄ administration for 4 weeks, the functioning of the hepatocyte mitochondrial respiratory chain is impaired. Development of liver pathology was accompanied by adipose dystrophy, fibrosis, and an increase of triglycerides and lipid peroxidation products in the liver tissue. The endogenous respiration rate in hepatocytes isolated from the pathologically altered liver was 34% higher than in the control. Cell respiration was not stimulated by the addition of the substrates malate and pyruvate with digitonine. An uncoupler of oxidation and phosphorylation, 2,4-dinitrophenol, increased the hepatocyte oxygen consumption rate by 37%, while addition of the inhibitor of the I complex, rotenone, decreased cell respiration in pathologically altered hepatocytes by 27%. The states 3 (V₃) and 4 (V₄) of mitochondrial respiration with malate + glutamate as substrates were found to be higher by 70% and 56%, respectively, as compared with the control level. When using malate + glutamate or succinate as substrates, V₃ and Vd (dinitrophenol respiration) in the toxic hepatitis hepatocyte mitochondria did not differ from the control, which indicates no uncoupling occurred of the oxidation and phosphorylation processes. Cytochrome c oxidase activity was elevated (+80%) as compared with the control. Administration of the hypolipidemic agent symvastatin simultaneously with ethanol and CCl₄ resulted in a reduction of the degree of liver adipose dystrophy, prevented activation of lipid peroxidation, and decreased the hepatocyte endogenous respiration rate. Addition of malate + pyruvate, dinitrophenol or rotenone produced oxygen consumption changes similar to those in the control. However, in mitochondria isolated from the pathologically altered liver, symvastatin induced an uncoupling effect on the respiratory chain in the presence of the substrates malate + glutamate, but did not change the cytochrome c oxidase activity. We suggest that functioning of the NCCR complex in the hepatocyte mitochondria of animals with experimental toxic hepatitis is impaired, which leads to an intensive superoxide anion production at the level of this complex. Under these conditions, the defect of the NADH-coenzyme Q-oxidoreductase is compensated by functioning of other complexes of the respiratory chain (SCCR, coenzyme Q-cytochrome c-reductase, cytochrome c oxidase, and ATP-synthase activities).     

Activation of mast cells after experimental myocardial infarction in 3 week-old rats

It is known that mast cells (MC) take an active part in regeneration processes in postinfarction heart in adult rats and humans. Behaviour of population of cardial MCs has been studied 20, 60, 75 and 90 days after experimental myocardial infraction induced in 3 week-old and adult rats by ligation of left coronary artery. The density of MC of different degrees of maturity was estimated in atrium and ventricle on paraffin sections stained with Alcian blue - Safranin. Findings were compared with MC density obtained in hearts of intact rats. The MC density in intact 1.5-2.5 month-old rats in atrium and ventricle was about 0.6 cells/mm2, in intact 3.5-4.0 month-old rats in atrium--1.2 cells/mm2, in ventricle--0.6 cells/mm2. The MC density in 3 week-old rats with infarction was significantly higher than in intact rats: 5-fold increase in 20 and 60 days in atrium, and 2-fold increase in 60 and 75 days in ventricle. In 60 days after infarction the MC density in adult rats was 3 times lower in atrium and 2 times lower in ventricle than in the same heart compartments of 3 week-old rats with infarction. After infarction in 3 week-old rats, a relative share of young cells with alcian-positive granules sharply increased in 20 days and then decreased by 60-75 days. This indicates a migration of immature MCs to infracted myocardium and their subsequent differentiation. The MC activation after infraction in young rats may result from a more active immune reaction in younger rats and/or functional peculiarities of their MC.