scholarly journals Dynamics of changes in nonspecific resistance of guinea pigs under conditions of formation of experimental periodontitis and immobilization stress

2021 ◽  
Vol 11 (11) ◽  
pp. 67-72
Author(s):  
P. Olekshij

The aim of our study was to determine the phagocytic activity of leukocytes and nitrosine tetrazolium test (NST - test) in the dynamics of experimental periodontitis (EP) and immobilization stress (IS). It is established in the work that the indicators studied by us, namely phagocytic number, phagocytic index and NST - test increase on the 3 rd, 5 th and 15 th days of our experiment. The above tests have a high diagnostic value and allow to characterize the degree of activity of the inflammatory process and determine the participation of individual parts of the body's defense mechanisms. The obtained results make it possible to express the opinion that polymorphonuclear leukocytes take an active part in the formation of EP and IS, as well as indicate the stimulation of metabolic processes in leukocytes.

2021 ◽  
Vol 11 (10) ◽  
pp. 263-268
Author(s):  
P. Olekshij

The aim of our work was to investigate the peculiarities of changes in endogenous intoxication rates: medium mass molecules (MMM) and erythrocyte intoxication index (EII) in the blood of guinea pigs in the formation of combined pathology - experimental periodontitis (EP) and immobilization stress (IS).The results of biochemical studies showed that at all stages of development of combined pathology - experimental periodontitis and immobilization stress there is a consistent increase in the degree of endogenous intoxication, which dominated on the 15th  day of the experiment, namely increased content of medium mass molecules (МMМ254 , MMM280) and  EII in the blood by 58.5% (p≤0.05), 80.3% (p≤0.05) and 95.7% (p≤0.05), respectively, compared with the first group of animals is a clear manifestation of the formation of endogenous intoxication. These changes are obviously the result of insufficient elimination of toxic products on the background of the inflammatory process in periodontal tissues and stress.


Author(s):  
A. Ye. Demkovych

Introduction. Activation of lipid peroxidation is one of the trigger mechanisms of periodontium injury, which is primary caused by cellular damage. Reactive oxygen and nitrogen species (RONS) are able to cause damage to a cell as well as final products of lipid peroxidation, including unsaturated aldehydes and other metabolites. Objective. The aim of the research was to determine the role of RONS and accumulation of lipid peroxidation derivatives in initial development and formation of chronical inflammatory process in periodontium. Methods. Experimental periodontitis was modeled in animals by injection of complex mixtures of microorganisms diluted in egg protein into periodontal tissues. The results of biochemical studies of free radical processes activity in blood serum were evaluated by content of diene, triene conjugates, TBA-active products and total quantity of metabolites of nitric oxide (NO2–+NO3–), which were determined on the 7th, 14th and 30th days of the experiment. Results. Generation of active forms of oxygen is more influential, providing longevity of inflammatory process. This pays attention to typical dynamics of changes in active processes of lipid peroxidation in the development and course of experimental periodontitis. The study of inflammatory process with a bacterial-immune component in the rats’ periodontal complex proved accumulation of lipid peroxidation and nitric oxide metabolites in blood serum.Conclusions. The preservation of increased lipid peroxidation and nitric oxide metabolites in blood serum of the experimental animals with acute periodontitis conduce enhance of alteration and delayed healing that result in its sequel into chronical periodontitis.


2019 ◽  
pp. 375-384
Author(s):  
E. PROKUDINA ◽  
L MASLOV ◽  
N. NARYZHNAYA ◽  
S. TSIBULNIKOV ◽  
Y. LISHMANOV ◽  
...  

The objectives of this study were to investigate the role of endogenous opioids in the mediation of stress-induced cardiomyopathy (SIC), and to evaluate which opioid receptors regulate heart resistance to immobilization stress. Wistar rats were subjected to 24 h immobilization stress. Stress-induced heart injury was assessed by 99mTc-pyrophosphate accumulation in the heart. The opioid receptor (OR) antagonists (naltrexone, NxMB – naltrexone methyl bromide, MR 2266, ICI 174.864) and agonists (DALDA, DAMGO, DSLET, U-50,488) were administered intraperitoneally prior to immobilization and 12 h after the start of stress. In addition, the selective µ OR agonists PL017 and DAMGO were administered intracerebroventricularly prior to stress. Finally pretreatment with guanethidine was used. Naltrexone did not alter the cardiac 99mTc-PP accumulation in stressed rats. NxMB aggravated stress-induced cardiomyopathy (P=0.005) (SIC). The selective µ OR agonist DALDA, which does not cross the blood-brain barrier, completely prevented (P=0.006) SIC. The µ OR agonist DAMGO exhibited weaker effect than DALDA. The selective δ ligand (DSLET) and κ OR ligand (U-50,488) did not alter stress-induced 99mTc-pyrophosphate accumulation in the heart. Intracerebroventricular administration of the µ OR agonists aggravated SIC. Pretreatment with guanethidine abolished this effect (P=0.01). Guanethidine alone exhibited cardioprotective properties. A stimulation of central µ OR promotes an appearance of SIC. In contrast, stimulation of peripheral µ OR contributes to an increase in cardiac tolerance to stress.


1987 ◽  
Author(s):  
A Del Maschio ◽  
E Corvazier ◽  
F Maillet ◽  
M Kazatchkine ◽  
J Maclouf

The degranulatlon of human PMNs by opsonlsed zymosan (OpZ) was studied In the presence or In the absence of platelet alone or after stimulation by thrombin. Evidence Is presented that the presence of platelets Increased the extent of the liberation of lysozyme from PMNs stimulated by OpZ with a maximal intensity when they were stimulated by thrombin. The extent of the amplification was higher when the PMNs trigger was lower (i.e. 0.5 x 108 particles/ml as compared to 3.0 x 108 particles). This effect was dependent on the platelet concentration (from 10-80 platelets/PMN). Platelets stimulated by thrombin could alsoactivate the resting PMNs with a maximum obtained ata thrombin concentration of 0.1 U/ml, corresponding to the maximal release by these cells of products stored In their granules. However, the substitution ofplatelet suspensions by the released products found In their supernatant after stimulation by thrombin, resulted In a comparable stimulation only at platelet concentrations above the ones for coincubation experiments. These findings suggest that the presence of platelets themselves or In combination with their released products are responsible for this amplification. The use of zymosan alone or coated with IgG, C3b1, C3b or OpZ did not reveal any specificity of the Inducer for this amplification suggesting that platelets and/or platelet products acted by enhancing acommon step of PMNs activation Independent of the stimulus carried by the particles. Additionally, It could be noted that the maximal effect of the amplification by platelets occurred when the level of stimulation of the PMNs alone was the weakest.


1998 ◽  
Vol 275 (1) ◽  
pp. H145-H150 ◽  
Author(s):  
Mohammad M. H. Khan ◽  
Satya P. Kunapuli ◽  
Yingzhang Lin ◽  
Abraham Majluf-Cruz ◽  
Raul A. Dela Cadena ◽  
...  

The binding of high-molecular-weight kininogen (HK) to neutrophils (polymorphonuclear leukocytes, PMN) is required for the stimulation of aggregation and degranulation by human plasma kallikrein as well as the displacement of fibrinogen from this cell surface. The putative receptor for HK is the leukocyte integrin αMβ2, and domains 3 (D3) and 5 (D5) of HK form its binding site. To further map the binding sites on HK for PMN, we used D3 recombinant exon products and designed peptides from D3 and D5. In D3, a heptapeptide, Leu271-Ala277, from exon 7 product, and a peptide, Cys333-Cys352, from exon 9 product can inhibit binding of kininogen to PMN. Two contiguous peptides from D5 in the histidine-glycine-rich region, Gly442-Lys458and Phe459-Lys478, each inhibit the binding of HK to PMN. This study has thus delineated three noncontiguous surface-oriented sequences on HK, which together comprise all or most of the binding site for human PMN.


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