Troponins in experimental studies

The aim of our study was to compare the diagnostic performance of cardiac troponin T (cTnT) and cardiac troponin I (cTnI) in three groups of rabbits: 1) control (saline 1 ml/kg i.v.); 2) daunorubicin (3 mg/kg i.v.); 3) daunorubicin (3 mg/kg i.v.) + dexrazoxane (60 mg/kg i.p.). The drugs were given once a week, 10 administrations. The concentration of cTnT was measured using Elecsys Troponin T STAT Immunoassay (Roche). The concentration of cTnI was measured using AxSYM Troponin I (Abbott). The linear regression model was applied to see if there is a dependence between cTnT and cTnI. The coefficient of determination (R2 = 0.79) was acceptable only in the control group. In the remaining cases (i.e. in the daunorubicin group and in the daunorubicin + dexrazoxane treated group) R2 was too small (0.53, and 0.06). We may conclude that in rabbits after repeated administration of cardiotoxic or cardioprotective drugs meaningful dependence between cTnT and cTnI was not found. The choice of the most suitable cardiomarker in laboratory animals deserves further studies.     

Immunopathology of experimental bronchiectasis

In human bronchiectasis, the bronchial wall is the seat of abnormal mononuclear cell infiltration, which suggests the presence of a cell-mediated immune reaction. The histopathology of a recently devised animal model of experimental bronchiectasis resembles that of the human disease. We have investigated its immunohistology to validate the similarity to that of human bronchiectasis in order to provide a model for the study of cellular immune aspects of the pathogenesis of bronchiectasis. The immunohistology of the bronchial wall mononuclear cell population in experimental rat bronchiectasis was compared with that in control and normal rats. The control rats did not develop bronchiectasis, and the composition and distribution of mononuclear cells in the bronchial wall were similar to those of normal animals. In the rats developing bronchiectasis, there was infiltration of T lymphocytes, macrophages, and dendritic cells (as defined by monoclonal antibodies) in all compartments of the lung, particularly in the bronchial wall and around vessels. The bronchus-associated lymphoid tissue was disrupted by heavy infiltration of T cells, and follicular aggregates of T lymphocytes were seen deeper in the lung parenchyma. Expression of Ia antigen increased in the bronchial epithelium and in large numbers of mononuclear cells throughout the lung. These findings suggest that a cell-mediated immune response appears during the development of experimental bronchiectasis in this rat model. This cellular immune response is similar to that described in human bronchiectasis and may enable this animal model to be used in defining the role of cellular immunity in the pathogenesis of bronchiectasis.     

Immunobiology of experimental leishmaniasis

Self-cure versus uncontrolled disease progression in experimental murine cutaneous leishmaniasis depends upon a delicate interplay among various activated cells of the host's immune system. Susceptibility or resistance to infection with Leishmania major is correlated with the ability of different inbred strains of mice to produce the characteristic spectra of lymphokines upon infection. Appropriate experimental interventions now allow the modulation of these reponses, providing the possibility to render genetically susceptible mice resistant to infection and, vice versa, to cause genotypically healer strains to express a non-healer phenotype. These experimental manipulations have proven to be powerful tools in the dissection of the underlying immune mechanisms and cellular parameters responsible for susceptibility and resistance, and will perhaps allow the identification of molecules of parasite origin that induce deleterious immune responses to infection with Leishmania, and thus to exclude them from future vaccines. More importantly, rational immune intervention could permit the diversion of established host-damaging immune responses to host-protective immunization.     

Model of experimental pollinosis

A model of experimental pollinosis was created in guinea pigs. The animals were kept in a chamber in which the allergen, a dialyzed aqueous extract of ragweed pollen, was dispersed by means of a coaxial nebulizer. As a result of aerosol sensitization the guinea pigs formed homocytotropic antibodies, an indication of their sensitization to the specific allergen. Sensitization of the animals to ragweed allergen was accompanied by increased sensitivity of the bronchopulmonary system and was characterized by reflex bronchospasm to a reacting inhalation or to intravenous injection of the specific allergen.Allergologic Research Laboratory, Academy of Medical Sciences of the USSR, Moscow. Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 84, No. 11, pp. 590–593, November, 1977.     

Endotoxemia in experimental acholia

The intensity of experimental endotoxemia is assessed by serum content of medium molecules. Serum creatinine and bilirubin contents and leukocyte count are also monitored. It is found that acholia leads to pronounced endogenous intoxication which can be prevented by early return of bile into the organism. Translated fromByulleten’ Eksperimental’noi Biologii i Meditsiny, Vol. 123, No. 1, pp. 101–102, January, 1997     

Gluten-induced experimental IgA glomerulopathy

The effect of alimentary gluten and of its lectin-like fraction gliadin in inducing IgA mesangial deposits in BALB/c mice was investigated. In the pilot study G1 (4 mice), G2 (4 mice) and G3 (6 mice) received ovalbumin, human gamma-globulins, and crude gluten, respectively. The antigens, 1 mg/ml, were given in drinking water for 14 weeks. G4 (20 mice) were fed with standard mouse fodder. Gluten, as well as other alimentary antigens, induced IgA mesangial deposits with intense IgA staining in each animal, however a positive IgA staining was also observed in 10 of 20 adult controls. Antigliadin IgA antibodies were detected in renal tissue eluates from gluten-immunized mice but were found in eluates from control animals too. IgA deposits and antigliadin IgA in renal tissue were also observed in 3 of 7 adult mice (G7) fed for 30 weeks with standard fodder, then for 1 month with a protein-free diet supplemented with 20% amino acids. Conversely, there were no IgA mesangial deposits or IgA anti-gliadin antibodies in renal eluates of 1- or 2-week-old mice (G5 and G6). For the definitive protocol, 4-week-old BALB/c mice were selected and fed with basal glutenfree diet. G8 (14 mice) did not receive any alimentary immunogen in the drinking water, whereas G9 (15 mice) and G10 (15 mice) received ovalbumin and gliadin, respectively. G11 (15 mice) had standard gluten-containing diet. IgA deposits semiquantified by immunofluorescence scores were found to be significantly greater in G9 and G10 than in G8 (Student' t-test p1 less than 0.003, Mann-Whitney test p2 less than 0.001 and p1 less than 0.01, p2 less than 0.007, respectively), and in G11 than in G8 (p1 and p2 less than 0.05). The presence of positive IgA staining (greater than or equal to 2/6 scores) was significantly less frequent in G8 in comparison to G9 (chi-square test p3 less than 0.002), G10 (p3 less than 0.02) and G11 (p3 less than 0.04). Total serum IgA were significantly higher in orally immunized G9 and G10 than in G8 control mice (p1 less than 0.005, p2 less than 0.002). Anti-gliadin IgA in circulation as well as in renal deposit eluates were significantly increased in gluten-eating mice (G10 and G11) as compared with the gluten-free control group G8. These observations indicate that gliadin does induce IgA immune deposits in BALB/c mice.(ABSTRACT TRUNCATED AT 250 WORDS)     

Hyperpyruvaturia in experimental diabetes

1. The 24 hourly excretion of pyruvate and glucose has been measured in alloxan-diabetic rats.2. The animals were allowed a 6-day control period before being injected with alloxan (I.V. 50 mg/kg body weight). The diabetes was treated by daily injections of insulin for a period of 6 days from the 7th to the 12th day following the alloxan injection.3. The pyruvate excretion increased more than 5-fold following the induction of diabetes, the values being 189 +/- 130 (S.D.) mug/24 hr in the control period rising to an average of 1002 +/- 664 (S.D.) mug/24 hr over the first 6 days of diabetes. The administration of insulin over the second 6-day period of diabetes caused the pyruvate excretion to decrease-though not significantly. Upon the withdrawal of the insulin treatment the pyruvate excretion increased significantly from 785 +/- 315 (S.D.) mug/24 hr to 2105 +/- 679 (S.D.) mug/24 hr, measured over a 5-day period. The final period of pyruvate excretion was significantly greater than the excretion over the first diabetic period.4. The glucose excretion during the initial diabetic period was 6.75 +/- 2.64 (S.D.) g/24 hr. The administration of insulin caused a 42% decrease in glucose excretion compared to a decrease of 22% for the pyruvate. The withdrawal of insulin caused the glucose excretion to increase by 149% while the pyruvate excretion increased by 157%.5. Diabetes was also induced temporarily by injections of anti-insulin serum and diazoxide. In each case significant glycosuria and hyperpyruvaturia were produced.6. The possible causes of the hyperpyruvaturia in diabetes are discussed.