Morphometric changes of cardiac mast cells in rats acutely poisoned by T-2 toxin
ABSTRACT Wistar rats were treated with T-2 toxin (1 LD50; 0.23 mg/kg sc) and the surviving animals were sacrificed on days 1, 3, 5, 7, 14, 21 and 28 after treatment. At each time, control animals were sacrificed, too. Cardiac mast cells, previously stained by Giemsa method, were analyzed in whole visual fields, magnification x40. In the present study the following quantitative morphometric parameters of cardiac mast cells were evaluated: perimeter (P), area (A) and roundness (R). In the control groups of rats the majority of mast cells were small (P = 6.86 - 7.99 mm), hypogranular (A = 11.60 -14.30 mm2) and ovoid (R = 0.60 - 0.65 mm). Mast cells, with discrete granules, hypergranular, had significantly different quantitative parameters (P = 12.80 -14.90 mm; A = 16.70 -20.00 mm2; R = 0.35 -0.38 mm). The minority of mast cells, classified as degranulated, had a large (P=20.70-23.30 mm), irregular shape (A = 24.40 -30.90 mm2) and showed degranulation (R = 0.15 - 0.21 mm). In the heart of T-2 toxin-treated rats the quantitative parametar values of hypogranular mast cells and hypergranular mast cells were similar to the control group during the whole study. However, degranulated mast cells showed a significant increase in perimeter and area values (p<0.05), while their roundness was decreased (p<0.05) in comparison to the control groups of animals. It could be concluded that the chosen quantitative morphometric parameters of cardiac degranular mast cells are useful for the evaluation of the functional status of the rats' heart during acute T-2 poisoning. .
Full-textDOI: · Available from: Vesna Jacevic, Jun 12, 2015
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ABSTRACT: Radiation-induced heart disease (RIHD), characterized by accelerated atherosclerosis and adverse tissue remodeling, is a serious sequelae after radiotherapy of thoracic and chest wall tumors. Adverse cardiac remodeling in RIHD and other cardiac disorders is frequently accompanied by mast cell hyperplasia, suggesting that mast cells may affect the development of cardiac fibrosis. This study used a mast cell-deficient rat model to define the role of mast cells in RIHD. Mast cell-deficient rats (Ws/Ws) and mast cell-competent littermate controls (+/+) were exposed to 18 Gy localized single-dose irradiation of the heart. Six months after irradiation, cardiac function was examined by echocardiography and Langendorff-perfused isolated heart preparation, whereas structural changes were assessed using quantitative histology and immunohistochemical analysis. Mast cell-deficient rats exhibited more severe postradiation changes than mast cell-competent littermates. Hence, mast cell-deficient rats exhibited a greater upward/leftward shift in the left ventricular (LV) diastolic pressure-volume relationship (P = 0.001), a greater reduction in in vivo LV diastolic area (from 0.50 +/- 0.024 cm in age-matched controls to 0.24 +/- 0.032 cm after irradiation; P = 0.006), and a greater increase in LV posterior wall thickness (from 0.13 +/- 0.003 cm in age-matched controls to 0.15 +/- 0.003 cm after irradiation; P = 0.04). Structural analysis revealed more pronounced postradiation accumulation of interstitial collagen III but less myocardial degeneration in hearts from mast cell-deficient rats. These data show that the absence of mast cells accelerates the development of functional changes in the irradiated heart, particularly diastolic dysfunction, and suggest that, in contrast to what has been the prevailing assumption, the role of mast cells in RIHD is predominantly protective.Cancer Research 05/2005; 65(8):3100-7. DOI:10.1158/0008-5472.CAN-04-4333 · 9.28 Impact Factor
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ABSTRACT: Experiments were performed on pentobarbital-anesthetized cats to test the hypothesis that hypovolemia rather than cardiac failure is responsible for the acute lethal toxicity of the trichothecene mycotoxin, T-2 toxin (T2T). Measurements were made on mean arterial blood pressure (MAP), arterial pulse pressure (PP), and heart rate (HR) in eight otherwise untreated cats given T2T (2 mg/kg iv) and in three cats similarly injected with T2T but then transfused with plasma and blood. The transfusions to their available extent significantly delayed or counteracted the development of mycotoxic shock (i.e., depressed MAP and PP) and prevented or reversed a rise in the hematocrit. HR remained stable under all conditions. Plasmapheresis followed by whole-blood removal was found best to simulate mechanistically the mycotoxic shock syndrome in six blood donor cats free of T2T. It is concluded that hypovolemia with polycythemia resulting from plasma leakage and internal bleeding accounts for acute lethal T-2 mycotoxicosis.Toxicology and Applied Pharmacology 04/1991; 108(1):107-13. DOI:10.1016/0041-008X(91)90273-H · 3.63 Impact Factor
- Lloydia 38(1):21-35.