Non-Linear Mechanical Behavior of Visco-Elastic Biological Structures – Measurements and Models

Mechanical properties of biological structures affect functional ability of organism. Current knowledge is prevailingly concentrated on static characteristics. The present work analyzed dynamic mechanical responses of various biological materials. Following biological structures were measured: samples of aorta walls of human origin and from model organisms, human body surface, and samples of bones of various types and origin. Linear approximation leads in case of aortas and bones to simple Voight's model. Modules of elasticity (in tensile loading) of aortas were from 102 kPa to 103 kPa. Module of elasticity of bones were from 106 Pa to 1010 Pa. Viscous coefficients of aortas were from 102 Pa.s to 103 Pa.s. Viscous coefficients of bones were from 100 Pa.s to 102 Pa.s. Nonlinearities: We found that following types of nonlinearities are significant: strain-stress relationship, time-dependent changes in elastic as well as viscose bodies. Strain and stress is well approximated by quadratic function σ = a ε2 + b ε + c with parameters a = 1833, b = 135, c = 20.0 (porcine aorta). Time-dependence in elastic coefficient: At the beginning of responses the elastic coefficient was of 42% lower then at 0.02 s of duration of the response (porcine aortas). Analogical results follow also from experiments on other structures (skin, bones)

THE APPLICATION OF STEREOLOGICAL METHODS FOR THE QUANTITATIVE ANALYSIS OF THE ATHEROSCLEROTIC LESIONS IN RABBITS

Atherosclerosis is a chronic metabolic and inflammatory disease of vascular arteries. Insome cases, it comes the accumulation of the inflammatory cells and extracellular matrix in vessel intima, which lead to the narrowing of the vessel lumen. The aim of this study was introduce stereological methods for the quantification of atherosclerotic changes in the aorta of New Zealand White rabbits in dependence on the period of feeding with atherogenic diet containing 0.4% of cholesterol. The Cavalieri estimator was used for the estimation of the volume of atherosclerotic lesions. The area of the atherosclerotic lesions and the area fraction of free vessel lumen were determined with the image analysis software Lucia. The principle of the point counting method was used for the estimation of the volume fraction of collagen in atherosclerotic lesions and the principle of the optical disector was used for the estimation of the number of cells per unit volume in atherosclerotic lesions. The results obtained by the stereological methods confirmed the induction and progression of atherogenic changes in rabbit vessel wall in cholesterol fed animals. The methods applied in this study will be used in our prospective studies where the effect of hypolipidemic drug treatment on atherogenic process will be monitore

Intravenous rutin in rat exacerbates isoprenaline-induced cardiotoxicity likely due to intracellular oxidative stress

<p><b>Objectives</b>: Rutin, quercetin-3-<i>O</i>-rutinoside, a natural flavonol glycoside, has shown various <i>in vitro</i> benefits with potential use treating human diseases, especially cardiovascular system disorders. Antioxidant properties are assumed to underlie the majority of these benefits. Yet rutin pro-oxidant properties have been reported as well. Our research group has recently shown aggravating effects on isoprenaline (ISO)-induced cardiotoxicity in Wistar:Han rats after 24 hours.</p> <p><b>Methods</b>: This study was designed to examine in more detail the reasons for the negative effects of rutin (11.5 and 46 mg/kg, i.v.) after administration of ISO (100 mg/kg, s.c.) in rats within 2 hours of continuous experiment and in the H9c2 cardiomyoblast-derived cell line.</p> <p><b>Results</b>: Like our previous findings, rutin did not (11.5 or 46 mg/kg, i.v.) reduce the ISO-induced mortality within 2 hours although the lower dose significantly reduced cardiac troponin T (cTnT) and partly improved the histological findings. In contrast, the higher dose increased the mortality in comparison with solvent (1.26% w/v sodium bicarbonate). This was not caused by any specific haemodynamic disturbances. It appears to be associated with oxidative stress as rutin enhanced intracellular reactive oxygen species formation <i>in vitro</i> and had the tendency to increase it <i>in vivo</i>.</p> <p><b>Conclusions</b>: Rutin, likely due to its pro-oxidative effects, can exacerbate catecholamine cardiotoxicity depending on the dose used.</p