Overtraining does not induce oxidative stress and inflammation in blood and heart of rats.

The aim of our research was to evaluate the changes in levels of cytokines and redox state parameters in blood and isolated heart of rats subjected to different swimming protocols. Rats were divided into 3 groups: 1) controls, 2) moderately trained rats that during all 12 weeks swam 1 h/day, 5 days/week, and 3) overtrained rats that in 10(th) week swam twice, 11(th) week 3 times, and in 12(th) week 4 times a day for 1 h. After sacrificing, blood from jugular vein was collected, and the heart excised and perfused on a Langendorff apparatus. Samples of the coronary effluent were collected during coronary autoregulation. Levels of superoxide anion radical (O(2)(-)), hydrogen peroxide (H(2)O(2)), nitric oxide (NO) and thiobarbituric acid reactive substances (TBARS) were measured in plasma and coronary effluent, while reduced glutathione (GSH), activities of superoxide dismutase (SOD) and catalase (CAT) were measured in erythrocytes. Venous blood was also used for interleukin 6 (IL-6) and tumor necrosis factor alpha (TNF-alpha) determination. Moderate training protocol induced the decrease of TBARS in plasma, while both training protocols induced the decrease of O(2)(-) and H(2)O(2) in coronary effluent. There was no significant difference in levels of cytokines between groups. The results of study add evidence about beneficial effects of moderate-intensity training on blood and cardiac redox state of rats, and furthermore, shows that exercising frequently, if the intensity stays within moderate range, may not have detrimental effects.

Kinetics of thyroxine (T(4)) and triiodothyronine (T(3)) transport in the isolated rat heart.

The dynamics and kinetics of thyroid hormone transport in the isolated rat heart were examined using the modified unidirectional paired tracer dilution method. The uptake of (125)I-thyroxine ((125)I-T(4)) and (125)I-triiodothyronine ((125)I-T(3)) from the extracellular space into heart cells was measured relative to the extracellular space marker (3)H-mannitol. The thyroid hormone maximal uptake was 54.4 % for (125)I-T(4) and 52.15 % for (125)I-T(3). The thyroid hormone net uptake was 25.69 % for (125)I-T(4) and 25.49 % for (125)I-T(3). Backflux from the intracellular space was 53.17 % for (125)I-T(4) and 61.59 % for (125)I-T(3). In the presence of unlabelled thyroid hormones, (125)I-T(4) and (125)I-T(3) maximal uptakes were reduced from 10.1 to 59.74 % and from 34.6 to 65.3 %, respectively, depending on the concentration of the unlabelled hormone, suggesting a saturable mechanism of the thyroid hormone uptake by the heart cells, with K(m(T4))= 105.46 microM and the maximal rate of (125)I-thyroid hormone flux from the extracellular space to heart cells (V(max(T4))) = 177.84 nM min(-1) for (125)I-T(4) uptake, and K(m(T3)) = 80.0 microM and V(max(T3)) = 118.5 nM min(-1) for (125)I-T(3) uptake. Experimental Physiology (2001) 86.1, 13-18.

Design of a method for in vitro studies of polymer adhesion.

In this paper we describe a modified intestinal perfusion technique for investigation of bioadhesion phenomena. This technique is an in vitro method with well standardized experimental conditions which measures the intestinal intraluminal pressure and its oscillation. This also allows the vitality of the intestinal segment used in the experimental to be checked. Our results suggest that the longest adhesion occurred with polyacrylic acid, in comparison with carboxymethylcellulose sodium and the shortest with hydroxypropylcellulose.

Dynamic analysis of the three-phasic vascular response to histamine in coronary circulation.

In this work we tried to perform a dynamic analysis of coronary vascular response to histamine, using a simple mathematical analysis as a first step in the better understanding of complex histamine effects on coronary blood vessels of the isolated guinea pig heart. So, we defined more parameters, such as: I and delta I to quantify the intensity of coronary perfusion pressure (CPP) change, T and dt to quantify the time CPP change occurs and D to characterize the intensity and duration of CPP change, i.e. to quantify the dynamics of this change.

Tiazofurine uptake by the isolated guinea pig heart.

Tiazofurine is a selective inhibitor of the enzyme inosine monophosphate dehydrogenase, and exhibits potent antitumor activity. Considering the potential side effects on the heart, [3H] tiazofurine uptake into the cardiomyocytes, as well as the mechanism of transport, were studied in the isolated perfused guinea pig heart, using the rapid single circulation, paired-tracer technique. The maximal cellular uptake (Umax) of [3H] tiazofurine ranged from 19% to 25% of the injected dose, with total cellular uptake (Utot) ranging 12.1-15.6%. The addition of unlabeled tiazofurine caused inhibition of [3H] tiazofurine uptake, with a Umax value of 9.06 +/- 4.6%. Therefore, the uptake of tiazofurine into cardiomyocytes could be considered a saturable process. The inhibition of [3H] tiazofurine uptake caused by adenosine and dipyridamole was of the same degree as the inhibition by unlabeled tiazofurine. Thus, it can be assumed that nucleosides' transport system(s) are involved in transport of tiazofurine into myocardial cells.

Biphasic L-arginine uptake by the isolated guinea-pig heart.

L-Arginine is the physiological substrate for the formation of nitric oxide (NO) and accounts for the biological activity of endothelium-derived relaxing factor. We have studied L-arginine transport in the heart using a rapid dual-isotope dilution technique. The time course of L-[3H]arginine uptake (extraction) by the isolated perfused guinea-pig heart was found to occur in two phases. The first phase reached a plateau in 6.6 +/- 0.6 s and lasted 8.8 +/- 0.7 s, whereas the second phase developed a plateau after 16.3 +/- 0.8 s. The first phase of maximal uptake (Umax,1) accounted for 13.4 +/- 1.4% of the total uptake and the second (Umax,2) for 32.3 +/- 1.8%. The two phases of uptake were inhibited by unlabelled L-arginine in a dose-dependent manner, which suggests that both phases are carrier mediated. The degree of inhibition of Umax,1 and Umax,2 by unlabelled L-arginine was not significantly different. Studies of the kinetics of uptake of these processes revealed an apparent Km,1 of 183 +/- 10 microM with a Vmax,1 of 50 +/- 10 nmol min-1 g-1 for the first phase and Km,2 of 167 +/- 14 microM with a Vmax,2 of 93 +/- 13 nmol min-1 g-1 for the second phase of uptake. These results suggest a similar affinity for the receptors of both transport systems, but with different values for Vmax (P < 0.05). In contrast, 1 mM unlabelled D-arginine had no effect on either the first or second phase of uptake of L-[3H]arginine by the heart, which suggests that these processes are stereospecific. In the presence of the L-stereoisomer of nitro-arginine-mono-methyl ester (L-NAME), a potent inhibitor of NO synthesis, the Umax,1 was inhibited by about 60% while Umax,2 was inhibited by only 20%, which suggests that there is a difference in the effect of L-NAME on the two phases of L-arginine uptake. The first phase most probably represents uptake into the capillary wall, i.e. endothelium and smooth muscle, while the second phase represents entry into the extra-endothelial compartment, i.e. the cardiac myocytes and fibroblasts.

Characteristics of thiamin transport in the isolated perfused guinea pig heart.

The cellular uptake of (14C)-thiamin hydrochloride was studied in the isolated perfused guinea pig heart, using the rapid single circulation, paired-tracer technique, in which D-(3H)-mannitol serves as an extracellular marker. Cellular uptake of this vitamin was estimated by directly comparing venous dilution profiles of (14C) and (3H) radioactivities in the absence and presence of unlabelled thiamin hydrochloride and pyrithiamin hydrobromide. The maximal cellular uptake (Umax) of thiamin was very low (5.31 +/- 1.79%), while in the presence of 10 mM unlabelled thiamin and 1 mM pyrithiamin, Umax was significantly greater (9.71 +/- 1.57% and 12.30 +/- 0.82%, respectively). Our data suggest that there is a saturable mechanism of sarcolemmal thiamin transport out of myocardial cell, while this transport into the cell is unsaturable.

The effects of (R) alpha-methyl histamine on the isolated guinea pig aorta.

The effects of the H3 agonist (R) alpha-methyl histamine ( (R) alpha-MeHA) on the isolated guinea pig aorta were investigated. At all the concentrations of (R) alpha-MeHA used, a relaxation of the aorta, which had been preconstricted with KC1 (50mM), was produced. This response was abolished by the H3 antagonist mixture of cimetidine (100 microM) and impromidine (10 microM). In contrast the same concentrations of histamine produced vasoconstriction which could be abolished by the H1 antagonist pyrilamine (3 microM). The results show that (R) alpha-MeHA produces a vasodilation response which is most probably mediated by H3 receptors and provides further evidence of a functional role for H3 receptors in the control of the cardiovascular system.