This study investigated the effect of exercise training on the flow- mediated dilation (FMD) in gastrocnemius muscle arteries from spontaneously hypertensive rats (SHR). SHR and WKY rats were divided into sedentary and exercised groups. After swimming exercise for eight weeks, the isolated arteries were mounted on pressurized myograph and FMD re sponses examined. The role of nitric oxide (NO), prostaglandins (PGs) and endothelium derived hyperpolarizing factor (EDHF) on FMD were assessed by obtaining dilation responses in the presence and absence of pharmacological antagonists. Nω-nitro-L-arginine methyl ester (L-NAME), indomethacin (INDO) and tetraethylamonium (TEA) were used to inhibit nitric oxide synthase, cyclooxygenase and EDHF-mediated responses, respectively. The FMD response was significantly blunted in arteries of SHR compared with WKY rats, and, improved by exercise training in SHR (SHR-ET) group. In SHR arteries, L-NAME and TEA did not affect dilation responses to flow, while INDO led to a significant enhancement in this response. Although dilation response was not altered by L-NAME in arteries obtained from trained SHR, TEA caused a significant attenuation and INDO led to significant increases. These results demonstrate that exercise training improves FMD in SHR, and, this enhancement induced by exercise training occurs through EDHF-mediated mechanism(s)., F. Gündüz ... [et al.]., and Obsahuje bibliografii a bibliografické odkazy
In this study we have evaluated the effect of maximal incremental cycling exercise (IE) on the systemic release of prostacyclin (PGI2), assessed as plasma 6-keto-PGF1α concentration in young healthy men. Eleven physically active - untrained men (mean ± S.D.) aged 22.7 ± 2.1 years; body mass 76.3 ± 9.1 kg; BMI 23.30 ± 2.18 kg · m-2; maximal oxygen uptake (VO2max) 46.5 ± 3.9 ml · kg-1 · min-1, performed an IE test until exhaustion. Plasma concentrations of 6-keto-PGF1α, lactate, and cytokines were measured in venous blood samples taken prior to the exercise and at the exhaustion. The net exercise-induced increase in 6-keto-PGF1α concentration, expressed as the difference between the end-exercise minus pre-exercise concentration positively correlated with VO2max (r=0.78, p=0.004) as well as with the net VO2 increase at exhaustion (r=0.81, p=0.003), but not with other respiratory, cardiac, metabolic or inflammatory parameters of the exercise (minute ventilation, heart rate, plasma lactate, IL-6 or TNF-α concentrations). The exercise-induced increase in 6-keto-PGF1α concentration was significantly higher (p=0.008) in a group of subjects (n=5) with the highest VO2max when compared to the group of subjects with the lowest VO2max, in which no increase in 6-keto-PGF1α concentration was found. In conclusion, we demonstrated, to our knowledge for the first time, that exercise-induced release of PGI2 in young healthy men correlates with VO2max, suggesting that vascular capacity to release PGI2 in response to physical exercise represents an important factor characterizing exercise tolerance. Moreover, we postulate that the impairment of exercise-induced release of PGI2 leads to the increased cardiovascular hazard of vigorous exercise., J. A. Zoladz ... [et al.]., and Obsahuje seznam literatury
In some patients, heart failure (HF) is associated with increased pulmonary vascular resistance (PVR). The magnitude and the reversibility of PVR elevation affect the HF management. Sildenafil has been recently recognized as potent PVR-lowering drug in HF. The aim of the study was to compare hemodynamic effects and pulmonary selectivity of sildenafil to prostaglandin E1(PGE1). Right-heart catheterization was performed in 13 euvolemic advanced HF patien ts with elevated PVR (6.3±2 Wood's units). Hemodynamic parameters were measured at the baseline, during i.v. infusion of PGE1 (alprostadil 200 ng·kg-1·min-1 ) and after 40 mg oral do se of sildenafil. Both drugs similarly reduced systemic vascular resistance (SVR), but sildenafil had higher effect on PVR (-28 % vs. -49 %, p=0.05) and transpulmonary pressu re gradient than PGE1. The PVR/SVR ratio - an index of pulmonary se lectivity, did not change after PGE1(p=0.7) but it decreased by -32 % (p=0.004) after sildenafil. Both drugs similarly reduced pulmonary artery mean and wedge pressures and increa sed cardiac index (+27 % and +28 %). Sildenafil led more often to transplant-acceptable PVR while causing smaller drop of mean systemic pressure than PGE1. In conclusion, vasodilatatory effects of sildenafil in patients with heart failure are more pronounced in pulmonary than in systemic circulation., H. Al-Hiti ... [et al.]., and Obsahuje bibliografii a bibliografické odkazy