A patent ductus arteriosus (DA) was maintained in newborn rats (Wistar strain) by administering prostaglandin E2 (PG E2) in doses of 15 /ig.kg'1 at 30 min intervals up to 300 min after birth. In the control animals, the DA was functionally closed 300 min after birth. The lumen was blocked by clustered endothelial cells at various stages of degeneration. Elastic membranes of the media had disintegrated into irregular fragments and the smooth muscle cells were contracted. Cytoplasm excrescences formed on their surface as a result of contraction protruded as hernias into adjacent muscle cells and into endothelial cells. The smooth muscle cells degenerated. The administration of PG E2 inhibited contraction of the smooth muscle cells and so also the development of degenerative changes; 300 min after birth the DA was fully patent, the elastic membranes were structurally intact, regularly organized and continuous. The smooth muscle cells had the character of synthesizing cells with richly developed granular endoplasmic reticulum. The intima and its endothelial lining were likewise free from structural changes. The ultrastructural image of the wall of the DA correspondent to the state 10 min after birth, when the DA was fully patent. The administration of PG E2 did not induce any ultrastructural changes indicative of injury to the wall of the DA.
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
We studied the effects of hydrocortisone as a possible regulatory factor of bone blood flow and metabolism. Local bone blood flow in the tibia, distal femur, lumbar vertebra and some soft tissues (using 85Sr-microspheres), as well as 45Ca and 3H-proline incorporation into the tibia, bone density and ash weight per ml of the tibia were measured in sham-operated and oophorectomized female rats in which the influence of hydrocortisone administration (0.004 % diet for 5 weeks) was followed. Hydrocortisone markedly lowered 85Sr-microsphere uptake and blood flow through the bones of non-castrated female rats as well as elevated circulatory values in oophorectomized rats. The changes were nearly identical in the three bone samples measured; among the soft tissues only the kidneys showed a less pronounced decrease. Circulatory changes in the bones seem to be caused by local vascular reactions. Hydrocortisone also lowered the 24-hour incorporation of 45Ca and 3H-proline into the tibia of both non-castrated and oophorectomized females. In the tibia of oophorectomized rats, hydrocortisone normalized the decreased bone density and ash weight. The adrenocortical hormones are known to block eicosanoid synthesis by the inhibition of arachidonic acid production. It is possible, therefore, that local circulatory changes in the bones of rats, induced by hydrocortisone, are mediated by the changes in prostaglandin production.
The role of afferent sensory neurones in gastric mucosal protection is discussed. The principal effects of substance P and capsaicin on gastric motility and mucosal blood flow are taken in correlation with gastric mucosal injury. It seems likely that the protective effect of sensory neuropeptides is dependent on gastric mucosal blood flow and is mediated through the nitric oxide-generating system and partly the prostaglandins. The interaction between these two systems and the primordial effect of one of them on gastric mucosal blood flow and mucosal integrity after neuropeptide release is still not clear.
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