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Öğe Calcium channel blockers and intimal hyperplasia(2006) Kerry Z.; Yasa M.Smooth muscle cell (SMC) proliferation and migration is considered to play a major role in the development of intimal hyperplasia, an early stage in the progression of atherosclerosis and restenosis. The underlying mechanism of the development of the formation of intimal hyperplasia is still under investigation. With regard to the involvement of calcium in cellular processes such as proliferation and migration, the effects of calcium channel blockers (CCBs) in the development of atherosclerosis have always been deemed a subject worthy of investigation. This brief review will discuss the effects of CCBs in intimal hyperplasia.Öğe The effect of cigarette smoke on the plasma piroxicam concentrations in rats(1990) Lermioglu F.; Berkan T.; Yasa M.; Kerry Z.; Yalçinkaya C.; özer A.Abstract— The plasma concentration of unchanged piroxicam has been determined at 15, 30, 60 and 90 min after 10 mg kg-1 oral administration of the drug to rats exposed to cigarette smoke or pretreated with phenobarbitone, 3,4-benzpyrene or ethanol. Plasma piroxicam concentrations decreased in rats pretreated with phenobarbitone, 3,4-benzpyrene and ethanol and in rats 24 h after exposure to cigarette smoke. 1990 Royal Pharmaceutical Society of Great BritainÖğe Effect of the model of early atherosclerosis on systemic hemodynamic parameters in rabbits [Tavşanlarda erken dönem ateroskleroz modelinin sistemik hemodinamik parametreler üzerindeki etkisi](Gulhane Askeri Tip Akademisi, 2005) Türkseven S.; Yasa M.The purpose of this study was to investigate the effects of perivascular collar application, a model that induces intimal thickening seen in early atherosclerosis, on systemic hemodynamic parameters of rabbits. Rabbits were divided into two groups. In the first group, on the 1st day of the experiment (collared group, n=10), a soft silicone collar was implanted around the left carotid artery. The second group (perivascular manipulation group, n=10), served as control, was subjected only to perivascular manipulation on their left carotid artery without implanting the collar. Hemodynamic parameters of the rabbits were measured for half an hour on the first day and the final day (day 15) before the surgical operation. Statistical analysis was carried out by Wilcoxon signed rank test. A p value of <0.05 was considered statistically significant. This study has shown that neither collar implantation nor the perivascular manipulation affected the systemic hemodynamic parameters. In the collared group, positioning of the collar around the carotid artery resulted in an increase in intimal cross sectional area as compared to the normal arteries (0.091±0.015 mm vs 0.009±0.000 mm2, respectively, p=0.000, n=10). However, perivascular manipulation did not alter intimali cross sectional area (normal 0.009±0.001 mm2, manipulation 0.008± 0.001 mm2, p=0.172, n=7). In this model, a significant relationship between collar-induced intimal thickening and systemic hemodynamic parameters has not been found. Systemic hemodynamic parameters may not account for intimal thickening in this model. © Gülhane Askeri Tip Akademial 2005.Öğe How to interpret relationship between ischemic time and ischemia/reperfusion injury in langendorff perfused rat hearts [Langendorff-perfüze si{dotless}çan kalbinde i·skemi süresi ile i·skemi/reperfüzyon hasari{dotless} arasi{dotless}ndaki i·lişki: Degerlendirme kriterleri neler olmali{dotless}?](Turkiye Klinikleri, 2013) Ertuna E.; Türkseven S.; Hayran H.M.; Sargon M.F.; Yasa M.Objective: Diversities in ischemia time and injury assessment criteria used in Langendorff perfused isolated heart models complicate evaluation of the results. In this study, relationship between myocardial functional recovery, tissue viability and ultrastructural changes following ischemia were investigated in order to determine criteria which should be used to make precise interpretations. Material and Methods: Hearts were perfused in the constant flow Langendorff mode and were subjected to either continuous perfusion (Control), or to 15 (Ischemia15), 30 (Ischemia30) or 45 (Ischemia45) minutes ischemia followed by 30 minutes reperfusion. Left ventricular developed pressure, maximum contraction and relaxation rates, heart rate, arrhythmia incidence and duration were evaluated. Coronary effluent and heart cross-sections were used for creatine kinase-MB (CK-MB) measurements and morphological studies, respectively. Results: All functional parameters remained unchanged in Control and Ischemia15 groups. In Ischemia30 group, LVDP, +dP/dtmax and -dP/dtmax declined in early reperfusion, +dP/dtmax returned to basal values and heart rate declined at the end of reperfusion. In Ischemia45 group, all functional parameters except for heart rate declined in early reperfusion and returned to basal values at the end of reperfusion. Arrhythmia scores increased in all hearts subjected to ischemia. CK-MB was not elevated and triphenyltetrasolium staining showed that tissues were viable in Control, Ischemia15 and Ischemia30 groups. Necrotic fields were found and CK-MB increased in Ischemia45 group. Despite low myofibril scores, most marked ultrastructural pathological changes were found in Ischemia15 group. As ischemia time increased, the ultrastructural changes expressed as edema, glycogen, mitochondria and nuclei scores decreased. Conclusion: Our findings show that functional parameters should be evaluated in conjunction with morphological and biochemical data to make precise interpretation in ischemia reperfusion studies in isolated Langendorff perfused rat hearts. © 2013 by Türkiye Klinikleri.Öğe Low-dose fluvastatin prevents the functional alterations of endothelium induced by short-term cholesterol feeding in rabbit carotid artery(2012) Sevin G.; Akcay Y.D.; Ozsarlak-Sozer G.; Yasa M.3-Hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, commonly known as statins, are the medical treatment of choice for hypercholesterolemia. In addition to lowering serum-cholesterol levels, statins appear to promote pleiotropic effects that are independent of changes in serum cholesterol. In this study, we investigated the effects of low-dose fluvastatin on antioxidant enzyme activities (superoxide dismutase, SOD; catalase), total nitrite/nitrate levels, and vascular reactivity in 2% cholesterol-fed rabbits. This diet did not generate any fatty streak lesions on carotid artery wall. However, SOD activity significantly increased with cholesterol feeding whereas the catalase activities decreased. The levels of nitrite/nitrate, stable products of NO degradation, diminished. Moreover, dietary cholesterol reduced vascular responses to acetylcholine, but contractions to serotonin were augmented. Fluvastatin treatment abrogated the cholesterol-induced increase in SOD, increased the levels of nitric oxide metabolites in tissue, and restored both the impaired vascular responses to acetylcholine and the augmented contractile responses to serotonin without affecting plasma-cholesterol levels. Phenylephrine contractions and nitroglycerine vasodilatations did not change in all groups. This study indicated that fluvastatin treatment performed early enough to improve impaired vascular responses may delay cardiovascular complications associated with several cardiovascular diseases. Copyright 2012 Gulnur Sevin et al.Öğe Methylglyoxal causes endothelial dysfunction: The role of endothelial nitric oxide synthase and amp-activated protein kinase(Walter de Gruyter GmbH, 2014) Turkseven S.; Ertuna E.; Yetik-Anacak G.; Yasa M.Background: Methylglyoxal is a major precursor in the formation of advanced glycation end products and is associated with the pathogenesis of diabetes-related vascular complications. The aim of this study was to evaluate whether methylglyoxal induces endothelial dysfunction and to determine the contributors involved in this process. Methods: Rat thoracic aortic rings were treated for 24 h with 100 µM methylglyoxal by using an organ culture method. A cumulative dose-response curve to acetylcholine was obtained to determine endothelium-dependent relaxation. The protein levels of endothelial nitric oxide synthase (eNOS) and its phosphorylated form at the serine 1177 site [p-eNOS (Ser1177)], heat shock protein 90 (Hsp90), AMP-activated protein kinase (AMPK?) and its phosphorylated form at the threonine 172 site [p-AMPK? (Thr172)] were evaluated. Superoxide production was determined by lucigenin-chemiluminescence. Results: Treatment with 100 µM methylglyoxal for 24 h decreased acetylcholine-induced vascular relaxation. The levels of eNOS and p-eNOS (Ser1177) were reduced while no effect on Hsp90 was observed. Levels of p-AMPK? (Thr172) were significantly decreased without any change in total AMPK? protein levels. Superoxide level was not affected by methylglyoxal treatment. Conclusions: In rat aortic rings, methylglyoxal determines a reduction in endothelium-dependent relaxation. This effect seems to be mediated via a reduction in p-eNOS (Ser1177) and p-AMPK(Thr172).Öğe Vasoprotective effects of nitric oxide in atherosclerosis(2005) Yasa M.; Türkseven S.The endothelium plays a crucial role in the process of atherosclerotic disease by means of its regulatory functions on the vasculature, such as control of vasomotor tone, local hemostasis and proliferative processes. One of the most important substances released by the endothelium is nitric oxide (NO), which acts as a vasodilator, and inhibits the proliferation of vascular smooth muscle cells, the aggregation of platelets and the infiltration of inflammatory cells. A reduction in NO production or activity has been proposed as a major mechanism of endothelial dysfunction and a contributor to atherosclerosis. Since endothelial dysfunction is considered an early marker for atherosclerosis and can be detected before structural changes in the vascular wall, an impairment of NO bioactivity or synthesis will reduce its braking effect on processes involved in atherogenesis. This review briefly describes the vasoprotective actions of NO, its role in the pathogenesis of atherosclerosis, and the novel therapeutic strategies improving endothelial dysfunction.Öğe Vasorelaxant effects of glibenclamide on rat thoracic aorta(2005) Ertuna E.; Yasa M.The purpose of this study was to investigate the effect of glibenclamide, a selective ATP-sensitive K+ (KATP) channel blocker, on agonist-induced contractions in isolated rat aortic rings. The possible involvement of endothelium in glibenclamide-induced response was also investigated. The concentration-response curves of prostaglandin F 2?(PGF2?; 0.1 nM-30 µM), serotonin (5-hydroxytryptamine, 5-HT; 1 nM-30 µM) and phenylephrine (1 nM-30 µM) were obtained in the absence or presence of glibenclamide (1, 3 or 10 µM). Maximum agonist-induced contractions in the presence of glibenclamide 1, 3 and 10 µM were decreased by 30±5, 64±3 and 86±2 percent for PGF2? and 41±11, 50±11 and 65±5 percent for 5-HT respectively. Phenylephrine-induced contractions remained unaltered by glibenclamide 10 µM. The inhibitory effect of glibenclamide (10 µM) on PGF2?- or 5-HT-induced contractions were attenuated upon N ?-nitro-L-arginin (L-NNA; 100 µM) plus indomethacin (10 µM) incubation. The inhibitory effect of glibenclamide on PGF 2?-induced contractions was also assessed in endothelium-denuded arteries and the inhibitory effect of glibenclamide was greater in endothelium-denuded arteries than in endothelium-intact arteries pretreated with L-NNA plus indomethacin (64±4% versus 46±10%, respectively). These results suggest that glibenclamide could act through multiple sites in either endothelium or the underlying arterial smooth muscle and thus serve as a non-selective muscle relaxant at high concentration.
