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    Effect of oral pyridoxine hydrochloride supplementation on arterial blood pressure in patients with essential hypertension
    (Ecv-Editio Cantor Verlag Medizin Naturwissenschaften, 1995) Aybak, M; Sermet, A; Ayyildiz, MO; Karakilcik, AZ
    The purpose of this study was to test the effect of vitamin B-6 (pyridoxine-HCl, CAS 58-56-0) supplementation on arterial blood pressure in essential hypertension. The trial comprised 9 normotensive subjects (7 men and 2 women, aged between 32-58 years, mean +/- SD, 48 +/- 11) and 20 patients with essential hypertension (16 men and 4 women, aged between 32-69 years, mean +/- SD, 56 +/- 12). The patients were treated during 4 weeks with a single oral dose of pyridoxine (5 mg/kg body weight/day). After a 5-min rest, measurements were made in the supine position. When compared with the normotensive subjects, the hypertensive subject group had a significantly higher systolic and diastolic blood pressure (p < 0.001) and higher level of plasma norepinephrine (E) (p < 0.01) before pyridoxine treatment. On the other hand there, were no significant differences in plasma epinephrine (E) and heart rates. Treatment of hypertensive patients with pyridoxine significantly reduced systolic (p < 0.01) and diastolic blood pressure (p < 0.005), plasma NE (p < 0.005) and E (p < 0.05) within 4 weeks. However, there was no significant difference in heart rate at the end of pyridoxine treatment. These results indicate a relationship between pyridoxine status and arterial blood pressure in the essential hypertensive patients.
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    The effect of pyridoxine supplementation on plasma lipoproteins and its relationship with atherogenic risk
    (Faculty Press, 1999) Sermet, A; Atmaca, M; Diken, H; Kelle, M; Deniz, B
    The effect of pyridoxine-HCl on cholesterol in plasma lipoprotein fractions and its relationship with atherogenic risk were investigated in mate Sprague-Dawley rats and healthy human volunteers. Plasma cholesterol, very low and low density lipoprotein cholesterol (VLDL-C and LDL-C) decreased, and high density lipoprotein cholesterol (HDL-C) increased, in rats treated with pyridoxine. Although the cholesterol content of the liver did not change, it decreased significantly in the aorta. Atherogenic risk decreased in rats treated with pyridoxine because of a decrease in the plasma/HDL or LDL/HDL cholesterol ratio and the aorta cholesterol. Plasma cholesterol and cholesterol in the lipoprotein fractions of healthy volunteers given a placebo did not change significantly at the end of the experimental period. Pyridoxine affected the plasma cholesterol and cholesterol in lipoproteins in healthy persons as well as in the rats. Plasma cholesterol, VLDL-C and LDL-C decreased while HDL-C increased. Thus, the atherogenic risk decreased significantly. These findings; indicate that pyridoxine may be an antiatherogenic agent.
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    Effect of Ramadan fasting on platelet aggregation in healthy male subjects
    (Springer, 1996) Aybak, M; Turkoglu, A; Sermet, A; Denli, O
    The purpose of this study was to examine platelet aggregation during Ramadan fasting. A group of 20 healthy non-smoking male volunteers were studied, whose mean age was [21 (SD 2.4) years range 19-24]. The average fast was about 15 h. Venous blood samples were taken on 4 different days; 1 day before Ramadan (day 0), then on the 1st, 14th and 28th day of Ramadan, On each of these 4 days, blood samples were taken at 4 p.m. (1 h before the evening meal). Body mass index and platelet count did nor change during fasting. Bleeding and coagulation time had increased significantly by the end of Ramadan fasting (P < 0.05, P < 0.005 respectively), but these changes remained within physiological Limits. Ramadan fasting induced a reduction in platelet sensitivity to adenosine 5'-diphosphate (ADP) and collagen on days 14 (P < 0.05) and 28 (P < 0.05, P < 0.005 respectively). However, adrenaline-induced. platelet aggregation decreased only on day 25 (P < 0.05). This study indicated that Ramadan fasting led to a decrease in the platelet responses of different aggregating agents (ADP, adrenaline and collagen) in vitro. It also led to an increase in bleeding and coagulation time.
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    Platelet aggregation in type two diabetes mellitus and its relationship with lipoprotein levels
    (Faculty Press, 1998) Sermet, A; Kocyigit, Y; Atmaca, M; Kelle, M; Diken, H
    The relationship between in vitro platelet aggregation and plasma lipoprotein concentrations, in 32 type hive non-insulin dependent diabetes mellitus (NIDDM) patients and 32 healthy subjects, was studied. An increase in the fasting plasma glucose and serum fructosamine concentrations in NIDDM patients was determined. No significant difference was found between platelet counts of the diabetic and control groups, but platelet aggregation induced by adenosine diphosphate (ADP), epinephrine and collagen were significantly higher than in healthy controls. Plasma total cholesterol, low density lipoprotein cholesterol (LDL-C) and triglyceride levels were significantly higher, and the plasma high density lipoprotein cholesterol (HDL-C) level was significantly lower than the controls. In vitro platelet aggregation induced by ADP, epinephrine and collagen correlated positively with LDL-C levels and the LDL-C/HDL-C ratio in both groups, and negatively with HDL-C levels in the diabetic group.
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    Time-dependent changes in superoxide dismutase, catalase, xanthine dehydrogenase and oxidase activities in focal cerebral ischaemia
    (Faculty Press, 2000) Sermet, A; Tasdemir, N; Deniz, B; Atmaca, M
    Time-dependent changes in the activities of antioxidant enzymes and an oxidant enzyme, xanthine oxidase (XO), were detected in primary and peri-ischaemic brain regions during permanent occlusion of the middle cerebral artery (MCAO) in rats. There were no changes in superoxide dismutase (SOD) and catalase (CAT) activities after 3 h of MCAO, whereas antioxidant enzyme activities decreased significantly in ischaemic brain areas following 24 h of ischaemia. After 48 h, the enzyme activities returned to the baseline but then a further increase was observed in ischaemic brain areas by 72 h post-ischaemia. Normally, XO exists as a dehydrogenase (XD), but it is converted to XO which contributes to injury in some ischaemic tissues. The XO activity increased slightly at 3 h after ischaemia, but after 24 h of ischaemia it returned to the baseline and then remained relatively unchanged in ischaemic areas. Pretreatment with allopurinol before ischaemia prevented changes in SOD and CAT activities and attenuated brain oedema during 24 h of ischaemia. Neither XO nor XD activity changed in allopurinol-treated rats at the times of ischaemia. These results indicated that ischaemic brain tissue remained vulnerable to free radical damage for as long as 48 h after ischaemia, and XO was probably not an important source of free radicals in cerebral ischaemia.