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    Involvement of cholinoceptors in cadmium-induced endothelial dysfunction
    (2003) Bilgen, İbrahim; Öner. Gülşen; Cirrik, Selma; Edremitlioglu, Mustafa; Alkan, Zeliha
    Cadmium (Cd) toxicity was produced in male rats to study the role of cholinoceptors in Cd-induced endothelial dysfunction. The changes in the tension of the aortic rings to constrictor and dilator agonists were compared with those of controls. A Cd-induced significant increase in phenylephrine response was associated with a decrease in basal dilator prostanoid release. In Cd-exposed rings, despite an obvious depression in the acetylcholine (ACh) response, the receptor-independent dilation to the calcium ionophore A23187, which elicits a receptor-independent endothelial relaxation, was slightly elevated (p< 0.01), but the smooth muscle cell response to the NO donor, sodium nitroprusside (SNP) remained unaltered. Cadmium decreased both the maximal response to ACh (10-5M) and its pirenzepine (Prz) sensitive component. The M1 type cholinoceptor-mediated response to ACh decreased in Cd-exposed rings to 10.30 ± 5.00% from 38.40 ± 6.90% (p< 0.001). Cadmium also reduced the share of indomethacin 1.64% to 13.92 ± 2.89% (p< 0.01), which correlated well with the changes in the M1-mediated response (r= 0.991, p < 0.0001). Most of the deleterious effect of Cd appears to Abbreviations: Cd = Cadmium, ACh = Acetylcholine, PG12= Prostacyclin, Indo = Indomethacin, L-NAME = N (G)-nitro-L-arginine methyl ester, EDHF = Endothelium-derived hyperpolarizing factor, Galla = Gallamine, PE = Phenylephrine, Prz = Pirenzepine, Atr = Atropine be restricted to the M1-dependent ACh response. These findings suggest that Cd produces an endothelial dysfunction by impairing the Ml type cholinoceptor mediated response, which seems to be involved in prostanoid release. © 2011, by Walter de Gruyter GmbH & Co. All rights reserved.
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    Mild Hypothermia Improves Survival During Hemorrhagic Shock Without Affecting Bacterial Translocation
    (Taylor & Francis Inc, 2009) Deniz, Turgut; Agalar, Canan; Özdoğan, Mehmet; Edremitlioglu, Mustafa; Eryılmaz, Mehmet; Devay, Seda Duygulu; Ağalar, Fatih
    Background: Accidental hypothermia in patients with hemorrhagic shock (HS) is associated with increased mortality. However, experimental mild and moderate hypothermia has beneficial effects. The mechanisms for beneficial effects of hypothermia have not been completely understood. Therefore, the aim of this study was to investigate the effect of hypothermia on survival, bacterial translocation (BT), and remote pulmonary injury in a controlled HS model in rats. Methods: HS was achieved by blood withdrawal through femoral vein. Rats in the normothermia group (group I) were maintained at 37C. Mild hypothermia group (group II) was observed at 32C that was spontaneously induced by exposure to ambient temperature. Moderate hypothermia of 28C was actively induced by external cooling in group III for 90 min. Survival and neurological deficit scores (NDS) were recorded at 24th hr. Mesenteric lymph nodes, liver and spleen samples were collected. Myeloperoxidase (MPO) and malondialdehyde (MDA) levels were measured in lung tissue. Results: Blood pressure significantly increased in hypothermia groups. Mild hypothermia significantly increased survival. No difference was found in BT rates in groups. Hypothermia was found to significantly decrease the NDS points in group III, compared to group I. There was no difference in lung tissue MPO levels among groups. Lung tissue MDA levels increased significantly in groups II and III. Conclusions: Mild hypothermia improved blood pressure, survival, and neurological outcome with a possible detrimental effect on pulmonary ROS production during HS in rats. These effects of hypothermia are not associated with BT.
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    The Role Of Cholesterol On The Pressure Sensing Ability Of Kidneys In Rats
    (2003) Edremitlioglu, Mustafa; Öner, Gülsen
    We studied the effect of hypercholesterolemia on the pressure-sensing and regulating ability of the kidneys, using an acute hemorrhage model to provide 40% and 60% reduction in the blood pressure of hypercholesterolemic and control rats. The control group (n = 22) was fed a normal rat pellet diet and tap water; the experimental group (n = 22) received a diet containing 2% cholesterol/0.2% thaurocholate. Half the animals were subjected to 6 mL/kg bw and the others to 12 mL/kg bw of bleeding for 1 min. Blood pressure recording and proper samplings were done before bleeding and during the 20 min posthemorrhagic period for analysis. Despite a finding of hypercholesterolemia in the experimental group, kidney cholesterol content as well as its function remained unchanged. Following an initial 40% decrease in rats bled 6 mL/kg bw, 20 min later the mean blood pressure returned to 90% of its initial value in control rats and to 70% of its basal level in hypercholesterolemic rats. A similar delay in pressure normalization occurred in rats subjected to 12 mL/kg of bleeding. Plasma renin activity remained unaffected. We conclude that dietary hypercholesterolemia delays the normalization of blood pressure after hemorrhage without affecting the sensing ability of kidneys, and that the kidneys are less sensitive than other organs to plasma cholesterol levels. © 2011 by Walter de Gruyter GmbH & Co. All rights reserved.