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  1. Home
  2. Browse by Author

Browsing by Author "Kurdal T."

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    The effect of beta-blocking agents on morbidity und mortality following coronary artery bypass surgery; [Kronik beta bloker kullaniminin koroner baypas cerrahisi sonrasi morbidite ve mortalite üzerine etkileri]
    (2013) Öztürk T.; Koçan A.A.; Yildirim F.; Alp D.; Kurdal T.
    Objective: Aim of this study was to investigate the effect of beta-blocking agents on both short and long-term morbidity and mortality in patients undergoing coronary artery bypass surgery. Material and Methods: Between January 2010 and March 2012, the patients undergoing coronary artery bypass surgery in our cardiovascular surgery clinic were divided into two groups; Group B included the patients who had (Group B) or had not (Group C) been using beta-blocking agents preoperatively, Demographic and clinical characteristics, intraoperative and postoperative clinical parameters as well as short (30-days) and long-term (1 year) rates of morbidity and mortality were retrospectively evaluated. Results: Number of patients with atrial fibrillation was significantly lower in Group B (n=17, 20% vs. n=28, 35%; p<0.01). Frequency of agitation-delirium in Group B was also significantly less than Group C (n=2, 3% vs. n=8, 10%; p=0.05). Thirty-day morbidity was also higher in Group C than Group B (n=28, 35% vs. n=17, 20%; p<0.04), however this difference disappeared after 1 year (n=30 38% vs. n=24, 28%; p=0.2). Neither 30-day nor 1 year-mortality rates were statistically significant between Groups B and C (p=0.4 and p=0.2, respectively). Conclusion: Compared to the control group, the frequencies of both atrial fibrillation and agitation-delirium were significantly lower in Group B in this cohort of patients. The long term use of beta-blocking agents prior to coronary artery bypass surgery appears to markedly reduce 30-day morbidity, despite this effect was not reflected on short and long-term mortality rates.
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    Acute and Chronic Pretreatment With Atenolol Attenuates Intestinal Ischemia and Reperfusion Injury in Hypercholesterolemic Rats
    (W.B. Saunders, 2016) Öztürk T.; Vural K.; Tuğlu İ.; Var A.; Kurdal T.; Aydemir I.
    Objective To evaluate the protective effects of preinjury atenolol (acute v chronic) on apoptosis, contractility, oxidative stress, and inflammatory markers in hypercholesterolemic rats undergoing intestinal ischemia-reperfusion (I/R) injury. Design Prospective, experimental animal study. Setting University laboratory. Participants Male Wistar rats (n = 32). Interventions Rats were divided into the following 4 groups: 1 group was fed a normal diet (ND) (group ND+NoAT [no atenolol]), and the other 3 groups were fed a high-cholesterol diet (HCD)—group HCD+NoAT, group HCD+ChAT (chronic atenolol, 3 mg/kg/day for 8 weeks), and group HCD+AcAT (acute atenolol, 1.5 mg/kg, given 5 minutes before intestinal clamping). All rats underwent I/R injury. The superior mesenteric artery was clamped for 60 minutes, then opened for 120 minutes (reperfusion). Apoptotic cells and stimulated contractions of ileal segments were examined. Tissue markers of intestinal I/R injury were examined. Intestinal malondialdehyde, superoxide dismutase, and nitrate/nitrite levels were measured. Measurements and Main Results The chronic atenolol group had fewer apoptotic cells and higher superoxide dismutase activity compared with the other groups. Intestinal contraction was higher in both atenolol pretreatment groups compared with the NoAT groups. Chronic and acute atenolol resulted in lower ileal levels of malondialdehyde and immunolabeling-positive cells (intestinal inducible nitric oxide synthase, endothelial nitric oxide synthase, interleukin-1, and interleukin-8) after I/R injury compared with the no atenolol groups. Conclusions Both chronic and acute pre-I/R injury treatment with atenolol attenuated I/R injury in this hypercholesterolemic rat model. These findings should encourage future studies of atenolol in hypercholesterolemic patients undergoing procedures with a high risk of intestinal ischemia. © 2016 Elsevier Inc.

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