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Biomedical subjects

R Türköz

Publications and source records attributed to R Türköz.

6 recordsLinked to original sources
PubMed2001

The effects of aprotinin and steroids on generation of cytokines during coronary artery surgery.

OBJECTIVE: To compare the efficacy of aprotinin and methylprednisolone in reducing cardiopulmonary bypass (CPB)-induced cytokine release, to evaluate the effect of myocardial cytokine release on systemic cytokine levels, and to determine the influence of cytokine release on perioperative and postoperative hemodynamics. DESIGN: Prospective, randomized clinical trial. SETTING: University teaching hospital and clinics. PARTICIPANTS: Thirty patients undergoing elective coronary artery bypass graft surgery. INTERVENTION: Patients were randomly allocated into groups treated with aprotinin (n = 10) or methylprednisolone (n = 10) or into an untreated control group (n = 10). Aprotinin-treated patients received aprotinin as a high-dose regimen (6 x 10(6) KIU), and methylprednisolone-treated patients received methylprednisolone (30 mg/kg intravenously) before CPB. MEASUREMENTS AND MAIN RESULTS: Patients were analyzed for hemodynamic changes and alveolar-arterial PO2 difference (AaDO2) until the first postoperative day. Plasma levels of proinflammatory cytokines (tumor necrosis factor [TNF]-alpha, interleukin [IL]-1beta, IL-6, and IL-8) were measured in peripheral arterial blood immediately before the induction of anesthesia, 5 minutes before CPB, 3 minutes after the start of CPB, 2 minutes after the release of the aortic cross-clamp, 1 hour after CPB, 6 hours after CPB, and 24 hours after CPB; and in coronary sinus blood immediately before CPB and 2 minutes after the release of the aortic cross-clamp. The hemodynamic parameters did not differ among the groups throughout the study. After CPB, AaDO2 significantly increased (p < 0.05) in all groups. A significant decrease in AaDO2 was observed in aprotinin-treated patients at 24 hours after CPB compared with the other groups (p < 0.05). TNF-alpha level from peripheral arterial blood significantly increased in control patients 1 hour after CPB (p < 0.01) and did not significantly increase in methylprednisolone-treated patients throughout the study. In all groups, IL-6 levels increased after the release of the aortic cross-clamp and reached peak values 6 hours after CPB. At 6 hours after CPB, the increase in IL-6 levels in methylprednisolone-treated patients was significantly less compared with levels measured in control patients and aprotinin-treated patients (p < 0.001). In control patients, IL-8 levels significantly increased 2 minutes after the release of the aortic cross-clamp (p < 0.05), and peak values were observed 1 hour after CPB (p < 0.01). IL-8 levels in control patients were significantly higher compared with patients treated with aprotinin and patients treated with methylprednisolone 1 hour after CPB (p < 0.05). CONCLUSION: This study showed that methylprednisolone suppresses TNF-alpha, IL-6, and IL-8 release; however, aprotinin attenuates IL-8 release alone. Methylprednisolone does not produce any additional positive hemodynamic and pulmonary effects. An improved postoperative AaDO2 was observed with the use of aprotinin.

Aged↗
PubMed2001

[Peripheral vascular injuries].

Between 1994-2000, 60 peripheral vascular injuries were admitted to the Turgut Ozal Medical Center Thoracic and Cardiovascular Surgery Clinic. Forty eight (80%) of patients were male, twelve (20%) were female and their age ranged from 5 to 70 years (mean 28.9 years). The causes of injuries were related to penetrating device in 34 (56.6%), gun shots in 14 (23.3%), blunt trauma in seven (11.6%) and iatrogenic causes in five(8.3%). Total laceration, partial laceration and pseudoaneurysm were observed in 45 (75%), 14 (23.3%) and one (1.6%) respectively. The localization of injuries were the upper limbs in 34(56.6%) and the lower limbs in 26 (43.4%). The vascular injury localizations in order of frequency were femoral artery in 12 cases (20.75%), radial artery in ten cases (17%), popliteal artery in ten cases (15%), brachial artery in nine cases (15%), axillary artery in nine cases (13.2%), ulnar artery in six cases (11.3%) and tibial artery in four cases(7.4%). There were nearby venous injuries in nine patients (15%) and neural injuries in ten patients (16.6%). The patients' mean admission time to the hospital was 3 hours and 30 minutes and mean operation time for revascularization was within 95 minutes. The operative techniques were autogenous saphenous vein graft interposition in 27 cases (45%), resection and end-to-end anastomosis in 19 cases (31.6%), lateral repair in ten cases (16.6%), synthetic graft insertion in three cases (4.8%) and ligation in one case (1.6%). Our success rate was 98.2% in salvaging the limbs. Mean length of hospital stay was 14.4 days. Mortality was not observed during the hospital stay.

Adolescent↗
PubMed1997

Evaluation of pentoxifylline in experimental spinal cord ischemia.

OBJECTIVE: Despite the advance of anesthesia and surgery, postoperative neurological dysfunction has remained a challenging problem after descending and thoracoabdominal aortic surgery. The pathophysiology of early and especially late paraplegia is not clearly understood. The effect of pentoxifylline (PTX), an agent known to inhibit in vitro neutrophil activation and improve recovery after cerebral ischemia in animals, was investigated on spinal cord protection. METHODS: Twenty four New Zealand white rabbits were used for spinal cord ischemia models. Infrarenal aortic occlusion devices were placed. After 48 h, the rabbits were randomly taken for study. The PTX groups (n = 12) were given PTX 40 mg/kg i.v. bolus followed by 0.2 mg/kg/min infusion. The control (CT) group (n = 12) received normal saline. Two groups underwent temporary (20-24 min) spinal cord ischemia in a conscious state. After the operation, the spinal cord function was assessed at 6, 12, 24, 48 and 72 h by the scale (score of 5 = normal hop, score of 0 = no movement). Histological analysis of the spinal cords was carried out immediately after acute paraplegia or within 24 h after development of delayed paraplegia. RESULTS: During the aortic occlusion, the distal aortic pressures were the same in both groups (PTX group: 14.92 +/- 3.78 mmHg; CT group: 17.42 +/- 3.2 mmHg). At the 72nd h, the scores were not different in the PTX group (1.58 +/- 2.11) and in the CT group (0.83 +/- 1.95) (P = 0.817). Acute paraplegia developed in 3 rabbits (25%) of each group. Delayed paraplegia was observed in 6 rabbits (50%) in the PTX group and 7 rabbits (58%) in the CT group. On morphological examination on the spinal cords, ischemic changes were observed in both groups. Although neutrophil leukocytes were noted in the control group with acute paraplegia and macrophage infiltration was noted in the control group with delayed paraplegia, there was not any leukocyte or macrophage sequestration in the PTX group. CONCLUSIONS: Neurological deficits after spinal cord ischemic/reperfusion injury were not directly responsible for blood-originated phagocytic cells and the inhibition of this type of cell function did not change the outcome.

Animals↗
PubMed1996

The effect of pentoxifylline on the lung during cardiopulmonary bypass.

Cardiopulmonary bypass (CPB) produces an inflammatory response due to the interaction of blood with a foreign body surface. The lungs are most affected by this inflammatory response. Pentoxifylline (PTX), a phosphodiesterase inhibitor and an inhibitor of leukocyte activation, is used to minimize damage in lungs where leukocytes play an important role. Twenty patients with mitral valve stenosis with planned mitral valve surgery were included in the study. The ten patients receiving pentoxifylline (PTX group) were administered 400 mg PTX orally TID for 3 days preoperatively and, following anesthetic induction, a 300 mg PTX infusion was given. The ten patients receiving no PTX were the control group (CT). Platelet and leukocyte counts, mean pulmonary arterial pressure (mPAP), pulmonary capillary wedge pressure (PCWP), cardiac index (CI), pulmonary vascular resistance (PVR), alveolar-arterial PO2 gradient (AaDO2) were measured just before and after CPB, and 2 h postoperatively. The number of the leukocytes increased in the blood samples drawn 15 min after CPB in both groups and 2 h postoperatively showed no statistical change. The number of platelets had decreased significantly at the end of the CPB in both groups and, 2 h postoperatively, there was a further decrease in the blood count in the control group (P < 0.05). There was no significant difference in either the preoperative or postoperative PAP, PAWP, and CI. Pulmonary vascular resistance increased in both groups following the CPB (CT, before: 136 +/- 44, after: 177 +/- 94 dyne. sec.cm-5; PTX, before: 151 +/- 82, after 182 +/- 43 dynes.sec.cm-5). Two hours postoperatively, a considerable increase continued in the control group (CT 219 +/- 170 dynes.sec. cm-5), while there was an insignificant increase in the PTX group (PTX 193 +/- 51 dynes.sec.cm-5) (P < 0.05). The alveolar-arterial PO2 gradient increased after the CPB in both groups but a moderate decrease was observed 2 h postoperatively. In lung biopsy specimens taken before and after the CPB, there was marked leukocyte sequestration in the control group, whereas the number of leukocytes was seen to be insignificant in the PTX group (P < 0.005). This dosage regimen of PTX inhibits the postoperative increase in PVR and greatly minimized leukocyte sequestration in the lung due to CPB.

Adult↗