The aim of the present study is to evaluate whether blood count parameters differ according to the stages of Fontaine’s classification and to investigate the relationship between hemogram parameters and the severity of the disease. Eighty-two peripheral arterial disease patients were examined prospectively. Patients were classified according to the Fontaine classification system. Fifty newly diagnosed patients were included in the study. The neutrophil-to-lymphocyte ratio, mean platelet volume, and red blood cell distribution width values were recorded. Mean neutrophil-to-lymphocyte ratio values were found to be 3.31 ± 1.1% in Stage I, 3.11 ± 1.3% in Stage II, and 3.48 ± 1.1% in Stage III (p > 0.05). Mean platelet volume values were found to be 7.8 ± 0.6 fl (Stage I), 8.2 ± 1.0 fl (Stage II), and 9.0 ± 0.9 fl (Stage III) (p < 0.05). Red blood cell distribution width values were found to be 13.6 ± 1.0% in Stage I, 14.8 ± 1.7% in Stage II, and 15.4 ± 2.3% in Stage III, being significantly different among all three stages (p < 0.05). Both red blood cell distribution width and mean platelet volume are found to be associated with the severity of atherosclerotic disease in patients with peripheral arterial disease. This finding hypothesizes that complete blood counting parameters may serve as a beneficial and cost-effective method for monitoring atherosclerotic peripheral disease.

Ventricular shunts are used to drain cerebrospinal fluid into extra-cranial spaces. Ventriculoatrial (VA) shunts are provided to transfer cerebrospinal fluid from the cerebral ventricle into the right atrium of the heart. A single center experience of indications, procedure, and clinical outcomes in VA shunt was presented in current study. VA shunts were applied in 10 patients who had repeated previous shunt dysfunction or infection. The reasons, clinical findings, replacement methods, and postoperative clinical follow-ups and outcomes were recorded retrospectively. There were seven female (70%) and three (30%) male patients; their ages ranged from 5 to 13 years (mean ± SD; 8.5 ± 2.6 years). Shunt re-placement reasons were as follows: Shunt occlusion in five patients, intraperitoneal infection in four patients and a distal catheter was kinked and knotted in one patient. Postoperative early complications were seen in one patient as early catheter thrombosis and catheter revision were applied. Late complications were seen in two patients as follows: Catheter infection and infective endocarditis occurred in one patient and pulmonary thrombus occurred in one other patient. There was not any catheter-related mortality observed at the one year follow-up period. VA shunts may be an option for cerebrospinal fluid drainage at necessary conditions. However, sterilization and general training on asepsy and antisepsy are the most important determinants affecting the clinical outcome due to the cardio systemic relationship.

Ischemia reperfusion injuries can be threatening to end organ viability and can progress, with mortal and morbid outcomes. In particular, neural tissues are highly sensitive to hypoxia and reperfusion stress. This study aimed to determine the neuroprotective effects of rosuvastatin on spinal cord ischemia reperfusion injury. Forty male Sprague– Dawley rats were divided into four equal groups: group I (control), group II (sham with simple laparotomy), group III (ischemia-reperfusion), group IV (ischemia-reperfusion group with continuous rosuvastatin utilization), and group V (ischemia-reperfusion group with rosuvastatin-withdrawal after reperfusion). Spinal cord ischemia was induced by clamping the aorta below the left renal artery and above the aortic bifurcation. Reperfusion was provided after 72^nd hours of ischemia. After reperfusion, blood samples and spinal cord tissue samples were taken from all the rats. Oxidative and antioxidant markers from both serum and tissue samples were evaluated, and tissues were examined histopathologically. There were no significant differences between the control and sham groups. A notable increase in oxidative markers was observed in group III compared to group I. In addition, a significant decrease in antioxidant markers was detected in group III. However, there was a marked preservation in the tissue and blood samples of groups IV and V compared to group III in terms of oxidative damage. Additionally, definitive prophylaxes were seen in the histopathological examination of the tissue samples in groups IV and V compared with group III. These significant findings show that rosuvastatin has a considerable protective effect on neural tissue against oxidative damage. Likewise, the early withdrawal of rosuvastatin has a clear neuroprotective effect similar to that of continuous therapy. Nevertheless, other systematic effects and beneficial neural effects of statins should be investigated in further clinical trials.

Objective: The aim of this study was to determine the relationship between oxidative stress markers and the duration of ischemia in rat mesenteric and peripheral ischemia models. Methods: Forty rats were divided into five equal groups, as follows: rats in Group I (control group) were sacrificed to determine the baseline characteristics of the serum markers; the superior mesenteric artery was clamped via a simple laparotomy to induce mesenteric ischemia in Groups II and III; the right common femoral artery was clamped to induce peripheral ischemia in Groups IV and V. Blood samples were taken at 2 (Groups II and IV) and 6 (Groups III and V) hours after these procedures. The serum total oxidative status (TOS), total antioxidant capacity (TAC), oxidative stress index (OSI) and paraoxonase-1 (PON-1) enzyme activities were evaluated in the samples obtained from each group. Results: The OSI level of the control group was 91.00±5.46 (mean ± SD). The OSI levels taken 2 hours after the induction of mesenteric ischemia and peripheral ischemia were significantly higher (194.50±11.16 and 301.75±19.98, respectively (p<0.05)). However, these levels decreased to 151.88±17.02 (mesenteric ischemia) and 108.88±9.46 (peripheral ischemia) after 6 hours. The PON-1 levels of Group III (mesenteric ischemia at 6 hours) (99.75±7.26), Group IV (peripheral ischemia at 2 hours) (96.88±4.09), and Group V (peripheral ischemia at 6 hours) (111.25±10.33) were slightly elevated over that of the control group (87.38±5.31). However, the PON-1 level of Group II (mesenteric ischemia at 2 hours) (42.88±3.14) was lower than that of the other groups (p<0.05). Conclusion: Despite the increment of oxidative markers in early periods of ischemia (2^nd hour), which was a hypoxic response of ischemic cells, they have decreased markedly in prolonged ischemia. This might have been caused by the opening of some collateral circulation or the destruction of the ischemic cells.