Objectives Oxidative stress and inflammation have a critical role in the pathogenesis of ischaemic stroke. Alpha‐pinene is a monoterpenoid molecule with anti‐inflammatory and antioxidant properties. The nobility of the present study was to evaluate the neuroprotective effect of α‐pinene in ischaemic stroke. Methods Ischaemic stroke was induced by transient middle cerebral artery occlusion followed by 24 h reperfusion in male Wistar rats. Alpha‐pinene (25, 50 and 100 mg/kg, i.p.) was administered in the beginning of reperfusion. Then, the neurobehavioural function, infarct volume, brain oedema, antioxidant enzyme activity and the concentration of malondialdehyde (MDA), nitric oxide (NO) and interleukin‐6 (IL‐6) were evaluated by different methods in the brain. Key findings Alpha‐pinene (50 and 100 mg/kg) elicited a significant decrease in the brain oedema and infarct size as well as an improvement in the neurobehavioural function. Besides, α‐pinene (100 mg/kg) restored the function of superoxide dismutase, catalase and glutathione peroxidase and reduced the concentration of MDA, NO and IL‐6 in the hippocampus, cortex and striatum. Conclusions It was ultimately attainted that α‐pinene exerts neuroprotective effect in ischaemic stroke in rat through the restoration of antioxidant enzymes activity, attenuation of lipid peroxidation and reduction of inflammation in the ischaemic brains.

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Total hip arthroplasty (THA) is associated with high intraoperative and postoperative blood loss. Antifibrinolytic drugs have been used to minimize the potential risks of bleeding and blood transfusion. Studies on the effect of tranexamic acid on decreasing blood loss in THA have revealed interesting results, but most have focused on cemented THA. Yet its benefits in THA, especially in cementless THA, have not been proved. We conducted a prospective double-blind randomized controlled study on 64 patients who were candidates for cementless THA under epidural anesthesia between 2006 and 2008. Patients were randomly assigned into study and control groups. Patients in both groups were well matched regarding preoperative characteristics. Five minutes preoperatively 32 patients of the study and control groups received 15 mg/kg tranexamic acid or normal saline intravenously respectively. Our findings showed a significantly smaller decrease in 6- and 24-hour postoperative hemoglobin levels, less intraoperative and postoperative bleeding, and less need for allogenic blood transfusion in the tranexamic acid group. Our results also revealed a higher mean of 6- and 24-hour hematocrit level and shorter hospital stay in the tranexamic acid group compared to the control group, which were not statistically meaningful. In our study no thromboembolic event was seen; except 1 patient in the control group. Our study showed that administering tranexamic acid before the start of cementless THA under epidural anesthesia can reduce intraoperative and postoperative bleeding as well as need for blood transfusion.

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Recent studies suggest that dietary virgin olive oil (VOO) reduces hypoxia-reoxygenation injury in rat brain slices. We sought to extend these observations in an in vivo study of rat cerebral ischemia-reperfusion injury. Four groups, each consisting of 18 Wistar rats, were studied. One group (control) received saline, while three treatment groups received oral VOO (0.25, 0.5, and 0.75 mL/kg/day, respectively). After 30 days, blood lipid profiles were determined, before a 60-min period of middle cerebral artery occlusion (MCAO). After 24-h reperfusion, neurological deficit scores, infarct volume, brain edema, and blood brain barrier permeability were each assessed in subgroups of six animals drawn from each main group. VOO reduced the LDL/HDL ratio in doses of 0.25, 0.5, and 0.75 mL/kg/day in comparison to the control group (p < 0.05), and offered cerebroprotection from ischemia-reperfusion. For controls vs. doses of 0.25 vs. 0.5 vs. 0.75 mL/kg/day, attenuated corrected infarct volumes were 207.82 ± 34.29 vs. 206.41 ± 26.23 vs. 124.21 ± 14.73 vs. 108.46 ± 31.63 mm3; brain water content of the infarcted hemisphere was 82 ±± 0.25 vs. 81.5 ± 0.56 vs. 80.5 ± 0.22 vs. 80.5 ± 0.34%; and blood brain barrier permeability of the infarcted hemisphere was 11.31 ± 2.67 vs. 9.21 ± 2.28 vs. 5.83 ± 1.6 vs. 4.43 ± 0.93 µg/g tissue (p < 0.05 for measures in doses 0.5 and 0.75 mL/kg/day vs. controls). Oral administration of VOO reduces infarct volume, brain edema, blood brain barrier permeability, and improves neurologic deficit scores after transient MCAO in rats.