In the study the authors aimed to demonstrate the expression and protective effect of heme oxygenase-1 (HO-1) in the delayed preconditioning (PC) on cultured myocardiac cells. Neonatal rat cardiac myocytes were exposed to ischemic (ischemic medium [IM] for 20 min) and pharmacological (adenosine, epinephrine, opioid) PC. Twenty-four hours later cells were subjected to a simulated ischemia (SI)--culturing for 3 h in IM, followed by 2-h reperfusion in normal medium--and then lactate dehydrogenase (LDH), live/death ratio, and apoptosis were measured. For demonstrating the protective role of HO-1, its enzymatic activity was competitively inhibited by administration of zinc protoporphyrin IX (ZnPPIX), and HO-1 synthesis was blocked with HO-1 siRNA. Cells in control group were cultured under normoxic conditions. In SI group, cells underwent only an SI without PC. HO-1 expression in all of the groups was demonstrated with immunostaining. Our results showed a significant decrease of LDH release, apoptosis, and cell death in PC groups versus SI group, which has been risen in ZnPPIX- and HO-1 siRNA-treated groups. HO-1 immunostaining showed an appreciable HO-1 expression in PC groups, which was abolished with HO-1 siRNA administration, but not in ZnPPIX group. The results therefore suggest that HO-1 expression increases in both ischemic and pharmacological PC, and HO-1 has cellular protective effect against cell death and apoptosis in ischemia-reperfusion-induced oxidative injury.

The study confirmed significant improvement in quality of life measured by SF-36 questionnaire after both conventional and cryostripping with no difference between the two stripping techniques. Cryostripping results in less bruising than conventional stripping.

Pre- and postconditioning are powerful endogenous adaptive phenomenon of the organism whereby different stimuli enhance the tolerance against various types of stress. Urocortin (Ucn), member of the corticotropin-releasing factor (CRF) family has potent effects on the cardiovascular system. The aim of this article was to investigate the action of Ucn on cultured cardiomyocytes in the process of pre- and postconditioning. Isolated neonatal rat ventricular myocytes were preconditioned with adenosine, simulated ischemia, and Ucn (10-min treatment followed by 10-min reperfusion/recovery). For detecting the effect of alternative types of preconditioning, necrosis enzyme (lactate dehydrogenase [LDH]) release, vital staining (trypan blue), and ratio of apoptosis/necrosis were examined after cardiac cells were exposed to 3-h sustained ischemia and 2-h reperfusion. Same parameters were measured in the postconditioned groups (30- or 60-min ischemia followed by postconditioning with 10-min ischemic stimulus or Ucn and 2-h reperfusion). Cells exposed to 3-h ischemia followed by 2-h reperfusion were shown as control. Our results show that LDH release a number of trypan blue-stained dead cells and the ratio of apoptotized and necrotized cells was decreased in all preconditioned groups compared with control group. In postconditioned groups LDH content of culture medium, trypan blue-positive cardiomyocytes, and the rate of apoptotic/necrotic cells was reduced contrasted with non-postconditioned group. We can conclude that preconditioning with Ucn induced such a powerful cell protective effect as adenosine and ischemia. Furthermore, postconditioning with Ucn after 60-min ischemia was more cardioprotective than ischemic postconditioning.

Acute kidney injury (AKI) remains an independent risk factor for mortality and morbidity after vascular surgery (affecting the renal arteries) or aortic surgery (requiring suprarenal aortic clamping). These types of vascular surgery produce renal ischemia/reperfusion (I/R) injury, a common cause of AKI. The present studies aimed at monitoring the course of renal I/R injury at the cellular level and investigating the efficacy of long-term preoperative and single-shot intraoperative administration of sodium pentosan polysulfate (PPS) to protect renal tissue from acute I/R injury both in native and diabetic kidneys in rats. Western blot analyses of the proapoptotic (bax) and antiapoptotic (bcl-2) signaling pathways, as well as the extent of DNA damage (phospho-p53), were performed. Oxidative stress followed upon the termination of malondialdehyde, reduced glutathione, thiol group, and superoxide dismutase plasma levels. Inflammatory changes were measured by the determination of serum tumor necrosis factor-α and interleukin-1 levels. Morphological changes were detected by histological examinations. Our results showed that the long-term administration of PPS has an advantage in reducing I/R kidney injury in diabetic rats, while high-dose, single-shot parenteral administration of PPS prior to revascularization might be useful in nondiabetic rats.

Introduction: The challenge against reperfusion injury and tissue oxidative stress, especially in vascular surgical interventions has an essential importance to reach the optimal clinical result. Numerous experimental attempts have proved the positive antioxidant effect of vitamin E in both chronic and acute phase models. In our study we monitored the effect of continuous preoperative treatment with vitamin E, on oxidative stress and tissue inflammation reactions developed after reconstructive operations.Patients and methods: 32 patients have been involved in a randomized, prospective study, all suffering from AFS occlusion proved by angiography, and all undergone supragenual reconstruction. Duration of ischemia and amount of tissues under vascular clamping were almost the same in all patients. In the group treated with E-vitamin, we administered 1 × 200 mg of vitamin E p/o from the preoperative day till the 7th post operative day. Patients of the second group did not receive vitamin E.Materials and methods: Peripheral blood samples were collected immediately before operation and at the end of the second reperfusion hour (early reperfusion period). Late reperfusion period has been monitored by analyzing blood samples taken at 24th hour and 7th day next to the operative ischemia. Among oxidative stress parameters, direct measurement of reactive oxygen intermediator (ROI) and determination of antioxidant state (GSH, Total-SH group, SOD) have been performed. Malondialdehyde was chosen as marker for lipidperoxidation. Inflammation reactions were monitored up on expression of adhesion molecules (CD11a and CD18). We also controlled the oscillation of myeloperoxidase (MPO) activity.Results: Our study has proved that preoperative (from the preoperative day till the 7th post operative day) administration of 200 mg vitamin E could reduce the level of oxidative stress developed after ischemic-reperfusion insult (lipidproxidation, antioxidant enzymes). According to our results, the prooxidant-antioxidant imbalance also diminished in the group with E-vitamin treatment. We proved that elective administration of vitamin E could decrease the WBC activity (MPO activity, free radicals production, expression of adhesion molecules) and its consequential local inflammation process, during early reperfusion.