Exposure to sixty minutes of hyperoxia upregulates myocardial humanins in patients with coronary artery disease - a pilot study.

In experimental setting the concept of myocardial preconditioning by hyperoxia has been introduced and different intracellular protective mechanisms and their effects have been described. To study whether similar protective phenotype can be induced by hyperoxia also in humans, gene expression profile after hyperoxic exposure was analyzed. Adult patients were randomized to be ventilated with either FiO2 0.4 (n = 14) or 1.0 (n = 10) for 60 minutes before coronary artery bypass grafting. A tissue sample from the right atrial appendage was taken for gene analysis and expression profile analysis on genome wide level by RNA-seq analysis was applied. Exposure to > 96% oxygen for 60 minutes significantly changed the expression of 20 different genes, including upregulation of two different humanins - MTRNR2L2 and MTRNR2L8, and activated a "cell survival" network as detected by Ingenuity Pathway Analyses. We concluded that administration of > 96% oxygen for 1 hour changes gene expression in the myocardium of the patients with coronary artery disease and may enhance cell survival capability.

Cardioprotection by breathing hyperoxic gas-relation to oxygen concentration and exposure time in rats and mice.

OBJECTIVES: Breathing a hyperoxic gas (> or =95% O(2)) protects against ischaemia-reperfusion injury in rat and mouse hearts. The present study investigated how oxygen concentration and duration of hyperoxic exposure influenced cardioprotection, and whether hyperoxia might induce delayed cardioprotection (after 24 h). METHODS: Animals were kept in normal air or in a hyperoxic environment, and their hearts were isolated and Langendorff-perfused immediately or 24 h thereafter. Global ischaemia was induced for 25 min in rats and 40 min in mice, followed by 60 min of reperfusion. Infarct size was determined by triphenyl tetrazolium chloride staining. RESULTS: In rats exposure to > or =95, 80, and 60%, but not to 40% of oxygen immediately before heart isolation and perfusion improved postischaemic functional recovery. Eighty or more percent of oxygen also reduced infarct size. A preconditioning-like effect could be evoked by 60 or 180 min of hyperoxia, giving both immediate and delayed protection. In the mouse heart protection could be induced by pretreatment for 15 or 30, but not by 60 min with > or =95% oxygen. The protective effect of hyperoxia in mice could be evoked in the immediate model only. CONCLUSIONS: Hyperoxia protects the isolated rat and mouse heart against ischaemia-reperfusion injury, but some species-different responses exist. The protection depends on both oxygen concentration in inspired air, and duration of hyperoxic exposure.

Initial experience with lung transplantation in Estonia.

BACKGROUND: A lung transplant program in Estonia was initiated in cooperation with the Medical University of Vienna. The first lung transplantation for an Estonian patient was performed in Vienna on April 28, 2009. The waiting list in Estonia was opened on May 28, 2010; the first transplantation was performed on October 7, 2010. The aim of this study was to present our initial results. PATIENTS AND METHODS: All lung transplantations performed in Estonia through the end of January 2012 included 2 female and 3 male patients of age from 52 to 64 years. Data regarding the donor, the transplant operation, postoperative period, and follow-up were extracted from case records. RESULTS: The cases included 1 bilateral lobar, 3 double, and 1 single lung transplantations. Two patients had chronic obstructive pulmonary disease, one alpha-1 trypsin deficiency, and two idiopathic pulmonary fibrosis. The operative duration varied from 172 to 337 minutes; the ischemia times for the first and second lung ranged from 191 to 351 and 303 to 455 minutes, respectively. Duration of postoperative mechanical ventilation ranged from 2 to 14 days (median 3) and the hospital stay from 28 to 72 days. The following complications were observed: prolonged air leak in 2 patients, one of whom required rethoracotomy; phrenic nerve palsy in 2, atrial fibrillation in 2, and mild renal failure in 1 subject. One patient needed readmission to the intensive care unit owing to acute respiratory failure; one, a tracheostomy for weaning from the ventilator, and one, noninvasive ventilation owing to hypercapnia. All patients remain well at 4-19 months after transplantation. No episodes of acute rejection or bronchiolitis obliterans have been diagnosed. CONCLUSION: The first 1.5-year experience with lung transplantation in Estonia has been satisfactory. Although there have been several complications, no posttransplant or waiting list mortality has occurred.