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Introduction: To determine the course of ischemic mitral regurgitation (IMR) after coronary artery bypass grafting (CABG), and evaluate preoperative factors which predict the development of the severity of IMR after CABG.Methods: Between 1992–2005, 1995 patients underwent CABG and 170 of them had IMR. Data of 131 patients were retrospectively analyzed and living patients (n = 112) had a clinical follow-up visit. The mean follow-up time was 6.5 years.Results: At the time of CABG, 66% of the 131 cases analyzed had mild, 31% had moderate, and 3% had severe IMR. At the time of follow-up, 52% of patients had either no IMR or mild IMR, 27% had moderate IMR, 6% had severe IMR and 15% suffered from cardiac related death. During follow-up IMR grade reduced in 25% of study patients. None of the patient had re-operation due to the mitral regurgitation. Multivariate analysis showed that left ventricular ejection fraction (LVEF) was an independent predictor of good prognosis (O.R. 1.4, 95% C.I. 1.15–1.83/10% increase of LVEF, p = 0.02).Conclusion: Half of the patients, who have IMR at the time of CABG, have no IMR or only mild IMR postoperatively. Good LVEF adds to the probability that CABG only can reduce IMR.

Background and Aims: The aim of this study was to determine the risk factors of postoperative atrial fibrillation (AF) after coronary artery bypass grafting and to create predictive model and to evaluate the effects of AF on patients outcome.Material and Methods: Data of 3,676 consecutive patients were analysed to identify the predictors of AF. Multivariate logistic regression model was validated prospectively in 1,107 patients.Results: Increasing age (p < 0.001), preoperative use of digoxin (p = 003), need of intra-aortic balloon pump or inotropic medication in the weaning off cardiopulmonary by pass or during the first 24 hours postoperatively (p = 0.013), increasing body surface area (p = 0.006) and lower ejection fraction (p = 0.048) were independent risk factors for postoperative AF. The predictive model gave area under the receiver-operating characteristic (ROC) curve 0.682, 95 % confidence interval 0.663–0.701, and p < 0.001. The patients with AF incidence had more postoperative stroke (p = 0.008), confusion (p < 0.001) severe gastrointestinal complications (p = 0.005), readmission to ICU (p < 0.001), longer ICU (p < 0.001) and hospital stay (p < 0.001) when compared with the patients who remained in sinus rhythm.Conclusion: Logistic regression model with the parameters used was not accurate enough for clinical purposes. Postoperative AF is associated with postoperative stroke, severe gastrointestinal complications, readmission to ICU, and longer ICU and hospital stay.

To construct models for predicting mortality, morbidity and length of intensive care unit (ICU) stay after cardiac surgery and to compare the performance of these models with that of the EuroSCORE in two independent validation databases.

Chronic cigarette smoking is associated with dysfunction of the vascular endothelium. Smokers have also been shown to be insulin-resistant, at least in some studies. Since insulin-induced vasodilation is dependent on endothelial cell nitric oxide (NO) synthesis, we tested the hypothesis that decreased skeletal muscle blood flow causes insulin resistance in smokers. We studied 37 young normotensive normolipidemic nondiabetic men, of which 14 were smokers and 23 lifelong nonsmokers. The groups were similar with respect to age, body mass index (BMI), and maximal oxygen uptake (Vo2max). Basal and insulin-stimulated femoral muscle blood flow was measured using [15O]H2O and insulin-stimulated muscle glucose uptake using [18F]fluoro-2-deoxy-d-glucose ([18F]FDG) and positron emission tomography (PET). Whole-body glucose uptake was measured using the hyperinsulinemic (insulin infusion 5 mU/kg · min)-euglycemic clamp technique. In the basal state, muscle blood flow was 51% lower in smokers (17 ± 3 mL/kg muscle · min) versus nonsmokers (35 ± 17 mL/kg · min, P< .0001). Insulin increased muscle blood flow comparably in both groups; the mean rate of insulin-stimulated blood flow was 30 ± 10 and 55 ± 38 mL/kg · min (P= .049), respectively. Whole-body and skeletal muscle glucose uptake were similar in both groups during insulin infusion. We conclude that muscle blood flow is lower in chronic smokers compared with nonsmokers under both fasting and hyperinsulinemic conditions. The insulin-induced increase in muscle blood flow and insulin-stimulated glucose uptake appear normal, suggesting that the vasodilatory and metabolic effects of insulin are intact in smokers and the reduced muscle blood flow per se does not cause insulin resistance in these subjects.

Objective:To investigate granulocyte activation, as well as hypoxanthine and free radical production in children during the first day after cardiopulmonary bypass. Design: A prospective study of pediatric patients undergoing either cardiac surgery with a cardiopulmonary bypass or thoracotomy and extracardiac vascular surgery not requiring a cardiopulmonary bypass. Setting: Operative and intensive care units, Children’s Hospital, University of Helsinki, Finland. Patients: Seven consecutive patients undergoing elective correction of a ventricular septal defect and six patients undergoing extracardiac surgery for ligation of a patent ductus arteriosus or repair a coarctation of the aorta. Measurements and main results: Plasma concentrations of myeloperoxidase (140–334 µg/l preoperatively, 460–1692 µg/l at 0.2 h after declamping, 471–1386 µg/l at 0.5 h after declamping) and lactoferrin (77–258 µg/l preoperatively, 533–1783 at 0.2 h, 404–1482 µg/l at 0.5 h) as markers of granulocyte activation, and hypoxanthine (0–5.7 µmol/l preoperatively, 4.3–17.0 µmol/l at 0.2 h, 6.5–17.9 µmol/l at 0.5 h) increased in a biphasic manner at 0.2–0.5 h and 6–10 h postoperatively (all p<0.05). Expired ethane, as an index of free radical activity, increased at 10 h postoperatively (36–119 pmol/kg per min preoperatively, 72–152 pmol/kg per min, p<0.05). Conclusion: Granulocyte activation, and hypoxanthine and free radical production occur at least 10 h after cardiopulmonary bypass. In children undergoing open heart surgery, attempts to reduce free radical activity should be extended to the postoperative period.

1,5-Anhydro-D-glucitol (AG) is efficiently reabsorbed in renal tubuli by a mechanism that is saturated at high AG concentrations. To gain insight into the stereospecific requirements of the mechanism, we employed an in vivo loading test technique in which rats were injected with anhydrosugars and aldohexoses in doses that led to excretion of the sugar injected, thus saturating tubular reabsorption. Administration of AG elicited an increase in the excretion of D-mannose (P<0.0005), while D-mannose caused AG to appear in urine. Administration of 1,5-anhydro-D-mannitol led to increased excretion of D-mannose (P<0.0005) and the appearance of AG in urine. The effects of 1,5-anhydro-D-mannitol on the excretion of D-mannose and AG, and the effect of D-mannose on AG were dependent on the dose. Myoinositiol, mannitol and C-3–C-6 epimers of AG did not interfere with the reabsorption. The mechanism was highly phlorizin-sensitive. Repeated administration of 1,5-anhydro-D-mannitol rapidly depleted the rat organism from mobilizable AG. The AG space calculated (53% of body weight) suggested the presence of considerable cellular stores of AG. D-Mannose and AG are regular components of the plasma monosaccharide profile. The data suggest that the two sugars are reabsorbed in renal tubuli by a common mechanism, which is distinct from the main D-glucose reabsorption system. The presence of a glucose-type C-3–C-6 and pyranose structure is required for a sugar to be transported by the system. The mechanism accommodates both an axial and an equatorial hydroxyl group at C-2, but a hydroxyl group at C-1 is not required.

Peroxidation of human erythrocyte membranes was followed in vitro with head space analysis of ethane and pentane and a thiobarbituric acid assay in a standardized system liberating free oxygen radicals. Simultaneously, the decrease of the membrane palmitic, linoleic, arachidonic and docosahexaenoic acid was monitored. The recoveries of the peroxidation products of the red cell ghost preparations were compared with those obtained by peroxidation of pure fatty acids.Experiments using purified fatty acids revealed that ethane was preferentially produced from docosahexaenoic and linolenic, and pentane from linoleic and arachidonic acids. Thiobarbituric acid-reactive material (TBAR) was produced from each unsaturated fatty acid tested, but the amount was dependent on the number of carbon chain double bonds.During peroxidation of the erythrocyte ghosts, 72% of ethane and 51% pentane were produced during the first 12 h of incubation, whereas TBAR was produced at a constant rate throughout the 36-h test period. Hydrocarbon and TBAR production were similarly inhibited by desferoxamine (at p < 0.005 and p < 0.0001, respectively). The total recoveries of ethane, pentane and TBAR exceeded the amount expected by 7.8-, 1.4-and 5.5-fold, respectively. It was concluded that measurement of pentane is a reliable method to monitor lipid peroxidation during oxidative damage of the erythrocyte membrane.

Feeding with a galactose-rich diet induced a substantial drop in blood plasma 1,5-anhydroglucitol concentration. The decline was proportional to the dose of galactose. The decline was less marked in xylose-fed rats.

Rat serum contains natural 1,5-anhydroglucitol. Injected or orally administered 1,5-anhydroglucitol was efficiently reabsorbed by the renal tubuli via a mechanism which had a saturation point at high serum 1,5-anhydroglucitol levels. The compound had a slow turnover rate in the body; its half-life is approximately 3 days. The compound was readily absorbed in the gut when administered orally.

Background: Airway epithelial sodium channel ENaC is critical to perinatal lung fluid clearance. Data on ENaC protein expression in developing human lung are limited and absent for infants with RDS or BPD.Objective: To characterize the expression of a-, ß-, and ?ENaC expression in lung tissue from human fetuses and newborns with and without RDS or BPD.Methods: Lung tissue was obtained from autopsies (n = 23) from fetuses (GA 12 - 21 wks), preterm infants with (GA 25 - 28 wks) or without RDS (GA 23 - 25 wks), and infants with BPD (GA 24 - 30 wks at birth). The primary antibodies were rabbit polyclonal aENaC (1:60 Sigma-Aldrich Inc, MO, US), ßENaC (1:2250 Aviva Systems Biology, CA, US) or ?ENaC (1:200 Lifespan Biosciences Inc, WA, US).Results: In fetal lung developing respiratory, glandular epithelium stained with a-, ß-, and ?ENaC from 12+3 wks GA. In preterm infants without RDS expression of a-, ß-, and ?ENaC was apparent in single type II pneumocytes, while type I pneumocytes remained unstained. In RDS and BPD the expression of ENaC subunits in alveolar epithelium was largely absent but reactive, hyperplastic type II pneumocytes stained strongly for a- and ßENaC. Throughout development, and in infants with RDS or BPD a-, ß-, and ?ENaC stained the bronchiolar epithelium.Conclusions: In human fetal lung all three ENaC subunits were expressed during the pseudoglandular stage of lung development. Expression of ENaC subunits in bronchioles may indicate a role for conductive airways in perinatal lung liquid clearance.

Objective: Reabsorption of lung fluid is critical for the adaptation of the newborn infant. Defective reabsorption may result in transient tachypnea of the newborn or contribute to respiratory distress syndrome. Perinatally, epithelial sodium channel (ENaC) is crucial for lung fluid reabsorption. ENaC is composed of 3 homologous subunits, the a-subunit being indispensable to ENaC function. Exogenous glucocorticoids (GC) regulate ENaC gene expression, but little is known whether an association exists between endogenous cortisol and ENaC.Subjects and methods: 69 term infants delivered vaginally (n=22) or by elective cesarean section (CS) (n=47) were included. We collected cord blood and saliva for cortisol analyzes with ELISA. Airway epithelium ENaC mRNA was quantified with real-time RT-PCR and normalized to cytokeratin 18 (CK18). Saliva and airway epithelial sampling was performed < 3h, 24 ± 5 and 48 ± 8 h postnatally. In a subset of infants delivered by elective CS (n = 26) first airway samples were obtained < 30 min postnatally.Results: aENaC mRNA < 30 min postnatally correlated with cord cortisol; r = 0.64, p = 0.001 (n=22). Adjusted for GA the correlation remained significant; r = 0.59, p = 0.005. At < 3h postnatally aENaC correlated with salivary cortisol; r = 0.52, p = 0.004 (n=29).Conclusion: Cortisol seems to be an important physiologic regulator of ENaC expression at birth. Our finding suggests that lung fluid transport may respond to GC even in the term infant. This underlines the potentials of regulation of perinatal lung fluid reabsorption by GC.

Background: ENaC is considered critical for the movement of liquid across respiratory epithelium. Functional impairment of liquid transport may participate in the pathogenesis of respiratory insufficiency. In preterm infants with respiratory distress syndrome ENaC expression is lower than in healthy term infants. We wanted to study how expression of ENaC changes over the first postnatal days.Methods: We studied 35 healthy term infants (GA 39.5±1.3 wks). Samples of respiratory epithelium were obtained by scraping both nostrils at 1–4, 23–27 and 45–48 hours after birth. The samples were subjected to RT-PCR using real-time PCR for analysis of expression of alpha-, beta- and gamma-ENaC and cytokeratin 18 (CK18) which was used as an epithelial marker. Reactions were performed in singleplex format.Results: In healthy term infants expression of alpha-ENaC was 8.2±4.0, 7.7±6.6 and 7.5±5.9 amol/fmol CK18 at 1–4, 23–27 and 45–48 hours after birth, respectively. Expression of beta-ENaC decreased significantly during the first 27 postnatal hours from 12.0±8.1 to 4.1±4.2 amol/fmol CK18 (p= 0.0001). At 45–48 hours after birth beta-ENaC was 2.7±3.6 amol/fmol CK18. Expression of gamma-ENaC was 19.2±34.9, 8.7±23.6 and 27.5±101.6 at 1–4, 23–27 and 45–48 hours after birth, respectively.Conclusion: In the healthy newborn infant, expression of alpha- and gamma-ENaC remain constant over the first 48 postnatal hours, whereas there is a significant decrease in the expression of beta-ENaC. Beta-ENaC has been considered to have a regulatory function in the ENaC complex. We conclude that the expression of beta-ENaC may play a role in the postnatal pulmonary adaptation of the healthy newborn infant.