SF-36 (Physical Functioning) and 6-MWT are useful indicators for predicting postoperative complications and LOS. Patients undergoing major surgery answered SF-36 and performed 6-MWT. Physical Functioning as a component of the SF-36 correlated with LOS. The 6-MWT had a negative correlation with LOS and with complication grade. SF-36 and 6-MWT are useful predictors of postoperative complications.

Background: The aim of the study is to examine the effect of limited and prolonged hyperoxia on neonatal rat lung. This is done by examining the morphologic changes of apoptosis, the expression of ceramide, an important mediator of apoptosis, the expression of inflammatory mediators represented by IL-1β and the expression of 2 proto-oncogenes that appear to modulate apoptosis (Bax and Bcl-2).

BackgroundHyperoxia triggers the release of toxic reactive oxygen species (ROS). Pomegranate Juice (PJ) is a rich source of potent antioxidants. We assessed the effects of PJ supplementation on Acute Lung Injury (ALI) in adult rats exposed to hyperoxia for 5 days.MethodsAdult rats were divided into four different groups: control, hyperoxia, hyperoxia + PJ and PJ. Animals were placed in chambers containing either room air or oxygen above 95% for a total of 5 days. Two different PJ concentrations were utilized and the control group received placebo water. Animals were euthanized and their lungs were excised. Assessment of lung injury was accomplished by: a) wet to dry ratio (W/D) method, b) measurement of albumin concentration in the bronchoalveolar lavage fluid (BALF), c) oxidative stress, d) histological evaluation of the lung e) apoptosis and f) transcriptional expression levels of the inflammatory mediators IL-1β, IL-6 and TNF-alpha.ResultsAn increase in the W/D and albumin leak was noted in Hyperoxia (p < 0.05). Those findings were attenuated by the higher dose of PJ supplementation. Hyperoxia increased ROS production. Again PJ significantly reduced oxidative stress. Lung sections showed significant reduction in inflammation, edema, and infiltrating neutrophils in Hyperoxia + 80 μmol/kg when compared with Hyperoxia. TUNEL demonstrated significant apoptosis in the Hyperoxia, which was diminished in the Hyperoxia + 80 μmol/kg. Furthermore, increase in IL-1β and IL-6 was noted in Hyperoxia. Again, 80 μmol/kg of PJ significantly reduced the expression of inflammatory mediators.ConclusionIn this animal model, PJ supplementation attenuated ALI associated with hyperoxia.

BackgroundCigarette smoke (CS) increases oxidative stress (OS) in the lungs. Pomegranate juice (PJ) possesses potent antioxidant activities, attributed to its polyphenols. This study investigates the effects of PJ on the damaging effects of CS in an animal model and on cultured human alveolar cells (A549).MethodsMale C57BL/6J mice were divided into the following groups: Control, CS, CS + PJ, and PJ. Acute CS exposure was for 3 days, while chronic exposure was for 1 and 3 months (5 days of exposure/week). PJ groups received daily 80 μmol/kg via bottle, while other groups received distilled water. At the end of the experiments, different parameters were studied: 1) expression levels of inflammatory markers, 2) apoptosis, 3) OS, and 4) histopathological changes. In vitro, A549 cells were pretreated for 48 hours with either PJ (0.5 μM) or vehicle. Cells were then exposed to increasing concentrations of CS extracted from collected filters. Cell viability was assessed by counting of live and dead cells with trypan blue staining.ResultsAcutely, a significant increase in interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α expression, apoptosis, and OS was noted in CS when compared to Control. PJ significantly attenuated the expression of inflammatory mediators, apoptosis, and OS. Chronically (at 1 and 3 months), increased expression of TNF-α was observed, and lung sections demonstrated emphysematous changes when compared to Control. PJ supplementation to CS animals attenuated the increased expression of TNF-α and normalized lung cytoarchitecture. At the cellular level, CS extract reduced cellular proliferation and triggered cellular death. Pretreatment with PJ attenuated the damaging effects of CS extract on cultured human alveolar cells.ConclusionThe expression of inflammatory mediators associated with CS exposure and the emphysematous changes noted with chronic CS exposure were reduced with PJ supplementation. In vitro, PJ attenuated the damaging effects of CS extract on cultured human alveolar cells.

To assess the effect of chronic hypoxia on cardiomyocyte apoptosis, we used an animal model that mimics cyanotic heart disease. Rats were placed in a hypoxic environment at birth, and oxygen levels were maintained at 10% in an air-tight Plexiglas chamber. Controls remained in room air. Animals were killed, and the hearts were harvested at 1 and 4 wk. Significant polycythemia developed in the hypoxic rats at 1 and 4 wk. Right ventricular mass in the hypoxic rats was 192% and 278% that of controls, and hypoxic left ventricular mass was 140% and 178% that of the controls at 1 and 4 wk, respectively. The increase in cardiac mass was paralleled by only mild hypertrophy (10 to 20%). Contrary to previous reports showing increased apoptosis in response to hypoxia in cultured cardiomyocytes, there was no difference in the number of apoptotic cardiomyocytes between the chronically hypoxic rats and controls, as assayed by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling and Hoechst staining. We then examined the role of the sphingolipid ceramide because of its reported role in the stress response, growth suppression, and apoptosis. We found that the right ventricular ceramide content was significantly decreased in the hypoxic rats to 73% of control levels at the age of 4 wk. We suggest that the decrease in the ceramide content in the hypoxic right ventricular rat heart may be an adaptive response to chronic hypoxia and pulmonary hypertension. Lower ceramide levels may help suppress apoptosis and allow compensatory right ventricular cardiomyocyte proliferation. Apoptosis, or programmed cell death, is a mechanism of regulated cell death that plays a major role during development and homeostasis, and in many disease states. Apoptosis in cardiomyocytes has been demonstrated after injury caused by ischemia and reperfusion (1, 2), myocardial infarction (3, 4), cardiac aging (5), ventricular pacing (6), heart failure, and coronary embolization (7,8).Conflicting data regarding apoptotic changes, in response to hypoxia, have been described (9 -12). The failing myocardium is subject to regional ischemia and hypoxia, an abnormality that can trigger cardiomyocyte apoptosis (13). Long et al. (14) reported that cultured neonatal rat cardiomyocytes exposed to in vitro hypoxia for 48 h exhibited apoptotic changes. However, Bishopric et al. (15) found that induction of apoptosis of cardiac myocytes by hypoxia required acidosis, and that chronic hypoxia alone did not cause apoptosis of cardiomyocytes in culture. Hypoxia can induce cellular adaptive responses, such as c-Jun expression, that overcome apoptosis signals to minimize injury or damage (16). The in vivo effect of chronic hypoxia on the neonatal heart has not been investigated, and differentiating the effect of hypoxia and ischemia from that of hypoxia alone on apoptosis in the neonatal heart is important.Although no universal definition of apoptosis currently exists, morphologic and biochemical characteristics of apoptosis have been described that distinguis...