Despite high in-hospital mortality associated with acute respiratory distress syndrome (ARDS), there is no effective therapeutic strategy. We tested the hypothesis that combined melatonin-mitochondria treatment ameliorates 100% oxygen-induced ARDS in rats. Adult male Sprague-Dawley rats (n = 40) were equally categorized into normal controls, ARDS, ARDS-melatonin, ARDS with intravenous liver-derived mitochondria (1500 μg per rat 6 hr after ARDS induction), and ARDS receiving combined melatonin-mitochondria. The results showed that 22 hr after ARDS induction, oxygen saturation (saO2 ) was lowest in the ARDS group and highest in normal controls, significantly lower in ARDS-melatonin and ARDS-mitochondria than in combined melatonin-mitochondria group, and significantly lower in ARDS-mitochondria than in ARDS-melatonin group. Conversely, right ventricular systolic blood pressure and lung weight showed an opposite pattern compared with saO2 among all groups (all P < 0.001). Histological integrity of alveolar sacs showed a pattern identical to saO2 , whereas lung crowding score exhibited an opposite pattern (all P < 0.001). Albumin level and inflammatory cells (MPO+, CD40+, CD11b/c+) from bronchoalveolar lavage fluid showed a pattern opposite to saO2 (all P < 0.001). Protein expression of indices of inflammation (MMP-9, TNF-α, NF-κB), oxidative stress (oxidized protein, NO-1, NOX-2, NOX-4), apoptosis (mitochondrial Bax, cleaved caspase-3, and PARP), fibrosis (Smad3, TGF-β), mitochondrial damage (cytochrome C), and DNA damage (γ-H2AX+) exhibited an opposite pattern compared to saO2 in all groups, whereas protein (HO-1, NQO-1, GR, GPx) and cellular (HO-1+) expressions of antioxidants exhibited a progressively increased pattern from normal controls to ARDS combined melatonin-mitochondria group (all P < 0.001). In conclusion, combined melatonin-mitochondrial was superior to either treatment alone in attenuating ARDS in this rat model.

MDCT angiography is clinically feasible for evaluating the complete vascular tree of failing AVFs and in showing uncommon complications, including brachial aneurysms and central vein lesions.

SUMMARYThe integrity of myocardial structures plays a crucial role in signal transductions and cardiac function. The aim of this study was to test the hypothesis that diabetes mellitus (DM) exerts adverse effects on the integrity of gap junctions (GJs) and induces cellular apoptosis in rat cardiomyocytes that can be abolished by simvastatin or losartan therapy. An experimental model of DM (induced by streptozocin 60 mg/kg body weight) in adult male rats (n = 24) was utilized to investigate the integrity of GJs containing connexin43 (Cx43) and the incidence of cellular apoptosis in the left ventricular myocardium. These rats were divided into 3 groups; group I (insulin therapy only), group II (insulin plus simvastatin 20 mg/kg/day), and group III (insulin plus losartan 20 mg/kg/day). Diabetic rats and 8 healthy rats (group IV) were sacrificed at 3 weeks following DM induction for immunofluorescence analysis. The experimental results demonstrated that the number of intact Cx43 GJs and the integrated area (µm 2 ) constituted by clusters of Cx43 spots were significantly higher in groups II and IV than in group III, and in groups II-IV than in group I (all P values < 0.05). Additionally, the number of apoptotic bodies was remarkably higher in group I than in groups II-IV, and notably higher in groups II-III than in group IV (all P values < 0.05).Simvastatin is more effective than losartan at inhibiting the effects of DM on the integrity of myocardial ultrastructures. Both drugs effectively prevent cellular apoptosis in diabetic rat heart. (Int Heart J 2007; 48: 233-245)