Aim: To investigate the effect of a new inotropic drug, levosimendan compared with dobutamine on levels of brain natriuretic peptide (BNP), interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-a), and malondialdehyde (MDA) in patients with severe decompensated heart failure. Methods and results: Twenty-nine consecutive patients (22 males and 7 females), mean age 70.5 F 9.9 years, with decompensated heart failure on standard medical therapy, were randomised to receive either a 24 h infusion of levosimendan (n = 15) or dobutamine (n = 14). Blood samples were drawn at baseline, 48 h and 5 days post infusion. Levosimendan produced a significant reduction in BNP compared to baseline, at both 48 h (744.1 F100 vs 1136.3 F 93.7 pg/ml, p = 0.04) and 5 days (446 F 119.3 vs 1136.3 F 93.7 pg/ml, p = 0.03), while IL-6 values decreased after 5 days (4.8 F 1.3 vs 8.6 F 1.5 pg/ml, p = 0.01). MDA levels were significantly lower 5 days after levosimendan compared to baseline (2.3 F 0.2 vs 3 F 0.3 AM, p = 0.01). TNF-a levels did not differ between the groups. The comparison of percentage alteration compared to baseline showed that BNP (À44.5 F 7.6% vs 4.8 F 18.7%, p = 0.025), MDA (À21.8 F 5.1% vs 14.9 F 8.5%, p = 0.001) and IL-6 (À38.8 F 12.5% vs 70.2 F 24%, p = 0.001) levels were significantly lower in the levosimendan group 5 days after treatment compared to the dobutamine group. Conclusions: Treatment with levosimendan in advanced decompensated heart failure exerts a beneficial hemodynamic, anti-inflammatory and antioxidant effect. These findings may give an insight into the favourable impact on mortality that levosimendan appears to have in published multicenter trials.

Melatonin has marked antioxidant properties. The aim of the present study was to evaluate the therapeutic effect of melatonin on acute liver injury induced in rats by carbon tetrachloride (CCl4), allyl alcohol (AA) and their combination. A total of 108 male Wistar rats were divided into 12 experimental groups according to their treatment regimen (n = 5-10 rats in each group). Melatonin (100 mg/kg body weight, BW) was administered 6 hr (a) after a single dose of CCl4 (intragastrically 0. 66 mL/kg BW diluted 1:1 v/v with corn oil); (b) a single dose of AA (intraperitonealy, 0.62 mmol/kg BW 1:50 v/v in 0.9% saline solution); and (c) a combination of the above substances. Rats were sacrificed at 24 and 48 hr post-toxin administration and the therapeutic effect of melatonin was investigated by assessment of histopathological changes and lipid peroxidation alterations determined by measuring tissue malondialdehyde plus 4-hydroxy-nonenal (MDA + 4-HNE), plasma MDA and plasma levels of liver enzymes. The levels of a key antioxidant, glutathione (GSH), were measured in liver tissue homogenates. Hepatic necrosis was significantly reduced in the melatonin-treated rats 48 hr after administration of CCl4, AA and CCl4 + AA. The levels of hepatic enzymes in plasma were found to be significantly reduced at 24 and 48 hr in the CCl4 + AA treated rats after melatonin administration. Additionally, MDA and MDA + 4-HNE concentrations were significantly reduced at 24 and 48 hr time-points in all groups that received melatonin. GSH levels were decreased in liver after the toxic substances administration, whereas melatonin reversed this effect. In conclusion, a single dose of melatonin decreased hepatic injury induced by CCl4, AA and CCl4 + AA. The inhibition of the oxidative stress and therefore lipid peroxidation by melatonin in CCl4 and AA administered animals, may constitute the protective mechanism of melatonin against acute liver injury.

The presence of calcium destabilized the admixtures, while the use of different commercial ingredients altered the admixtures' characteristics. Only 1 batch of the AIO admixtures studied was found to be compliant with USP <729> standards.

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