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Objectives: The aims of this study were to determine interrelationships between serum leptin, adiponectin and resistin, insulin-like growth factor-1 (IGF-1), total antioxidant capacity (TAC), non-esterified fatty acids (NEFA) and phospholipids concentrations in infants., Design and Methods: A cross-sectional study was conducted to assess serum levels of leptin, adiponectin, resistin, IGF-1, TAC, NEFA and phospholipids in 45 breast-fed infants enrolled at 4-30 days after birth., Results: Serum leptin and adiponectin concentrations were positively correlated. Serum resistin concentrations were inversely correlated to serum leptin and adiponectin concentrations. Serum TAC was positively correlated to serum leptin and adiponectin, and inversely to serum resistin concentrations. Serum adiponectin concentrations were positively related to serum NEFA and phospholipid concentrations. Serum resistin concentrations were inversely related to serum NEFA, and phospholipid concentrations., Conclusion: These data show that circulatory levels of leptin, adiponectin and resistin are interrelated and they apparently interact with the anti-oxidant system of infants., (Copyright © 2012 The Canadian Society of Clinical Chemists. Published by Elsevier Inc. All rights reserved.)

Previous studies has report the modulation of K+ channels play key roles in the induction of peripheral antinociception induced by many types of drugs. However, the possible participation of 4-aminopyridine-sensitive K+ channels to local antinociception induced by tramadol, a mu opioid receptor agonist, and lidocaine, a local anaesthetic, has been less studied. In this study, we therefore investigated this by using thermal plantar test. Tramadol or lidocaine administered intraplantarly into the hind paw elicited an antinociceptive effect. 4-aminopyridine caused an increase in the antinociception produced by lidocaine. However, tramadol induced antinociception remained unaffected by intraplantar administration of 4-aminopyridine. These results suggest that 4-aminopyridine-sensitive K+ channels may play an important role in the thermal peripheral antinociception produced by lidocaine, but not tramadol.

Several studies have suggested that systemic tramadol, an opioid, can represent a valuable treatment in severe pain conditions because of their effects on central pain pathways. However, there are not enough studies supporting that tramadol is efficacious when administered locally. Therefore, we studied the potential local analgesic effects of tramadol in peripheral nociception. In addition, we tested the antinociceptive effects of tramadol-CaCl(2) or naloxone combinations after subcutaneous intraplantar injection in a validated rat model of acute thermal nociception. Local analgesic effects of tramadol were compared with those of lidocaine. The effects of tramadol on thermal paw withdrawal latencies were monitored using the plantar test. The antinociceptive potency of tramadol is higher and long-lasting than that of lidocaine. Naloxone was unable to inhibit the increased antinociceptive response produced by tramadol. Ca(2+) modified the effect of tramadol. When Ca(2+) dose was increased in the solution, thermal antinociceptive potency of tramadol, but not lidocaine was prolonged. Thermal nociceptive responses were not affected in the non-injected paws, indicating a lack of systemic effects with doses of tramadol and lidocaine that elicited local analgesia. These results suggest that intraplantar tramadol administration can produce local analgesic effect with a different action mechanism than that of lidocaine. In addition, extracellular Ca(2+) may play an important role in the local analgesic action of tramadol.

The aim of the present study was to investigate the action of lidocaine and tramadol on the abnormal impulse characteristics of injured peripheral nerves. The ultrastructure of nerves was studied with electron microscopy and the action of lidocaine and tramadol on intact and injured rat sciatic nerves was examined by using the sucrose gap recording technique. Tramadol and lidocaine caused concentration- and frequency-dependent decreases in the amplitude of the compound action potential. Injured nerves were more sensitive to lidocaine than to tramadol. Lidocaine suppressed the delayed depolarization and decreased the hyperpolarizing afterpotentials to a greater extent than did tramadol. A low concentration of lidocaine may restore the abnormal impulse characteristics of injured nerves without changing the normal impulse pattern. The efficacy of lidocaine and inefficacy of tramadol on abnormal impulse characteristics may contribute, at least in part, to our understanding of the mechanisms of action of these drugs in neuropathic pain therapy.

The experiments were done on frog sciatic nerves, using a sucrose-gap recording technique. The aim of our study was to investigate and to compare the tonic and phasic conduction blocking potency of tramadol and lidocaine on whole nerve and their interactions with Ca(2+). The concentration of a tramadol solution producing the same amount of tonic and phasic conduction blocks was three and six times higher than that needed for lidocaine, respectively. Increasing the Ca(2+) concentration in the test solution enhanced the conduction blocking potency of tramadol, but decreased that of lidocaine. It is concluded that tramadol blocks nerve conduction like a local anesthetic but with a weaker effect than that of lidocaine. Interactions of Ca(2+) and these drugs suggested that these drugs might have either different binding sites or different action mechanisms.