ABSTRACT
The present study was designed to assess the anti-inflammatory activity of hyperbaric oxygen treatment by comparing it with that of diclofenac, a nonsteroidal anti-inflammatory drug, and also to investigate whether hyperbaric oxygen treatment enhances the anti-inflammatory effect of diclofenac in carrageenan-induced paw edema which is commonly employed as an acute inflammation model in rats. Hyperbaric oxygen treatment and diclofenac (20 mg/kg) markedly reduced the carrageenan-induced paw edema in rats. In other words, they displayed anti-inflammatory activity. On the other hand, hyperbaric oxygen treatment did not consistently modify the anti-inflammatory effect of diclofenac in this model.
Subject(s)
Edema/therapy , Hyperbaric Oxygenation , Inflammation/therapy , Animals , Anti-Inflammatory Agents, Non-Steroidal/administration & dosage , Anti-Inflammatory Agents, Non-Steroidal/therapeutic use , Carrageenan , Combined Modality Therapy , Diclofenac/administration & dosage , Diclofenac/therapeutic use , Disease Models, Animal , Edema/chemically induced , Hindlimb , Inflammation/chemically induced , Male , Rats , Rats, Sprague-DawleyABSTRACT
Single Photon Emission Computed Tomography (SPECT) and radiopharmaceutical stabilizing agents allowed us to investigate regional cerebral blood flow (CBF) distribution in six resting healthy subjects during acute laboratory hypobaric hypoxic conditions. In the hypobaric experiment stabilized 99mTc-D, L-hexamethyl-propylene amine oxime was injected 40 min after reaching hypoxic conditions corresponding to an altitude of 5500 m above sea level. Arterial blood sample was taken after five additional minutes. Mean arterial oxygen pressure and haemoglobin saturation were 28 mmHg and 56%, respectively. The control experiment was performed similarly, apart from barometric pressure and blood gas analysis. We analysed CBF distribution in 12 regions of functional interest bilaterally in frontal, parietal, temporal, occipital cortex, in the hippocampus, in the basal ganglia and other central structures of brain. No overall effect of hypoxia on normalized regional CBF distribution in the considered regions was found. Motor cortex (Brodmann 4) and basal ganglia were the only regions in which hypobaric hypoxia significantly increased relative distribution of the radiopharmaceutical [F(1,5)=18.30; P < 0.008 and F(1,5)=10.85; P < 0.022, respectively]. Despite severe hypoxia, we did not observe any major regional CBF redistribution. We found a small relative increase in blood flow to the motor cortex and the basal ganglia, at rest after 40 min of hypobaric hypoxia, suggesting a preferential compensatory mechanism of these functional regions of brain.
