There is a balance between oxidative stress, antioxidant capacity and immune response. Their roles in physiological and behavioural mechanisms are important for the maintenance of the organism’s internal equilibrium. This study aimed to evaluate the antioxidant effects of the exogenous alga Spirulina platensis (Arthrospira platensis) in a stress-induced rat model, and to describe its possible mechanism of action. Thirty-six adult male Sprague Dawley rats were separated into four groups: control (C), stress (S), S. platensis (Sp), and S. platensis + stress (SpS). The rats in groups Sp and SpS were fed with 1,500 mg/kg b.w./day Spirulina platensis for 28 days. All rats were exposed to prolonged light phase conditions (18 h light : 6 h dark) for 14 days. The SpS and S groups were exposed to stress by being kept isolated and in a crowded environment. Blood samples were obtained by puncturing the heart on the 28th day. The effect of stress on serum corticosterone, oxidative stress markers (TOS, TAC, PON1, OSI) and immunological parameters (IL-2, IL-4, IFN-ɣ) were tested. Also, the brain, heart, intestines (duodenum, ileum, and colon), kidney, liver, spleen, and stomach of the rats were weighed. Serum corticosterone levels were higher in the S group than in the C group, and significantly lower in the SpS group than in the S group. Mean total antioxidant capacity were lower in the S group than in the C group, and Spirulina reversed this change. Although not significantly different, IL-2 was lower in the S group than in the C group. However, in the SpS group, IL-2 increased due to Spirulina platensis mitigating effects of stress. Male rats fed a diet with Spirulina platensis could experience significantly milder physiological changes during stress, although stress patterns may be different. Exogenous antioxidant supplements merit further investigation in animals and humans where the endogenous defence mechanism against stress may not be sufficient.

OBJECTIVE To determine whether isoflurane-anesthetized cats with demonstrated resistance to the immobilizing effects of fentanyl would exhibit naltrexone-reversible sparing of the minimum alveolar concentration (MAC) of isoflurane when fentanyl was coadministered with the centrally acting catecholamine receptor antagonist acepromazine. ANIMALS 5 healthy male purpose-bred cats. PROCEDURES Anesthesia was induced and maintained with isoflurane in oxygen. Baseline isoflurane MAC was measured by use of a standard tail clamp stimulus and bracketing study design. Afterward, fentanyl was administered IV to achieve a plasma concentration of 100 ng/mL by means of target-controlled infusion, and isoflurane MAC was remeasured. Next, acepromazine maleate (0.1 mg/kg) was administered IV, and isoflurane MAC was remeasured. Finally, isoflurane concentration was equilibrated at 70% of the baseline MAC. Movement of cats in response to tail clamping was tested before and after IV bolus administration of naltrexone. Physiologic responses were compared among treatment conditions. RESULTS Isoflurane MAC did not differ significantly between baseline and fentanyl infusion (mean ± SD, 1.944 ± 0.111% and 1.982 ± 0.126%, respectively). Acepromazine with fentanyl significantly decreased isoflurane MAC to 1.002 ± 0.056% of 1 atm pressure. When isoflurane was increased to 70% of the baseline MAC, no cats moved in response to tail clamping before naltrexone administration, but all cats moved after naltrexone administration. CONCLUSIONS AND CLINICAL RELEVANCE Acepromazine caused fentanyl to decrease the isoflurane MAC in cats that otherwise did not exhibit altered isoflurane requirements with fentanyl alone. Results suggested that opioid-mediated increases in brain catecholamine concentrations in cats counteract the opioid MAC-sparing effect.

OBJECTIVE To evaluate whether cell-based and tissue-based immunofluorescent assays (IFAs) run in parallel could be used to detect glial fibrillary acidic protein (GFAP) autoantibodies in the CSF of dogs with meningoencephalitis of unknown origin (MUO) and other CNS disorders ANIMALS 15 CSF samples obtained from dogs with presumed MUO (n = 5), CNS disease other than MUO (5), and idiopathic epilepsy (5). PROCEDURES All CSF samples underwent parallel analysis with a cell-based IFA that targeted the α isoform of human GFAP and a tissue-based IFA that involved mouse brain cryosections. Descriptive data were generated. RESULTS Only 1 CSF sample yielded mildly positive results on the cell-based IFA; that sample was from 1 of the dogs with presumed MUO. The remaining 14 CSF samples tested negative on the cell-based IFA. All 15 CSF samples yielded negative results on the tissue-based IFA. CONCLUSIONS AND CLINICAL RELEVANCE Results suggested that concurrent use of a cell-based IFA designed to target the human GFAP-α isoform and a tissue-based IFA that involved mouse tissue cryosections was inadequate for detection of GFAP autoantibodies in canine CSF samples. Given that GFAP autoantibodies were likely present in the CSF samples analyzed, these findings suggested that epitopes differ substantially between canine and human GFAP and that canine GFAP autoantibody does not bind to mouse GFAP. Without a positive control, absence of GFAP autoantibody in this cohort cannot be ruled out. Further research is necessary to develop a noninvasive and sensitive method for diagnosis of MUO in dogs.