No abstract

The administration of hypertonic saline solution in experimental AP attenuated hemodynamic alterations, decreased inflammatory cytokines, diminished systemic lesions and pancreatic acinar necrosis, prevented pancreatic infection, and reduced the mortality rate.

Objectives To assess the prevalence of antibodies to Toxoplasma gondii and Neospora caninum in a population of dogs with a diagnosis of suspected inflammatory meningoencephalitis. Materials and Methods Medical records of three referral centres were reviewed from 2008 to 2016 to identify a cohort of dogs diagnosed and treated for suspected inflammatory meningoencephalitis after testing for evidence of exposure to these pathogens. Results In our sample of 400 dogs the prevalence for exposure (IgG>1:50) to Toxoplasma gondii was 8/201 (3∙98%). Active infection (IgG titre >1:400 or/and an IgM titre >1:64 and/or positive PCR in CSF) was suspected in 1/400 (0∙25%). The prevalence for exposure [Indirect fluorescent antibody (IFA) titre >1:50] and active infection (IFA titres ≥⃒1:400 and/or positive PCR in CSF) with Neospora caninum were 14/201 (6∙96%) and 9/400 (2∙25%), respectively. Clinical Significance In view of the low prevalence of protozoan infections, the risk associated with starting immunosuppressive medication in dogs with evidence of inflammatory meningitis or encephalitis in the UK appears low.

Liver fibrosis occurring as an outcome of non-alcoholic steatohepatitis (NASH) can precede the development of cirrhosis. We investigated the effects of sorafenib in preventing liver fibrosis in a rodent model of NASH. Adult Sprague-Dawley rats were fed a choline-deficient high-fat diet and exposed to diethylnitrosamine for 6 weeks. The NASH group (n=10) received vehicle and the sorafenib group (n=10) received 2.5 mg·kg-1·day-1 by gavage. A control group (n=4) received only standard diet and vehicle. Following treatment, animals were sacrificed and liver tissue was collected for histologic examination, mRNA isolation, and analysis of mitochondrial function. Genes related to fibrosis (MMP9, TIMP1, TIMP2), oxidative stress (HSP60, HSP90, GST), and mitochondrial biogenesis (PGC1α) were evaluated by real-time quantitative polymerase chain reaction (RT-qPCR). Liver mitochondrial oxidation activity was measured by a polarographic method, and cytokines by enzyme-linked immunosorbent assay (ELISA). Sorafenib treatment restored mitochondrial function and reduced collagen deposition by nearly 63% compared to the NASH group. Sorafenib upregulated PGC1α and MMP9 and reduced TIMP1 and TIMP2 mRNA and IL-6 and IL-10 protein expression. There were no differences in HSP60, HSP90 and GST expression. Sorafenib modulated PGC1α expression, improved mitochondrial respiration and prevented collagen deposition. It may, therefore, be useful in the treatment of liver fibrosis in NASH.

Cerebrospinal fluid (CSF) analysis is commonly used in the diagnostic investigation of seizure disorders in order to exclude possible inflammatory underlying aetiology. The medical records were searched for dogs presenting with epileptic seizures (ES) that had normal interictal neurological examination, normal complete blood count and biochemistry analysis, unremarkable MRI of the brain and had CSF analysis performed as part of the diagnostic investigation. A total of 200 dogs met the inclusion criteria. The CSF was abnormal in 30 dogs with a median total nucleated cell count of two cells/µl (IQR 1.5–6) and median protein concentration of 0.37 g/l (IQR 0.31–0.41). Pleocytosis was recorded in 14/30 dogs and the CSF protein was increased in 22/30. There was no correlation between abnormal CSF and the type or number of seizures or the time interval between the last seizure and CSF collection. A significant correlation was found between the number of red blood cells on CSF and having an abnormal CSF. The prevalence of having a diagnosis other than suspected idiopathic epilepsy (IE) was 0.5 per cent (1/200). These results suggest that performing CSF analysis in dogs with recurrent ES that have normal interictal neurological examination and unremarkable MRI has a low diagnostic value.

Objective. The inhalation anesthetic sevoflurane has presented numerous biological activities, including anti-inflammatory properties and protective effects against tissue ischemic injury. This study investigated the metabolic, hemodynamic, and inflammatory effects of sevoflurane pre- and postconditioning for short periods in the rescue of liver ischemia-reperfusion (IR) injury using a rat model. Materials and Methods. Twenty Wistar rats were divided into four groups: sham group, control ischemia group (partial warm liver ischemia for 45 min followed by 4 h of reperfusion), SPC group (administration of sevoflurane 2.5% for 15 min with 5 min of washout before liver IR), and SPPoC group (administration of sevoflurane 2.5% for 15 min before ischemia and 20 min during reperfusion). Results. All animals showed a decrease in the mean arterial pressure (MAP) and portal vein blood flow during ischemia. After 4 h of reperfusion, only the SPPoC group had MAP recovery. In both the SPC and SPPoC groups, there was a decrease in the ALT level and an increase in the bicarbonate and potassium serum levels. Only the SPPoC group showed an increase in the arterial blood ionized calcium level and a decrease in the IL-6 level after liver reperfusion. Therefore, this study demonstrated that sevoflurane preconditioning reduces hepatocellular injury and acid-base imbalance in liver ischemia. Furthermore, sevoflurane postconditioning promoted systemic hemodynamic recovery with a decrease in inflammatory response.

Purpose: Liver ischemia-reperfusion injury is a phenomenon presents in events like liver resections and transplantation. The restoration of blood flow may leads to local and systemic injury. Several techniques have been developed in order to avoid or ameliorate ischemia-reperfusion injury in clinical situations. The application of a sttuter reperfusion after the ischemic event (postconditioning) could alters the hydrodynamics and stimulates endogenous mechanisms that attenuate the reperfusion injury. The present study was designed to evaluate the potential protective effect of postconditioning in a model of ischemia-reperfusion in rats. Methods: Hepatic anterior pedicle of median and left anterolateral segments were exposed and clamped for 1 hour. Two hours later, clamp was released in two different ways: Control Group (n=7): clamp was release straightforward; Postconditioning Group (n=7): clamp was released intermittently. Lipid peroxidation (malondialdehyde) and expression of the glutathione-s-transferase--3 gene were studied. Results: Lipid peroxidation was significantly decreased in ischemic and non-ischemic liver by postconditioning. GST-3 gene was overexpressed in postconditioned group, but not significantly. Conclusion: Postconditioning induced hepatoprotection by reducing lipid peroxidation in the ischemic and non-ischemic liver. Key words: Liver. Ischemia. Reperfusion. Lipid Peroxidation. Rats. RESUMOObjetivo: A lesão de isquemia-reperfusão hepática é um fenômeno presente em eventos tais como ressecções hepáticas e transplante de fígado. A restauração do fluxo sangüíneo após a isquemia gera lesões locais e sistêmicas. Várias técnicas foram desenvolvidas com o objetivo de evitar ou diminuir a lesão de isquemia-reperfusão hepática em situações clínicas. A utilização da reperfusão intermitente após o evento isquêmico (pós-condicionamento) pode alterar a hidrodinâmica e estimular mecanismos endógenos que atenuam o dano da reperfusão. O presente estudo foi realizado para avaliar o potencial efeito protetor do pós-condicionamento em um modelo de isquemia-reperfusão em ratos. Métodos: O pedículo dos lobos mediano e ântero-lateral foi isolado e clampeado por 1 hora. Após 2 horas, o pedículo foi liberado de duas maneiras diferentes: Grupo Controle (n=7): clampe liberado de uma só vez; Grupo Pós-condicionamento (n=7): clampe liberado de maneira intermitente. Malondialdeído (MDA) e expressão do gene GST-3 foram estudadas nos grupos. Resultados: A peroxidação lipídica foi significativamente diminuída no fígado isquêmico e no fígado não isquêmico pelo pós-condicionamento. A expressão do gene GST-3 aumentou, porém não significativamente, no grupo pós-condicionamento. Conclusão: O pós-condicionamento induziu hepatoproteção pela redução da peroxidação lipídica nos fígados isquêmico e não isquêmico. Descritores: Fígado. Isquemia. Reperfusão. Peroxidação de Lipídeos. Ratos.

Peritoneal lavage has a systemic anti-inflammatory effect in severe AP and may be able to decrease the severity of severe AP.