We report the successful anaesthetic management of a young girl with Alagille's syndrome and severe aortic stenosis (resting pressure gradient 88 mm Hg) undergoing living related donor liver transplantation (LRDLT). The patient had end-stage liver disease and LRDLT was performed before replacement of the aortic valve. Anaesthesia was conducted uneventfully with the aid of a pulmonary artery catheter. Intra-aortic balloon pumping was used in the perioperative period for protection against myocardial ischaemia. Total clamping of the inferior vena cava was avoided during surgery and volume administration was guided by the pulmonary artery pressure. A stable circulation was maintained in the reperfusion period. The patient was discharged from hospital on day 54 after operation with normal liver function. Two years later her aortic valve was replaced successfully.

Corticotropin-releasing factor (CRF) is released in response to various types of stressors and mediates endocrine, autonomic, immune, and behavioral responses to stress through interaction with CRF1 and CRF2 receptors. To investigate the role of CRF1 receptors in physiological responses to surgical stress, we analyzed the effects of two different non-peptide selective CRF1 receptor antagonists (JTC-017 and CP-154,526) and a peptide non-selective CRF receptor antagonist (astressin) on laparotomy-induced sympathetic nervous responses in isoflurane-anesthetized rats. JTC-017, CP-154,526, and astressin similarly suppressed plasma ACTH elevation induced by laparotomy. JTC-017 and CP-154,526 significantly augmented plasma noradrenaline and adrenaline responses to laparotomy, while astressin showed no effect on these responses. Laparotomy-induced maximum increases in mean blood pressure and heart rate were augmented by JTC-017, but were not affected by astressin. The results suggested for the first time that there was a pathway to attenuate sympathetic nervous response to surgical stress through CRF1 receptors in the central nervous system.

Benzodiazepines potentiate the effect of CRH or forskolin on proopiomelanocortin gene expression. The potentiating effect is not mediated by the benzodiazepine receptors, but its mechanism probably involves inhibition of phosphodiesterase.

Background and aim Reactive microglia has been associated with neuroinflammation caused by the production of proinflammatory molecules such as cytokines, nitric oxide, and prostaglandins. The overexpression of these molecules may provoke neuronal damage that can cause neurodegenerative diseases. A traditional herbal medicine, Orengedokuto (OGT), has been widely used for treating inflammation-related diseases. However, how it influences neuroinflammation remains poorly understood. Experimental procedure This study investigated the effects of OGT on inflammatory molecule induction in BV-2 microglial cells using real-time RT-PCR and ELISA. An in vivo confirmation of these effects was then performed in mice. Results and conclusion OGT showed dose-dependent inhibition of prostaglandin E2 (PGE2) production in BV-2 cells stimulated with lipopolysaccharide (LPS). To elucidate the mechanism of PGE2 inhibition, we examined cyclooxygenases (COXs) and found that OGT did not suppress COX-1 expression or inhibit LPS-induced COX-2 upregulation at either the transcriptional or translational levels. In addition, OGT did not inhibit COX enzyme activities within the concentration that inhibited PGE2 production, suggesting that the effect of OGT is COX-independent. The inhibitory effects of OGT on PGE2 production in BV-2 cells were experimentally replicated in primary cultured astrocytes and mice brains. OGT can be useful in the treatment of neuroinflammatory diseases by modulating PGE2 expression.

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