In addition to their traditional role in centrally mediated analgesia, opiate compounds produce significant effects when administered peripherally. Using a recently characterized model of acute chemical injury to the rat cornea, we assessed the effects of morphine sulphate eye drops on corneal inflammation and hyperalgesia. Topical application of a 5 microM morphine sulphate eye drop preparation attenuated capsaicin-induced blinking in a concentration-dependent manner. However, morphine had no effect on capsaicin-induced blinking when applied to healthy, non-inflamed rat cornea. In addition, 5 microM morphine given every 2 h following cauterization retarded the development of both stromal edema and the infiltration of immune cells. Both the analgesic and anti-inflammatory effects of morphine were prevented by the opioid receptor antagonists naloxone, CTAP, and naltrindole. We conclude that morphine acts on mu and delta opioid receptors located in the rat cornea to attenuate inflammation and hyperalgesia.

The results indicate that respiratory acidosis was caused during CO2 insufflation for laparoscopic cholecystectomy, that was due to (1) decreased compliance, (2) increased CO2 load and (3) insufficient ventilation. Accumulated CO2 during laparoscopic cholecystectomy increased PaCO2 level in the recovery room.

Moxonidine-induced central sympathoinhibition attenuated brain oxidative stress, prevented cardiac dysfunction and remodelling, and improved the prognosis in rats with hypertensive heart failure. Central sympathoinhibition can be effective for the treatment of hypertensive heart failure.

Brief ReportGlucose intolerance during prolonged sevoflurane anaesthesia Purpose

Pressure overload enhances salt-induced sympathoexcitation through hypothalamic mineralocorticoid receptor (MR)-epithelial Na channel activation. Pressure overload also increases hypothalamic angiotensin type 1 receptors (AT1R). However, the role of AT1R in pressure overload-induced MR activation and salt-induced sympathoexcitation remains unknown. Therefore, the aim of the present study was to address this question. We performed aortic banding (AB) on mice from the Institute of Cancer Research. The expression of hypothalamic MR, serum/glucocorticoid-induced protein kinase-1 (SGK-1) and AT1R increased independently of plasma renin activity at 2 or 4 weeks after AB. Next, we performed AB in AT1aR-knockout (KO) mice and c57BL6/J wild-type (WT) mice. Sham-operated (Sham) mice were used as a control. Four weeks after AB (AB-KO or AB-WT), the expression of hypothalamic MR and SGK-1 increased in both AB-WT and AB-KO compared with Sham-WT and Sham-KO, respectively. The expression of AT1R was also greater in AB-WT than in Sham-WT. In addition, mice were fed a high-salt (8%) diet for an additional 4 weeks (ABH-KO and ABH-WT). High salt loading increased the urinary excretion of norepinephrine, a marker of sympathetic activity in ABH-WT, concomitant with hypothalamic MR activation, but not in ABH-KO. These results indicate that pressure overload activated hypothalamic MR independently of AT1R. After salt intake, however, AT1R was necessary to maintain hypothalamic MR activation and salt-induced sympathoexcitation.