The Hb concentration in the group administered low-dose carperitide at 0.01 µg/kg/min remained higher than that in the control group during surgery. Administration of low-dose carperitide may therefore reduce the risk of blood transfusion during surgery.

No abstract

Oxidative stress induced by reactive oxygen species such as hydrogen peroxide (H 2 O 2 ) has been implicated in the degeneration of motor neurons in amyotrophic lateral sclerosis (ALS). Astrocytes play a significant role in maintaining survival of neurons by supplying antioxidants such as glutathione (GSH) to neurons, and express many types of functional neurotransmitter receptors. It has been reported that dysfunction of astrocyte might be one of the cause of motor neuron degeneration in the transgenic mouse model of familial ALS. The decrease of GSH in the spinal cord has been also reported in the transgenic mice. Recently, we found that noradrenaline (NA) increased GSH in astrocytes via β 3adrenoceptor stimulation. Thus, NA may protect motor neurons from oxidative stress-induced death by increasing the supply of GSH from astrocytes to motor neurons via the stimulation of β 3 -adrenoceptor in astrocytes. In this study we investigated the neuroprotective effect of NA by using the single culture of mouse NSC34 motor neuron-like cell line or the co-culture of NSC34 cells and mouse astrocyte cell line C8-D1A. We established NSC34 cells overexpressed green fluorescence protein (GFP), and the cell viability was determined based on the morphology of GFP-positive cells under a fluorescence microscope. Pretreatment with NA (10-30 µM) for 24 h protected NSC34 cells from H 2 O 2 -induced death in co-culture with C8-D1A cells, but not in single culture. This neuroprotective effect of NA was inhibited by a β 3adrenoreceptor antagonist SR 59230A. In addition, pretreatment with CL316243, a β 3 -adrenoreceptor agonist, protected NSC34 cells from H 2 O 2 -induced death in co-culture. DL-buthionine-[S,R]-sulfoximine, a GSH synthesis inhibitor, negated the neuroprotective effect of NA. MK-571, which inhibits the export of GSH from astrocyte mediated by multidrug resistance-associated protein 1, also prevented the neuroprotective effect of NA. These results suggest that NA may protect motor neurons from H 2 O 2 -induced death by increasing the supply of GSH from astrocytes via β 3adrenoreceptor stimulation.