Evaluation of mean arterial blood pressure, heart rate, and sympathetic nerve activity in rabbits after administration of two formulations of etomidate.

Objective: To evaluate and compare the effects of the aqueous sulfobutyl ether beta-cyclodextrin (SBE-CD) etomidate formulation and the commercial etomidate formulation on mean arterial pressure (MAP), heart rate, and sympathetic outflow using neuraxis-intact and baro-denervated rabbits.

Study Design: Prospective experimental study.

Animals: Twenty-seven male New Zealand white rabbits.

Protamine after heparin produces hypotension resulting from decreased sympathetic outflow secondary to increased nitric oxide in the central nervous system.

To elucidate whether there are linkages among protamine-induced hypotension, nitric oxide (NO), and sympathetic nerve activity, we administered 3 mg/kg protamine sulfate after 300 U/kg heparin after 20 mg/kg of N(G)-nitro-D-arginine methyl ester (D-NAME) or N(G)-nitro-L-arginine methyl ester (L-NAME) as a pretreatment to baroreceptor-denervated rabbits and compared changes in hemodynamic variables and renal sympathetic nerve activity (RSNA). In the D-NAME group, heart rate (HR), mean arterial blood pressure (MAP), and RSNA significantly decreased to 93.7% +/- 0.

Inhibitory effects of extracellular matrix modulator(s) on lipopolysaccharide (LPS)- and acidosis-damaged glia containing cerebellar granule cell cultures.

The inhibitory effects of a novel chondroitin sulfate compound on lipopolysaccharide (LPS)- and acidosis-induced neuronal dysfunctions were examined. Cell viabilities in cultured neurons and/or astrocyte-rich cerebellar granule cells were measured by the calcein-AM method. Ten and 20 microg, as a final dosage, of LPS damaged less than 20% cells during a-2 h incubation.