Single and repeated sevoflurane or desflurane exposure does not impair spatial memory performance of young adult mice.

Volatile anesthetics are known to disturb the spatial memory in aged rodents, but there is insufficient information on their effects on young adult rodents. The aim of this study was to compare the effects of single and repeated exposure to desflurane and sevoflurane on spatial learning and memory functions in young adult mice. Balb/c mice (2 months old) were randomly divided into six equal groups (n = 8). The groups with single inhalation were exposed to 3.3% sevoflurane or 7.8% desflurane or vehicle gas for 4 h, respectively. The groups with repeated inhalation were exposed to 3.3% sevoflurane or 7.8% desflurane or vehicle gas for 2 h a day during 5 consecutive days. Spatial learning and memory were tested in the Morris water maze 24 h after exposure. In the learning phase, the parameters associated with finding the hidden platform and swimming speed, and in the memory phase, time spent in the target quadrant and the adjacent quadrants, were assessed and compared between the groups. In the 4-day learning process, there was no significant difference between the groups in terms of mean latency to platform, mean distance traveled and average speed (P > 0.05). During the memory-test phase, all mice exhibited spatial memory, but there was no significant difference between the groups in terms of time spent in the target quadrant (P > 0.05). Sevoflurane and desflurane anesthesia did not impair acquisition learning and retention memory in young adult mice.

Beneficial effects of levosimendan on cerebral vasospasm induced by subarachnoid haemorrhage: an experimental study.

BACKGROUND: The aim of this study was to investigate the ability of levosimendan to prevent cerebral vasospasm in a rabbit model of subarachnoid haemorrhage (SAH). ANIMALS AND METHODS: Eighteen New Zealand white rabbits were allocated into three groups randomly. SAH was induced by injecting autologous blood into the cisterna magna. (Group 1 = control:sham surgery group, Group 2 = SAH alone group, Group 3 = SAH plus levosimendan group). Histopathological examination was performed on day 3 as described. Intravenous levosimendan dose (initially 12 microg kg(-1) infusion, continuously for at least 10 minutes and then continued with a dose of 0.2 microg kg(-1) min(-1)) treatment was started after the induction of SAH. Three days later, the animals were sacrificed. RESULTS: In pathological investigation; there was statistically significant difference in luminal area and muscular wall thickness of the basilar artery between all groups (p < 0.005). Malondialdehyde level was also found significantly low in the levosimendan group compared with the SAH group. CONCLUSION: Intravenous levosimendan treatment was found effective by increasing the pathological luminal area and reducing muscular wall thickness measurements. This is the first study to show that intravenous administration of levosimendan is effective in preventing cerebral vasospasm induced by SAH in rabbits.

The mechanisms of the direct vascular effects of fentanyl on isolated human saphenous veins in vitro.

OBJECTIVE: The purpose of this study was to determine the mechanism of the direct effects of fentanyl on human veins in vitro. DESIGN: In vitro, prospective with repeated measures. SETTING: University research laboratory. INTERVENTIONS: Dose-response curves were obtained for cumulative doses of fentanyl (10(-9)-10(-5) mol/L) on saphenous vein strips precontracted with (10(-6) mol/L) 5-hydroxytryptamine incubated with either naloxone (10(-4) mol/L), Nomega-nitroL-arginine-methyl ester (L-NAME) (10(-4) mol/L), indomethacin (10(-5) mol/L), glibenclamide (10(-4) mol/L), tetraethylammonium (10(-4) mol/L), or ouabain (10(-5) mol/L). Vein strips were also exposed to a Ca++-free solution and 0.1 mmol/L of ethylene glycol-bis-(b-aminoethylether) N,N'-tetraacetic acid; 5-hydroxytryptamine (10(-6) mol/L) was added to the bath before cumulative Ca++ (10(-4)-10(-2) mol/L). The same procedure was repeated in the presence of fentanyl (10(-6) , 3 x 10(-6) , or 10(-5) mol/L) (p < 0.05 = significant). MEASUREMENTS AND MAIN RESULTS: Preincubation of vein strips with naloxone, L-NAME, or indomethacin did not influence the relaxant responses to fentanyl (p > 0.05). Tetraethylammonium, glibenclamide, and ouabain reduced the relaxation response to fentanyl (p < 0.05). A stepwise increase in tension was recorded with cumulative doses of Ca++ (p < 0.05). CONCLUSIONS: The present results show that fentanyl causes vasodilatation via both endothelium- and opioid receptor-independent mechanisms in the human saphenous vein. The relaxant effects of fentanyl are probably via activation of K+ channel and Na+K+-adenosine trisphosphatase and inhibition of Ca++ channel.