Delayed post-ischaemic administration of xenon reduces brain damage in a rat model of global ischaemia.

OBJECTIVE: Xenon and nitrous oxide have been shown to be neuroprotective in vivo and in vitro, but mainly in models of focal cerebral ischaemia. This study aimed to investigate whether the two gases are able to attenuate cerebral injury after global cerebral ischaemia. METHODS: Adult male Wistar rats underwent bilateral common carotid artery occlusion and were ventilated for 1 hour with 21% O2/78% N2. They were then randomized to three groups which continued to receive atmospheric air, 50% N2O/50% O2 and 50% Xe/50% O2 for an additional period of 45 minutes. The number of ischaemic neurons, the cortical volume loss and the immunochemical and molecular expression of c-fos and MMP-9 were evaluated. RESULTS: Xenon reduced the number of ischaemic neurons in the cortex and CA1 hippocampal region (p < 0.001) and decreased the cortical volume loss (p < 0.01). Immunochemical induction of c-fos in the cortex was significantly suppressed (p < 0.01) after administration of xenon. The molecular analysis revealed significant effects of N2O and xenon administration on c-fos and MMP-9 expression. CONCLUSIONS: The data indicate that N2O and xenon administration is neuroprotective 1 hour after bilateral common carotid artery occlusion. These findings provide valuable evidence on the beneficial role of N2O and xenon in global cerebral injury.

Effects of succinylcholine on the recovery of block produced by mivacurium in rats.

This study investigates the effects of succinylcholine on the recovery of neuromuscular blockade produced by mivacurium in rats. In 48 anesthetized animals, the sciatic nerve was prepared and stimulated, and twitches of the flexor digitorum longus muscle were recorded. Animals were randomly divided into four groups (n = 12 each): bolus dose of succinylcholine 0.1 mg/kg (GroupSch), bolus dose of mivacurium 0.15 mg/kg (GroupMiv), bolus dose of mivacurium 0.15 mg/kg, followed by succinylcholine 0.1 mg/kg at 25% neuromuscular recovery from mivacurium (Group-MivSch(25)), or bolus dose of mivacurium 0.15 mg/kg, followed by succinylcholine 0.1 mg/kg at 75% neuromuscular recovery from mivacurium (GroupMivSch(75)). Onset times of neuromuscular block following succinylcholine in mivacurium-treated groups were comparable and significantly shorter than in GroupSch (p < 0.001). Duration of action of succinylcholine was more prolonged when it was given in the presence of deeper neuromuscular block induced by mivacurium (p < 0.001 in GroupMivSch(25) and p < 0.01 in GroupMivSch(75)). Our results suggest that, in rats, mivacurium administration has a significant potentiating effect on a subsequent succinylcholine-induced neuromuscular block.

Effect of succinylcholine on the neuromuscular junction of hypoglycemic rats.

The aim of the present study was to investigate the effect of neuromuscular blocking drugs on the neuromuscular junction in hypoglycemic rats. Three groups of 6 white adult Wistar albino rats were used. Group A consisted of the control animals with normal blood glucose levels ranging between 80-120 mg/dl. Groups B and C consisted of animals which were made hypoglycemic by intravenous injection of insulin at a dose of 1 iU/100 g b.w. In this way, their blood glucose levels were reduced to 50% of the blood glucose levels of the control animals. The test animals (groups B and C) were sacrificed 40 min after the injection of insulin and the preparations of the phrenic nerve-hemidiaphragm were placed into a 100 ml_bath containing Paradelis-Zaimis solution. The bath was aerized with O2/CO2:95/5%, it's temperature was maintained at 37 degrees C and it's pH at 7.2. After the stabilization of the system and the recording of neuromuscular activity, succinylcholine was administered (1.5 x 10(-8) M in groups A and B and 3.0 x 10(-8) M in group C). For the statistical analysis of the results, student's t-test was used. According to our results, there is a statistically significant difference (with p < 0.02 being considered significant) between the n.bl/t% (magnitude of final neuromuscular blockage) values of the animals of groups B and C and those of the animals of group A. We also observed a statistically significant difference (with p < 0.001 being considered significant) between the t (time required for complete blockage in groups A and C or time required for stabilization of blockage in group B) values of the animals of groups B and C and those of the animals of group A. On the other hand, there was a statistically significant difference (p < 0.02 being considered significant) in the n.bl/5'% (magnitude of neuromuscular blockage 5 min after the administration of succinylcholine) values only between the animals of group A and B. Our results indicate that under hypoglycemic conditions, the amount of succinylcholine required for final neuromuscular blockage is two times greater than that needed under normal glucose blood levels. This finding suggests that the integrity of the neuromuscular junction is altered during hypoglycemia.

Pancuronium effect on the neuromuscular function of hypoglycemic rats.

An expected response in a hypoglycemic patient to a muscle relaxant formed the basis for the research presented in this study. There was no information available in the accessible literature and references gave no data on this subject. But because perioperative hypoglycemia is not unusual, we scheduled this experimental work. Four groups of 6 white adult Wistar albino rats were used in the study. Group A was the normoglycemia control group, with blood glucose levels of 80-120 mg/dl. Groups B, C and D were made hypoglycemic by i.v. injection of insulin 1 IU/100 g b.w. Blood glucose levels were reduced to 50% of the control values in hypoglycemic animals, which were sacrificed 40 min later. Phrenic nerve-hemidiaphragm preparations were placed in a 100 ml bath containing Paradelis-Zaimis solution, 37 degrees C, pH 7.2, aerated with O2/CO2:95/5%. After stabilization and recording of neuromuscular activity, pancuronium bromide was administered in doses of 1.5 x 10(-9) M in groups A and B, 3 x 10(-9) M in group D. Statistical analysis between A-B, A-C, A-D groups was done with Student's paired t test. Results showed that under hypoglycemic conditions the amount of pancuronium bromide needed for complete neuromuscular blockade was 2.5-fold greater than that needed in normoglycemic conditions. These findings suggest that the integrity of the neuromuscular junction is altered during hypoglycemia.