B-7601.

Constant infusion, exponentially declining infusion and program infusion of theophlline were administered to rabbits byadopting the rabbit population pharmacokinetic parameters in this laboratory, and the plasma concentrations of the drug was measured by ul- traviolet spectrophotometry. The results showed that the plasma drug concentrations following exponentially declining infusion and program infusion attained the desired steady-state level at only 30 min, though the T1/2?= 6. 08h, The median absolute value of performance error in pro-gram infusion and exponentially declining infusion was 7. 8% and 14% respectively.

Objective To investigate the effects of isoflurane on cyclic adenosine monophosphate (cAMP ) content of brain in the rats. Methods Fourty SD rats were allocated randomly to 5 groups: no administration(control group,n=8), inhalation of 1.4% isoflurane until losing of righting reflex(loss of righting reflex group,n=8), inhalation of 1.4% isoflurane lasting 30 min(anesthesia group,n=8) ,righting reflex recovery after cessation of 30-min inhalation of 1.4% isoflurane (recoveryⅠ group,n=8) and 30 min after cessation of 30-min inhalation of 1.4% isoflurane (recovery Ⅱ group,n=8). The rats of each group were decapitated at the end of procedures to measure the cAMP content of brain tissue with competitive protein binding assay.Results As compared with that in control group,the cerebrocortical cAMP content only in anesthesia group significantly increased by 49% (P

Objective To determine the effects of isoflurane on the amino acid neurotransmitter contents in rat cerebral cortex, hippocampus and spinal cord. Methods Sixteen male SD rats weighting 220-280g were randomly divided into two groups: isoflurane group (A) and control group (B). Animals in group A were killed after 30min inhalation of 1.3% isoflurane and cerebral cortex, hippocampus and spinal cord were removed immediately for determination of glutamic acid (Glu), aspartic acid (ASP), glutamine (Gln), GABA and glycine (Gly) levels by high-performance liquid chromatography (HPLC), whereas in group B O2 was inhaled instead of isoflurane. Results As compared with control group, Asp and Glu levels in cerebral cortex and hippocampus decreased markedly while Gly level increased significantly in hippocampus and spinal cord in isoflurane group. Conclusions The inhibition of excitatory amino acid synapse transmission and augmentation of inhibitory amino acid synapse transmission may be involved in the mechanism of isoflurane anesthesia.

Aim To observe the effects of ketamine on Na+,K+-ATPase,Ca2+-ATPase and NOSase activity in different cerebral cortex in convulsive mice.Methods The mice were randomly divided into blank group,normal saline(NS) group and ketamine 25 mg?kg-1 (KetⅠ),50 mg?kg-1(KetⅡ) group. The animals of blank group were killed directly.Convulsion was induced by intraperitoneally(ip) strychnine(1.5 mg?kg-1) in other groups,and correspond drugs were administered ip before five minutes.Action variety of mice was observed. Animals were killed on 30 minutes after strychnine injection.The activity of Na+,K+-ATPase,Ca2+-ATPase,TNOSase and iNOSase were assessed by spestrophotometric analysis in different cere-bral cortex(forehead,parietal and occipital area).Results Ketamine group could decrease mortality completely. The duration of tonic state in KetⅡ group was significantly shorter than that in KetⅠgroup.Compared with blank group,Na+,K+-ATPase and Ca2+-ATP ase activities were decreased in the group of NS and KetⅠ,and recovered normal level in the group of KetⅡ at parietal and occipital area. TNOS ase activity was decreased by 1/3 in KetⅡ group(P

Aim To investigate the effect of spinal substance P on the antinociceptive propoties of ketamine. Methods Using behaviors and Fos expression technique,the effects of intrathecal administration (it) of substance P of different dose on the ketamine induced antinociception were observed in the formalin test of mice. Results Compared with NS group, the amount of time that mice spent licking the injected paw was dose-dependently decreased in 20 and 30 mg?kg -1 groups(P

AIM:To study the protective effects of penehyclidine hydrochloride(PHC) on transient forebrain ischemia reperfusion injury in gerbils.METHODS:The model of transient forebrain ischemia reperfusion was established in gerbils by bilateral carotid artery clamping.The effects of PHC on neurological function scores and the morphous of hippocampal pyramidal neuron of gerbils were observed after receiving transient forebrain ischemia reperfusion.SOD activities and contents of MDA in the hippocampus and cortex of gerbils were measured.RESULTS:In the groups of PHC(0.08),(0.24)(mg?kg~(-1)) and atropine,the stroke index was decreased,compared with the ischemia-reperfusion group after the gerbils received transient forebrain ischemia reperfusion for six hours.PHC could reduce the degree of injury in hippocampal pyramidal neuron after ischemia reperfusion for three days.CONCLUSION: PHC has protective effects on transient forebrain ischemia reperfusion injury in gerbils.

AIM To investigate the protective effect of sodium gamma-hydroxybutyrate (?-OH) against cerebral ischemia-reperfusion injury in gerbils and the neuroprotective mechanism of ?-OH. METHODS The occlusion of bilateral carotid arteries of gerbil was used to make the cerebral ischemia-reperfusion models. Different doses of ?-OH were administered intraperitoneally 40 min prior to the onset of ischemia. After 10 min ischemia and 1 h reperfusion, bilateral hippocampus, cortex and striatum were taken out to measure ATPase, SOD and MDA. RESULTS The contents of MDA markedly elevated while Na +,K +-ATPase, Ca 2+ -ATPase and SOD activities decreased in hippocampus, cortex and striatum 1 h after ischemia-reperfusion. ?-OH administered prior to ischemia can partly reverse the elevation of MDA contents and the reduction of SOD activities. ?-OH given after ischemia can still provide partly protective effect. CONCLUSION ?-OH provides significant protective effect against cerebral ischemia-reperfusion injury by protecting ATPase and SOD activities, deleting free radicals and reducing the lipid peroxidation.

AIM:?To?investigate?if?alfentanil?protects?the?isolated?rat?heart?against?myocardial?reperfusion?injury?and?if?the?mechanism?of?this?protection?is?mediated?via?opioid?receptors?and?NO-dependent?pathways. METHODS: Langendorff rat hearts were perfused at constant pressure with Kreb-Henseleit(K-H) buffer for 20 min?and?then?were?perfused?with?test?solution:?K-H?buffer?or?K-H?buffer?containing?alfentanil? 50 ?g?L -1,?alfentanil? 100 ?g?L -1, naloxone 200 ?g?L -1, alfentanil 100 ?g?L -1+naloxone 200 ?g?L -1, L-NAME 100 ?mol?L -1 and alfentanil 100 ?g?L -1+L-NAME 100 ?mol?L -1. After 10 min of this, the hearts were subjected to 25 min normothermic( 37 ℃) global ischemia followed by 30 min reperfusion with the same test solution as before. To evaluate myocardial function, LVEDP, LVDP, ?dp/dt max, HR and CF were measured at the 20th, 25 and 30th minute of perfusion and the 1st, 3rd, 5th, 10th, 20th and 30th minute of reperfusion. After experiment, the NOS and ATP content of myocardium were assessed. RESULTS: Before ischemia, alfentanil 100 ?g?L -1 decreased the HR at the 30th minute compared with the 20th minute(P