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Objective To investigate the effects of repeated inhalation of sevoflurane on cognitive function in aged rats. Methods Twenty-four Wistar rats of beth sexes aged 18 months weighing 270-450 g were randomly divided into 3 groups(n=8 each):control group(C),2%aevoflurane group(S1)and 3% sevoflurane group (S2).Group C inhaled oxygen(2.5 L/min)and nitrogen(6L/min)only, while group S1 and S2 inhaled 2%and 3%sevonurane in oxygen(2.5 L/min)and nitrogen(6 L/min)100 min/d for 5 d respecfivelv. The Morris watemaze test was performed once a day for 6 consecutive clays after the last inhalation(T1-6).The swimming time and distance at T1-5 and probe time and swimming distance in the fourth quadrant at T6 were recorded. The aninlala were killed within 60 min after the last test and the hippecampus were immediately removed for determination ofthe expression of NMDAR, NRI and NR2B mRNA using RT-PCR.Results The swimming time and disl .ance were significantly longer at T1,and the probe time in the fourth quadrant shorter and expression of NMDAR mRNA hisher at T6 in group s2 than in group C(P<0.05).Conclusion Repeated inhalation of 2% sevoflurane can not induce cognitive disordel-,while 3%sevoflurane Call induce transient cognitive decline in aged rats.
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Objective To assess the effects of norephrine and dopamine on renal blood and renal function in a dog model of endotoxin shock. Methods Twenty-one mongrel dogs (weight 14-30 kg) were anesthetized with pentobarbital sodium and intubated. Spontaneous breathing was maintained. Swan-Ganz catheter was inserted via right external jugular vein. A 18G cannula was inserted via vein of the left upper limb for infusion of fluid and a 20G cannula in femoral artery for blood sampling and monitoring of arterial pressure. Abdomen was opened and right renal artery was exposed. A electromagnetic flowmeter (4mmφin interval diameter) was placed around the renal artery for measurement of renal blood flow. Shock was induced with intravenous administration of endotoxin 2mg/kg (LPS O55B5 Sigma). One hour after iv injection of LPS, the animals were divided into 3 groups with 7 dogs each: group Ⅰ (group NE) received norepinephrine infusion 40ng@ kg-1@ min-1 for 1h; group Ⅱ (group DA) received dopamine infusion 4μg.kg-1 @min-1 for 1h; group Ⅲ (group NE + DA) received NE 40 ng@ kg-1 @min-1 and 4 μg@ kg-1@min-1 for 1h. MAP, HR, cardiac output(CO), stroke volume index(SVI), CVP, PCVP, SVR, renal blood flow and renal function (serum Na+ , K+ , creatinine, urea nitrogen and uric acid ) were measured before LPS administration, lh after administration of LPS, at the end of norepinephrine and/or dopamine infusion, 1 and 2h after NE and/or DA infusion. Results MAP, CO and renal blood flow decreased significantly after LPS administration, but there was no significant change in renal function after LPS was given. After infusion of norepinephrine and/or dopamine MAP, SVI and CO increased significantly but there was little change in renal blood flow and renal function. Conclusions Low dose norepinephrine can improve hemodynamics and maintain renal blood flow and renal function especially when combined with dopamine during endotoxin shock in dogs.
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Objective: To determine the mechanism of protective effects of lidocaine on brain during ischemia. Method: Wistar rats within 24h after birth were enrolled. The brain cortex cells were separated and then cutured under normal or anoxic condition. The OD value of these cells were detected with rapid colorimetric assay after they were cultured 24h and 48h. According to the above values, other cells were cultured in different condition and divided intc three groups: control group(N) cultured under normal condition (37℃, 5%CO_2+95%air); anoxic group(A) and anoxic+ lidoeaine group(L) cultured under anoxic condition(37℃, 5%CO_2+95%N_2). 6.9?10~(-5)mol/L lidocaine was added to the medium in group L. Cells of these three groups were cultured under different condition for 48h, then malondiadehyde and lactate levels of each group were measured. Result: The survival cells of anoxic group were significantly lower than that of control group after cultured for 48h, the malondiadehyde levels were as follows (nmol/ml): group N(4.93 ?0.43, n=12), group A(5.56?0.34, n=12), group L(4. 80?0.25, n=11); the lactate levels (mmol/L): group N(8.05?1.64, n=21), group A (11.86?2.58, n=22), group L(9.96?1.88, n=21), Conclusion: Lidocaine may protect brain from ischemia through inhibiting malondiadehyde and lactate production induced by anoxia.
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Objective To determine the dose of ropivacaine leading to convulsion and the convulsant action of midazolam. Methods Twenty healthy adult rabbits weighing 2.5-3.5kg were randomly divided into two groups with ten animals in each group: ropivacaine group(R) and midazolam-ropivacaine group(MR). Middle artery of ear was cannulated for MAP, HR monitoring and blood sampling for blood gas analysis and determination of plasma lactate and ropivacaine concentrations. Edge vein of ear was cannulated for administration of drugs. In both groups animals received intravenous infusion of 0.75% ropivacaine at a rate of 0.5m1/min until convulsion occurred. In MR group midazolam 0.8 mg/kg was given intravenously before ropivacaine.Results The dose of ropivacaine leading to convulsion was 4.86mg/kg for R group and 12.26mg/kg for MR group. Plasma ropivacaine concentration was 11 .52pg/ml in group Rand 16.77pg/ml in MR group. Convulsion lasted for 7.25 mm(R group) and 8.59mm(MR group) . Plasma lactate concentration increased significantly during convulsion in R group but remained unchanged in MR group. Blood pH decreased significantly during convulsion in R group but there was little change in PaCO2 and PaO2. Blood pH, PaO2 and PaCO2 did not change significantly during convulsion in MR group. There was no significant change in MAP and HR during convulsion in R group. In MR group MAP and HR decreased by 31 % and 35% respectively during convulsion and returned to baseline value gradually after ropivacaine infusion was stopped. All animals survived the experiment in both groups. Conclusions Ropivacaine is less cardiovascular toxic. Pretreatment with 0 . 8mg/kg midazolam greatly increases the dose of ropivacaine leading to convulsion. Midazolam can effectively prevent and treat CNS toxicity of ropivacaine.
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Objective To investigate the effects of midazolam, ketamine and propofol on spatial cognitive function and the mRNA expression of N-methyl-D-aspartate (NMDA) receptor subunits NR1 and NR2B in the hippocampus of aged rats. Methods Thirty-two Wistar rats of both sexes aged 18 months were randomly divided into 4 groups: Ⅰ control group (n = 9); Ⅱ midazolam group (M, n = 8);Ⅲ propofol group (P, n = 7) and Ⅳ ketamine group (K, n = 8). The animals received intraperitoneal (IP) midazolam 30 mg?kg-1 or propofol 60 mg ?kg-1 or ketamine 80 mg?kg-1 once a day for 3 days whereas the animals in control group received IP normal saline 2 ml instead. One day after the last drug administration the animals underwent Morris water maze test 4 times a day for 3 consecutive days. The animals were killed at 1h after last test and the brains were immediately removed for determination of NR1 and NR2B mRNA expression in the hippocampus using RT-PCR.Results The latency period and swimming distance were significantly shorter on the 3rd day of water maze test than on the 1st day in control group and group K, P. The latency period on the 1st day was significantly longer in group K than in control group. The NR1 mRNA expression in group M was significantly higher while the NR2B mRNA expression in group K and P was significantly lower than that in control group (P
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Objective To investigate the effects of various concentrations of lidocaine on the N-methyl-D-aspartate ( NMDA)-mediated calcium currents in cultured rat hippocampal neurons. Methods Hippocampal neurons were obtained from newborn Wistar rats (0-24 h after birth) . The hippocampal neurons cultured for 12-14 days were divided into control group and 5 lidocaine groups in which lidocaine was added to the extracellular solution achieving the final concentrations of 10-3 , 10-4 , 10-3 , 10-2 and 10-1 . The neuronal cells were voltage clamped at - 80 mv. The currents evoked by NMDA 100 ?mol?L-1 were recorded. The NMDA-mediated Ca currents were isolated by blocking Na-currents with TTX, K-currents with CsCL and TEACL and non-NMDA receptor (to a large degree AMPA receptor) with CNQX. Current density was calculated (pA / pF) .Results Lidocaine significantly reduced the density of NMDA-mediated calcium currents at concentrations of 10-3- 10-1 ?mol?L-1 compared with that in the control group (P