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To establish rat model of lung ischemia/reperfusion (IR) in vivo, and to explore the effects of acidification pretreatment for respiratory acidosis on the expression of matrix metalloproteinase-9 (MMP-9) and the possible mechanisms. Methods: A total of 36 male Sprague-Dawley rats were divided into a sham group (S group), a IR group, and an experiment group (RA group) (n=12 in each group). The rat left lung hilum in the S group was dissociated, followed by perfusion without ischemia. After the left lung hilum in the IR group was blocked for 45 min, the rats were followed by reperfusion for 180 min. After left lung hilum in the RA group was dissociated, the respiratory parameters were adjusted so that pressure of end tidal carbon dioxide (PETCO2) reached 56-65 mmHg (1 mmHg=0.133 kPa) for 5 min, then the rats was subjected to IR. Lung tissue wet/dry (W/D) and lung permeability index (LPI) were calculated, while the lung histopathology was observed and the MMP-9 protein expression were measured. Results: Compared with the control group, the W/D and LPI in the IR group and the RA group increased after reperfusion (both P<0.05), and the levels of W/D and LPI in the group RA were lower than that in the IR group (P<0.05). LPI and pathology scores were significantly lower in the RA group than those in the IR group (both P<0.01). After IR, the expression of MMP9 in the lung tissues in the IR group and the RA group increased significantly (both P<0.01). The expression of MMP-9 protein in the RA group was significantly lower than that in the IR group (P<0.01). Conclusion: After lung IR injury, the expression of MMP-9 protein, vascular permeability and inflammatory exudation is increased. The acidification pretreatment for respiratory acidosis can inhibit the expression of MMP-9 protein and reduce inflammatory exudation after lung IR, showing a protective effect on lung IR injury.
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Animals , Male , Rats , Acidosis, Respiratory , Drug Therapy , Gene Expression Regulation, Enzymologic , Lung , Lung Injury , Matrix Metalloproteinase 9 , Genetics , Rats, Sprague-Dawley , Reperfusion Injury , Drug TherapyABSTRACT
Objective To investigate the effects of dexmedetomidine on renal function in patients with hemorrhagic shock undergoing emergency surgery.Methods Sixty patients (27 males, 33 females) with hemorrhagic shock, aged 18-69 years, ASA physical status Ⅲ or Ⅳ, required emergency surgery under general anesthesia, were randomized into two groups (n=30 each): dexmedetomidine group (group D) and control group (group C).The patients in group D receiving a loading dose of dexmedetomidine (0.5 μg/kg within 10 min) after the induction of anesthesia followed by a continuous infusion rate of 0.4 μg·kg-1·h-1 till 30 min before the end of surgery, while those in group C received equal volume of normal saline.Venous blood were obtained immediately before beginning of surgery (T1), immediately after surgery (T2), 24 h after surgery (T3) and 72 h after surgery (T4) for detecting the concentrations of the serum creatinine (Scr) and blood urea nitrogen (BUN), the contents of neutrophil gelatinase-associated lipocalin (NGAL) and high mobility group box-1 (HMGB1).The range ability of the concentration of the serum Scr from T4 to T1 (ΔScr) and the content of the serum HMGB1 from T4 to T1 (ΔHMGB1) were also calculated and recorded.Hemodynamic index (including MAP, HR) and arterial blood gas results were recorded during surgery.Results Compared with T1, MAP, CVP and BE were increased, meanwhile, HR and Lac were decreased at T2, but there was no statistically significant difference between the two groups.No statistical difference was found in BUN at any time point between group D and group C.Compared with T1, Scr decreased in both groups at T2-T4.The ΔScr in group D was higher than that in group C at T4 (P＜0.05).The content of serum NGAL at T4 in group D was significantly dropped when compared with T1 (P＜0.01) and was lower than that in group C (P＜0.05).Compared with T1, the content of serum HMGB1 was significantly decreased in both groups at T2 (P＜0.05);the content of serum HMGB1 at T3 in group C was significantly increased and was higher than that in group D;the ΔHMGB1 in group C was higher than that in group D.Conclusion Hemorrhagic shock could induce acute kidney injury.Perioperative continuous infusion of dexmedetomidine facilitated renal function recovery after ischemia-reperfusion injury in patients with hemorrhagic shock through inhibiting the elevation of serum HMGB1.
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Objective To evaluate the effects of prolonged anesthesia with propofol during the early pregnancy on cognitive function of offspring rats.Methods One hundred and twenty female Sprague-Dawley rats at 5-7 days of gestation,weighing 280-320 g,were randomly divided into 4 groups (n =30 each) using a random number table:control group (group C),and propofol 2,4 and 8 h groups (P2,P4,P8 groups).In P2,P4,P8 groups,after propofol 20 mg/kg was injected intravenously,propofol was infused at 20 mg· kg-1 · h-1 for 2,4 and 8 h,respectively.In group C,normal saline 2 ml/kg was infused intravenously.At 30,31,32,33,34,35 and 36 days after birth,Morris Water maze was performed to evaluate the learning and memory abilities of offspring rats.At the end of Morris water maze test,the hippocampus of offspring rats was removed for microscopic examination of pathological changes with light and electron microscope.Results Compared with group C,the escape latencywas significantly prolonged,the frequency of crossing the original platform was decreased,and the time of staying at the original platform quadrant was shortened in p4 and P8 groups,and no significant changes were found in the indices mentioned above in group P2.The pathological changes of hippocampi were not found in C and P2 groups,while the pathological changes were obvious in P4 and P8 groups.Conclusion Prolonged anesthesia with propofol during the early pregnancy can induce cognitive dysfunction of offspring rats and the mechanism is related to the damage to hippocampal tissues.
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Objective To investigate the effect of ketamine anesthesia in early pregnancy on expression of hippyragranin (HGN) mRNA in hippocampus in offsprings of rats.Methods One hundred and twenty pregnant Sprague-Dawley rats at 5-7 days of gestation,aged 7 weeks,weighing 270-300 g,were randomly divided into 4 groups (n =30 each):2 h anesthesia with ketamine group (group K1),4 h anesthesia with ketamine group (group K2),8 h anesthesia with ketamine group (group K3) and control group (group C).Ketamine 20 mg/kg was injected via the caudal vein,followed by continuous intravenous infusion at 130 mg· kg-1 · h-1 after loss of righting reflex,and the infusion lasted for 2,4 and 8 h in groups K1-K3,respectively.The equal volume of normal saline was given instead of ketamine in group C.The learning ability and memory of the offsprings were tested by Morris water maze test on postnatal day 30.The offsprings were sacrificed on 2nd day after the end of Morris water maze test,their brains were removed and hippocampi were isolated for determination of the expression of HGN mRNA by RT-PCR.Results Compared with group C,the escape latency was significantly prolonged,the frequency of crossing the original platform was decreased,the time of staying at the original platform quadrant was shortened,and the expression of HGN mRNA was up-regulated in groups K1-K3 (P ＜ 0.05).There was no significant difference in the escape latency,frequency of crossing the original platform and time of staying at the original platform quadrant among groups K1-K3 (P ＞ 0.05).The expression of HGN mRNA was significantly higher in group K3 that in group K1 (P ＜ 0.05).There was no significant difference in the expression of HGN mRNA between group K2 and group K3 (P ＞ 0.05).Conclusion The mechanism by which ketamine anesthesia in the early pregnancy induces impairment of learning ability and memory of the offsprings is related to up-regulation of HGN mRNA expression in hippocampus in offsprings of rats.
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Objective To investigate the neurotoxic effects of different concentrations of tetracaine and ropivacaine on the brachial plexus nerve in rats.Methods Forty-eight male Sprague-Dawley rats,weighing 410-430 g,were randomly divided into 8 groups (n =6 each):normal saline group (group NS),0.25％,0.50％ and 1.00％ tetracaine groups (groups T1-3 ),and 0.25％,0.50％,1.00％ and 2.00％ ropivacaine groups (groups R1-4 ).The rats received injection of normal saline 1.0 ml,0.25％,0.50％ and 1.00％ tetracaine 0.5 ml,0.25％,0.50％,and 1.00％ ropivacaine 1.0 ml and 2.00％ ropivacaine 0.5 ml in groups NS,T1-3 and R1-4 respectively through one side of the axillary sheath.The other side of the axillary sheath served as control side.Five days later,compound action potential and nerve conduction velocity (NCV) of the brachial plexus nerve were measured.Tne brachial plexus nerve was obtained as the specimen for microscopic examination with light and transmission electron microscope.Results Compared with the control side and group NS,the compound action potential and NCV of the brachial plexus nerve were significantly decreased in groups T2,3 and R3,4 ( P ＜ 0.05 ).The compound action potential and NCV of the brachial plexus nerve were gradually decreased with the increasing concentrations of tetracaine in groups T1 3 ( P ＜ 0.05 ).The compound action potential and NCV of the brachial plexus nerve were significantly decreased in group R4 as compared with groups R1-3 (P ＜ 0.05).The microscopic examination showed that the pathologic changes were more severe in groups T2,3 and R3,4 than those on the control side and than in group NS.Conclusion 0.50％ and 1.00％ tetracaine,and 1.00％ and 2.00％ ropivacaine can result in pathologic damage to the brachial plexus nerve in rats and the degree of damage is related to the concentration.
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Objective To investigate the effect of isoflurane anesthesia during early pregnancy on the cognitive function of offspring rats.Methods Thirty SD rats at 5-7 day gestation were randomly divided into 3 groups ( n =10 each):control group (group C) and 2 isoflurane groups (groups Ⅰ1,Ⅰ2).Groups Ⅰ1 and Ⅰ2 inhaled 1.4％ isoflurane in O2 for 4 and 8 h respectively while group C inhaled 95 ％ O2 for 8 h.At 20 and 30 days after birth,offspring rats from 5 pregnant rats were tested for learning and memory abilities using Morris water maze.The offsprings were sacrificed at 7 days after test and their hippocampi were isolated for determination of N-methyl-D-aspartate receptor subunit 2B (NR2B) mRNA and protein expression.Results There were no significant differences in the results of Morris water maze test and NR2B mRNA and protein expression among the three groups.Conclusion Isoflurane anesthesia during early pregnancy has no effect on the cognitive function of the offspring rats.
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Objective To investigate the effect of inhalation of enflurane on the expression of N-methyl-D-aspartate receptor subunit 2B (NR2B) in the hippocampus of the offsprings of rats.Methods Thirty SD rats pregnancy 8-10 day weighing 200-250 g were randomly divided into 3 groups ( n =10 each):control group (Group C),4 h inhalation of enflurane group ( group E1 ) and 8 h inhalation of enflurane group ( group E2 ).Group E1 and E2inhaled 1.7 ％ enflurane (in O2 2 L/min) for 4 and 8 h respectively,while group C inhaled oxygen 2 L/rin for 8 h.The learning and memory functions of the offsprings were assessed at 20 and 30 days after birth by Morris maze test.The expression of the NR2B mRNA were examined by RT-PCR,NR2B protein were examined by mmunohistochemistry.Results Compared with group C,the escape latency was significantly prolonged,the frequency of crossing the original platform was significantly decreased,the staying time at the original platform quadrant was significantly shortened at 3-5 days after the test in group E1 and E2 (.P ＜ 0.05 ),the expression levels of NR2B mRNA and protein were significantly decreased at 20 and 30 days after birth in group E1 and E2 ( P ＜ 0.05).There were no significant differences in the indexes mentioned above between groups E1 and F2 ( P ＞ 0.05).Conclusion Inhalation enflurane in the early pregnancy can result in cognition dysfunction through inhibiting NR2B expression in the hippocampus of the offsprings of the rats.
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Objective To investigate the effect of inhalation of enflurane in the early pregnancy on the cognitive function in the offsprings of rats. Methods Thirty 8-10 day pregnant SD rats were randomly divided into 3 groups ( n = 10 each): control group (group C), 4 h inhalation of enflurane group (group E1 ) and 8 h inhalation of enflurane group (group E2). Group E1 and E2 inhaled 1.7% entlurane (in O2 2 L/min) for 4 and 8 h respectively, while group C inhaled oxygen 2 L/min for 8 h. The learning and memory functions of the offsprings were assessed at 20 and 30 days after birth by Morris water maze test. Results Compared with group C, the escape latency was significantly prolonged, the frequency of crossing the original platform was significantly decreased and the staying time at the original platform quadrant was significantly shortened at 3-5 days after the test in group E1 and E2 ( P ＜ 0.05). There was no significant difference in the indexes metioned above between group E1 and E2 ( P ＞ 0.05). Conclusion Inhalation of enflurane in the early pregnancy can result in cognitive dysfunction in the offsprings of the rats.
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Objective To investigate the effect of ketamine anesthesia in the early pregnancy on the c-fos mRNA and c-jun mRNA expression in the offsprings of rats. Methods Thirty pregnant SD rats at 5-13 days of gestation were randomly divided into control group and ketamine group (n = 15 each). Ketamine 20 mg/kg was injected intravenously through tail vein followed by 2 h infusion at a rate of 130 mg·kg-1 ·h-1 in ketmine group.While the equal volume of normal saline was given instead of ketamine in control group. The learning and memory function of the offsprings were tested by Morris water maze test on postnatal day 20 and 30. The hippocampal tissues were taken to detect the expression of c-fos mRNA and c-jun mRNA and to observe the ultrastructure. Results Compared with group C, the escape latency was significantly prolonged at 2 days during the test which was performed on postnatal day 30, but there was no significant difference in the expression of c-fos mRNA and c-jun mRNA on postnatal day 20 and 30 and in the indices mentioned above on postnatal day 20 in ketamine group (P ＞0.05). The damage to hippocampal neurons happened in ketamine group. Conclusion The mechanism by which ketamine anesthesia in the early pregnancy inhibits the cognitive function of the offsprings is related to the hippocampal neuron damage, but not related to the expression of c-fos mRNA and c-jun mRNA in hippocampus.
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<p><b>OBJECTIVE</b>To investigate the influence of high frequency partial liquid ventilation (HFJV) on the cardiopulmonary function in dogs with inhalation injury.</p><p><b>METHODS</b>Sixteen mongrel dogs inflicted by hot steam inhalation were subjected to severe inhalation injury and were randomly divided into control (C) and treatment (T) groups. The dogs in both groups were all given HFJV. In addition, the dogs in T group were simultaneously supplied with perfluorocarbon liquid (3 ml/kg) into the lungs slowly via tracheal intubation for liquid ventilation. The blood gas analysis, pulmonary compliance, airway resistance and hemodynamic parameters were determined at 30, 60 and 90 minutes after ventilation.</p><p><b>RESULTS</b>The PaO(2) in T group increased progressively, which was significantly higher than the post-injury value at all time points (P < 0.05). While the PaO(2) in C group exhibited no difference to the post-injury value at all time points. The PaCO(2) in T group increased obviously and was higher than the post-injury value at 60 and 90 post-ventilation minutes (P < 0.05). Furthermore, the PaO(2) in all the time points in T group was a little higher than that in C group (P > 0.05) and PaCO(2) in T group was much higher than that in C group at 90 min after ventilation (P < 0.05). But there was no difference between the two groups in terms of dynamic/static pulmonary compliance and airway resistance as well as the hemodynamics.</p><p><b>CONCLUSION</b>Compared with simple HFJV, high frequency partial liquid ventilation seemed to be beneficial to the oxygenation after inhalation injury and to be no influence on the hemodynamics.</p>
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Animals , Dogs , Female , Male , Airway Resistance , Blood Gas Analysis , Burns, Inhalation , Therapeutics , High-Frequency Jet Ventilation , Liquid Ventilation , Lung Compliance , Pulmonary Circulation , Pulmonary Gas Exchange , Respiration, Artificial , Methods , Respiratory Function Tests , Time FactorsABSTRACT
Objective:To study the effect of growth hormone(GH) on acute lung injury induced by endotoximia and its’ mechanism.Methods:After introduction of acute lung injury(ALI) by endotoximia,one hundred and tweleve male Sprague-Dawley rats were randomly divided into ALI group and GH group. Western blot,immunofluorescence staining and semi-quantitive reverse transcription polymerase chain reaction(RT-PCR) were used to determine the expression and activation of nuclear factor kappa B(NF-?B), the levels of CC16 protein and the expression levels of CC16 mRNA in ALI rats’ lung.Results:Both the expression levels of CC16 mRNA and the contents of CC16 protein in ALI rats’ lungs began to decrease significantly 0.5 h post-injury,reached nadir at 6 h post-injury,and then began to recover.Both the expression levels of CC16 mRNA and the contents of CC16 protein in GH group were significantly lower than those in ALI group at different time intervals post-injury.The dynamic changes of the expression and activation of NF-?B were contrast to those of CC16 protein levels.Correlation analysis indicated that CC16 correlates significantly with the extent of lung injury and the expression and activation of NF-?B.Conclusion:Down-regulation of CC16 expression plays a critical role in the pathogenesis of acute lung injury induced by endotoximia.The application of GH can deteriorate the lung injury induced by endotoximia through down-regulating the expression of CC16.