Long Noncoding RNA H19 Overexpression Protects against Hypoxic-Ischemic Brain Damage by Inhibiting miR-107 and Up-Regulating Vascular Endothelial Growth Factor.

Long noncoding RNAs play critical roles in cellular homeostasis, and long noncoding RNA H19 (H19) is implicated in several pathologic conditions. The putative role of H19 in the pathogenesis and progression of hypoxic-ischemic brain damage (HIBD) is not yet understood. Therefore, a series of in vivo and in vitro experiments were designed to investigate the potential roles of H19 in neuronal apoptosis and cognitive dysfunction in HIBD. H19 expression was decreased in HIBD rat models established by partial occlusion of carotid artery. H19 bound to and decreased the expression of miR-107, which also increased VEGF expression. H19 overexpression reduced neuronal apoptosis and alleviated cognitive dysfunction in HIBD rats. The up-regulation of miR-107 reversed the protective effects conferred by H19. In addition, the cell model of HIBD was established by oxygen-glucose deprivation in neuronal cells used. H19 overexpression in oxygen-glucose deprivation neurons increased B-cell lymphoma-2 and decreased B-cell lymphoma-2-associated X, total and cleaved caspase-3 expressions. Taken together, the results showed that H19 expresses at a low level in HIBD. H19 overexpression decreased miR-107 and increased VEGF expression, which resulted in repressed neuronal apoptosis and alleviated cognitive dysfunction. Thus, H19 may serve as a molecular target for translational research for HIBD therapy.

MicroRNA-22-3p alleviates spinal cord ischemia/reperfusion injury by modulating M2 macrophage polarization via IRF5.

Cell death after spinal cord ischemia/reperfusion (I/R) can occur through necrosis, apoptosis, and autophagy, resulting in changes to the immune environment. However, the molecular mechanism of this immune regulation is not clear. Accumulating evidence indicates that microRNAs (miRs) play a crucial role in the pathogenesis of spinal cord I/R injury. Here, we hypothesized miR-22-3p may be involved in spinal cord I/R injury by interacting with interferon regulatory factor (IRF) 5. Rat models of spinal cord I/R injury were established by 12-min occlusion of the aortic arch followed by 48-hr reperfusion, with L4-6 segments of spinal cord tissues collected. MiR-22-3p agomir, a lentivirus-delivered siRNA specific for IRF5, or a lentivirus expressing wild-type IRF5 was injected intrathecally to rats with I/R injury to evaluate the effects of miR-22-3p and IRF5 on hindlimb motor function. Macrophages isolated from rats were treated with miR-22-3p mimic or siRNA specific for IRF5 to evaluate their effects on macrophage polarization. The levels of IL-1ß and TNF-α in spinal cord tissues were detected by ELISA. miR-22-3p was down-regulated, whereas IRF5 was up-regulated in rat spinal cord tissues following I/R. IRF5 was a target gene of miR-22-3p and could be negatively regulated by miR-22-3p. Silencing IRF5 or over-expressing miR-22-3p relieved inflammation, elevated Tarlov score, and reduced the degree of severity of spinal cord I/R injury. Increased miR-22-3p facilitated M2 polarization of macrophages and inhibited inflammation in tissues by inhibiting IRF5, thereby attenuating spinal cord I/R injury. Taken together, these results demonstrate that increased miR-22-3p can inhibit the progression of spinal cord I/R injury by repressing IRF5 in macrophages, highlighting the discovery of a promising new target for spinal cord I/R injury treatment.

PRR34-AS1 overexpression promotes protection of propofol pretreatment against ischemia/reperfusion injury in a mouse model after total knee arthroplasty via blockade of the JAK1-dependent JAK-STAT signaling pathway.

Long noncoding RNAs have been documented to be protective against ischemia/reperfusion (I/R) injury. However, few research works have focused on the protective effects of PRR34-AS1 on I/R injury after total knee arthroplasty (TKA). The objective of the present study was to investigate the possible effect of PRR34-AS1 on I/R injury after TKA. A mouse model with I/R injury after TKA was established. The interaction between PRR34-AS1 and Janus kinase 1 (JAK1) was examined and thoroughly investigated. Next, the effects of PRR34-AS1 on the expression of apoptosis-related proteins, JAS-signal transducer and activator of transcription (STAT) signaling pathways, and inflammation-related genes, chondrocyte proliferation, and apoptosis were analyzed after gain- and loss-of-function experiments. Attenuated symptoms were observed in mice pretreated with propofol, which was evidenced by decreased positive expression rate of JAK1 protein and superoxide dismutase content along with increased malondialdehyde content and IL-10 levels. PRR34-AS1 was poorly expressed in mice with I/R injury after TKA. JAK1 was a target of PRR34-AS1. Upregulated PRR34-AS1 diminished expression of JAK1, STAT1, JAK2, and STAT3 as well as cell apoptosis, while enhancing cell proliferation in vitro. Furthermore, JAK1 silencing could reverse the suppressed cell proliferation and enhanced cell apoptosis of chondrocytes imposed by silencing PRR34-AS1. Upregulation of PRR34-AS1 can potentially relieve I/R injury after TKA in mice pretreated with propofol through inhibition of the JAS-STAT signaling pathway by targeting JAK1.

Effect of ketamine combined with lidocaine in pediatric anesthesia.

BACKGROUND: We conducted a randomized clinical trial to determine whether adjunctive lidocaine diminishes the incidence of adverse effects in pediatric patients sedated with ketamine. METHODS: This case-control study involved 586 consecutive pediatric patients necessitating anesthesia. Then systolic blood pressure, heart rate, respiratory rate, and blood oxygen saturation were observed. Alanine aminotransferase (ALT), aspartate aminotransferase (AST), urea nitrogen (BUN), and creatinine (Cr) levels were tested. General dose of ketamine, the time of onset and duration of anesthesia and postoperative recovery, anesthesia effect, and adverse reaction were subsequently compared. High-performance liquid chromatography was employed to detect ketamine concentration at different time points after administration, and the postoperative cognition function was further evaluated. RESULTS: Intra- and post-operation, the rising degree of ALT, AST, BUN, and Cr in patients treated with ketamine was higher than those in patients treated with the ketamine-lidocaine complex. General dose of ketamine, the time of onset and duration of anesthesia, postoperative recovery time, and the incidence rate of adverse reaction in patients treated with ketamine-lidocaine complex were lower, but the concentration of ketamine was higher compared to the patients treated with ketamine. In patients treated with the ketamine-lidocaine complex, elimination half-life of ketamine was prolonged, the area under curve was increased, and the plasma clearance rate was decreased relative to those with ketamine alone. CONCLUSIONS: Ketamine combined with lidocaine may be beneficial in shortening the onset of anesthesia, promoting postoperative awake, prolonging elimination half-life, increasing area under curve, and decreasing plasma clearance rate and incidence of adverse reactions.

MiR-132-3p Modulates MEKK3-Dependent NF-κB and p38/JNK Signaling Pathways to Alleviate Spinal Cord Ischemia-Reperfusion Injury by Hindering M1 Polarization of Macrophages.

Spinal cord ischemia-reperfusion (SCIR) injury is a serious complication of open surgical and endovascular aortic procedures. MicroRNA-132-3p (miR-132-3p) has been reported to be involved in the progression of various diseases, but its role in SCIR injury is unclear. Thus, we aimed in this study to investigate the mechanism of miR-132-3p in SCIR injury and explore its pathway as a therapeutic target for SCIR injury. We first constructed a SCIR injury rat model and documented motor function in the model. Reverse transcription quantitative polymerase chain reaction (RT-qPC)R and Western blot analysis were used to detect the expression of miR-132-3p and mitogen-activated protein kinase kinase kinase 3 (MEKK3) in SCIR injury rats. The interaction between miR-132-3p and MEKK3 was identified by dual-luciferase reporter gene assay. Then, the effects of miR-132-3p and MEKK3 on macrophage M1 polarization were evaluated in vitro and in vivo by altering their expression in macrophages of SCIR injury rats, with treatments altering the nuclear factor-kappaB (NF-κB) and c-Jun N-terminal kinase (JNK)/p38 signaling pathways using SP600125, SB203580, or PDTC. The SCIR injury rats had a high Tarlov score and low miR-132-3p expression along with high MEKK3 expression. miR-132-3p could directly bind to MEKK3, and that macrophage M1 polarization and inflammation could be inhibited by overexpression of miR-132-3p through downregulating MEKK3 and inactivating the NF-κB and p38/JNK signaling pathways. Besides, increased miR-132-3p expression could decrease the injured rat Tarlov score. Overall, our study demonstrated that miR-132-3p can suppress M1 polarization of macrophages and alleviate SCIR injury by blocking the MEKK3-dependent activation of the NF-κB and p38/JNK signaling pathway. Thus, miR-132-3p and its downstream pathways may be useful targets to alleviate the symptoms of SCIR injury.

[Protective effect of hypothermic propofol on ischemic spinal cords].

OBJECTIVE: To evaluate the protective effect of hypothermic propofol infused via the aorta against ischemia/reperfusion injury of spinal cords in rabbits. METHODS: Sixty New Zealand white rabbits were randomly divided into six groups (n=10 in each group). The infrarenal circum-aortic clamping model was used in this study. During the 30-clamping time, 5 mL/kg of normal saline, 10% intralipid, propofol, 4 degrees C saline, 4 degrees C intralipid and 4 degrees C propofol were infused into the left femoral arteries of the rabbits in group SN, IPN, PN, SH, PH and IPH, respectively, at a rate 10 mL/(kg x h). The heart rates, blood pressures, respiratory rates and SPO2 were measured during the ischemic-reperfusion processes. The neurological status (Tarlov Scale system) were assessed 6 h, 24 h, and 48 h after the reperfusions. The spinal cords were harvested 48 h after the reperfusions for histological analysis. The concentrations of excitatory amino (EAA, aspartate and glutamate), malondialdehyde (MDA) and superoxide dismutas (SOD) in the harvested spinal cords were determined. RESULTS: Group PN, SH, PH and IPH had better neurological outcomes and less severe pathological changes than group SN and IPN (P<0.05). There were no significant differences between group SN and IPN (P>0.05). Group PN, SH, PH and IPH had lower concentrations of EAA in spinal cords than group SN and IPN (P<0.05). Group PH had the best neurological outcome, the least histopathological changes of spinal cords, and the lowest concentrations of EAA (P<0.05). Groups PN and PH had lower concentrations of malondialdehyde than group SN, IPN, SH and IPH. Groups PN and PH had higher concentrations of superoxide dismutas than group SN, IPN, SH and IPH (P<0.05). CONCLUSION: Both propofol and hypothermic liquids can protect spinal cords against ischemia/reperfusion injuries. Combined use of propofol and hypothermia results in significant recovery of spinal cord functions.

microRNA-128 enhances neuroprotective effects of dexmedetomidine on neonatal mice with hypoxic-ischemic brain damage by targeting WNT1.

OBJECTIVE: Hypoxic-ischemic brain damage (HIBD) is a major cause of acute mortality and chronic neurological morbidity in infants and children. Dexmedetomidine (DEX) is an effective choice in HIBD treatment. Recent findings have revealed that microRNA-128 (miR-128) is implicated in cerebral ischemia reperfusion. Hence, this study aimed to investigate the role of miR-128 in HIBD. METHODS: HIBD models of neonatal mice were established. HIBD mice were treated with DEX, and injected with agomir (ago)-miR-128 or antagomir (anti)-miR-128 into the lateral ventricles to explore the influence of miR-128 on the neuroprotective effects of DEX on HIBD. Subsequently, the mice body weight, left/right (L/R) brain weight ratio, left-brain water content as well as learning and memory abilities were measured. Furthermore, the pathological changes of brain tissues and apoptosis rate of nerve cells were determined. The potential relationship between miR-128 and WNT1 was analyzed. RESULTS: Over-expression of miR-128 caused an increase in mouse body weight, L/R brain weight ratio, and learning and memory abilities, while led to a decline in left-brain water content, brain tissue injury and apoptosis rate of nerve cells in DEX-treated HIBD mice. WNT1 was targeted and negatively regulated by miR-128. Silencing of WNT1 exerted the same effect as miR-128 on enhancing the neuroprotective effect of DEX on HIBD mice. CONCLUSION: Collectively, miR-128 enhanced neuroprotective effect of DEX on HIBD neonatal mice by inhibiting WNT1.

NF-κB signaling pathway inhibition suppresses hippocampal neuronal apoptosis and cognitive impairment via RCAN1 in neonatal rats with hypoxic-ischemic brain damage.

NF-κB is a core transcription factor, the activation of which can lead to hypoxic-ischemic brain damage (HIBD), while RCAN1 plays a protective role in HIBD. However, the relationship between NF-κB and RCAN1 in HIBD remains unclear. This study aimed to explore the mechanism of NF-κB signaling pathway in hippocampal neuron apoptosis and cognitive impairment of neonatal rats with HIBD in relation to RCAN1. Initially, microarray analysis was used to determine the differentially expressed genes related to HIBD. After the establishment of HIBD rat models, gain- or loss-of-function assay was performed to explore the functional role of NF-κB signaling pathway in HIBD. Then, the learning and memory ability of rats was evaluated. Expression of RCAN1, NF-κB signaling pathway-related genes and glial fibrillary acidic protein (GFAP), S-100ß and acetylcholine (Ach) level, and acetylcholinesterase (AchE) activity were determined with neuron apoptosis detected to further explore the function of NF-κB signaling pathway. RCAN1 could influence the development of HIBD. In the HIBD model, the expression of RCAN1 and NF-κB-related genes increased, and NF-κB p65 showed a significant nuclear shift. By activation of NF-κB or overexpression of RCAN1, the number of neuronal apoptosis, S-100ß protein level, and AchE level increased significantly, Ach activity decreased significantly, and GFAP positive cells increased. In addition, after the activation of NF-κB or overexpression of RCAN1, the learning and memory ability of HIBD rats was inhibited. All the results show that activation of NF-κB signaling pathway promotes RCAN1 expression, thus increasing neuronal apoptosis and aggravating cognitive impairment in HIBD rats.

Long non-coding RNA MALAT1 sponges microRNA-429 to regulate apoptosis of hippocampal neurons in hypoxic-ischemic brain damage by regulating WNT1.

Hypoxic-ischemic brain damage (HIBD) is a common neurological disorder. Emerging reports reveal that long non-coding RNAs and microRNAs (miRs) are implicated in the progress of HIBD. In this study we tried to ascertain whether lncRNA MALAT1, with the involvement of miR-429 and WNT1, affects HIBD. Initially, a HIBD mouse model was established. Then, we treated HIBD mice with dexmedetomidine (DEX) and then up- or down-regulated the expression of MALAT1, miR-429 and WNT1 in HIBD mice and neurons. Meanwhile, brain injury and hippocampal neuronal apoptosis were evaluated. Moreover, the interaction among MALAT1, miR-429 and WNT1 in HIBD was investigated. MALAT1 and WNT1 were high-expressed in brain tissues of HIBD mice while miR-429 was low-expressed in brain tissues from HIBD mice. Interestingly, MALAT1 silencing was observed to enhance the cerebral protection of DEX against HIBD. In addition, it was confirmed that MALAT1 sponged miR-429 downregulating expression of miR-429, thereby promoting apoptosis of hippocampal neurons. This effect was achieved through up-regulating the level of WNT1. Taken together, this study demonstrates that silencing of MALAT1 enhances the cerebral protection of DEX against HIBD by suppressing WNT1 expression through miR-429.

[Protective effect of pyrrolidine dithiocarbamate on erythrocytes during canine cardiopulmonary bypass].

OBJECTIVE: To investigate the protective effect of pyrrolidine dithiocarbamate (PDTC) on erythrocytes during canine cardiopulmonary bypass (CPB). METHODS: Twelve adult healthy dogs undergoing CPB were randomly divided into the control group (n = 6) and the PDTC group (n = 6). In the PDTC group, PDTC 30 mg/kg was administered intravenously before CPB. Dogs in the control group was intravenously administering with normal saline. The levels of interleukin (IL)-1beta, IL-8, malondiadehyde (MDA), free hemoglobin (F-HB) in plasma, erythrocyte adenosine triphosphate (E-ATP), and erythrocyte superoxide dismutase (E-SOD) were determined before CPB, 30 and 60 minutes after aortic cross-clamping (AC), and 30 and 60 minutes after declamping (DC). RESULTS: In the control group, plasma levels of IL-1beta and IL-8 significantly increased after CPB (P < 0.01). In the PDTC group, plasma levels of IL-1beta and IL-8 significantly increased after CPB (P < 0.05, P < 0.01). Plasma levels of MDA and F-HB significantly increased (P < 0.01) and the E-ATP level and E-SOD activity significantly decreased after CPB (P < 0.01) in both two groups. The E-ATP level and E-SOD activity in the PDTC group at 30 and 60 minutes after AC and 30 and 60 minutes after DC were significantly higher than those in control group (P < 0.01). However, the levels of IL-1beta, IL-8, MDA, and F-HB at 30 and 60 minutes after AC and 30 and 60 minutes after DC were significantly lower in the PDTC group than those in control group (P < 0.01). CONCLUSION: PDTC can protect erythrocytes by alleviating lipid peroxidation and inflammatory response during CPB.

[Effect of pyrrolidine dithiocarbamate on antioxidation of canine myocardium during ichemia/reperfusion injury].

OBJECTIVE: To assess the alterations in myocardial energy metabolism and lipid peroxidation during canine cardiopulmonary bypass (CPB), and to investigate the interventional effects of pyrrolidine dithiocarbamate (PDTC) pretreatment. METHODS: Twelve adult healthy dogs undergoing CPB were randomized into control group (Group C, n=6) and PDTC group(Group P, n=6). In Group P, 30 mg/kg PDTC was administered intravenously before CPB and in Group C animals were given physiological saline instead of PDTC. The contents of adenosine triphosphate (ATP), superoxide dismutase (SOD), glutathione peroxidase (GSH-PX), malondialdehyde (MDA) and mitochondrial swelling degree (MSD) of myocardium were determined before CPB, 60 min after aortic cross-clamping (AC) and 60 min after declamping (DC). Hemodynamics was monitored before CPB, 30 min and 60 min after DC. RESULT: Contents of ATP, SOD and GSH-PX in Group P at 60 min after AC and 60 min after DC were higher than those in Group C (P<0.01). MDA and MSD in Group P at 60 min after AC and 60 min after DC were significantly lower than those in Group C (P<0.01). Hemodynamics of Group P was recovered at 30 min and 60 min after DC. CONCLUSION: Pretreatment with PDTC is effective in improving antioxidation capacity of myocardium and ameliorates myocardial energy metabolism.

[Effect of reperfusion leukocyte-depleted blood on canine myocardial energy metabolism balance during cardiopulmonary bypass].

OBJECTIVE: To investigate the impact of myocardial energy metabolism of canine reperfused with leukocyte-depleted blood during cardiopulmonary bypass (CPB). METHODS: Eighteen adult healthy dogs undergoing CPB were randomly divided into 3 groups: the control group (group C, n=6), whole blood (group W, n=6) and the experimental group (group L, n=6) with use of the leukocyte depletion filter (LDF) on the bypass circuit. The contents of adenine nucleotide, superoxide dismutase (SOD), glutathione peroxidase (GSH-PX), myeloperoxidase (MPO), malondialdehyde (MDA) and mitochondrial swelling of myocardia were determined respectively before cross-clamping, at 40 min and 60 min after aortic cross-clamping (AC), 30 min and 60 min after declamping (DC) during CPB. RESULTS: Reperfused with leukocyte-depleted blood by LDF connected with bypass circuit, the dog hearts of group L at 60 min after AC, 30 min and 60 min after DC were much better in the recovery of myocardium energy metabolism, higher in contents of myocardium SOD and GSH-PX than those in group C and W (P < 0.01). The myocardium MPO, MDA and mitochondrial swelling degree at 60 min after AC, 30 min and 60 min after DC were distinctly lower in group L than those in group C and W (P < 0.01). CONCLUSION: Myocardium has serious energy exhaustion and deteriorated metabolism during CPB. Myocardial mitochondrial structure and function can be protected and myocardial energy depletion can be reduced by infusion of leukocyte-depleted blood to the heart before DC, which can distinctly attenuate myocardial ischemia/reperfusion injury.

[The reperfusion injury model improvement and the tolerance time investigation of rabbit spinal cord ischemia under normothermia].

OBJECTIVE: This study is designed to improve the rabbit model of ischemic- reperfusion injury and determine the safe clamping duration relevant to the spinal cord tolerance to ischemia at normothermia. METHODS: 50 New Zealand white rabbits were assigned randomly to 5 groups (Group C20, C25, C30, C40 and C60, 10 rabbits in each group) according to different clamping durations, ranging from 20 min to 60 min. The rabbits were endotracheally intubated for ventilation, and their left ear arteries were catheterized for monitoring the mean artery pressure. The spinal cord ischemia was induced by infrarenal aorta occlusion. A catheter was inserted into the aorta distal clamped site for monitoring the distal artery pressure. The neurological functional status of animal was assessed with the Tarlov scale system (0 or 1 meaning the rabbit paraplegia), at the moment of revival, 6 h, 24 h, and 48 h after the reperfusion. After last scoring, the lumbar segments of spinal cord (L4-L6) were removed for pathological examination, and the normal motor neurons of anterior horn were counted. RESULTS: Forty-eight hours after the infusion, the severe neurological impairments were not detected in the rabbits whose aorta were only clamped for 20 min (Group C20). However, the rabbits in Group CSO became totally paraplegic, and the rabbits in Group C25 C30 or C40 developed the paraplegia at 30% , 80% or 90% respectively. The median number of normal motor neuron was 12. 5, 10 or 2 respectively in Group C20, C25 or C30, and 0 median number resulted in Group C40 and C60. CONCLUSION: The rabbit model of ischemic-reperfusion injury is successfully improved, of which the safe clamping duration without spinal cord injury is not more than 20 min at normothermia.

Perfusion of gastrodin in abdominal aorta for alleviating spinal cord ischemia reperfusion injury.

OBJECTIVE: To observe the effects of perfusion of the gastrodin in abdominal aorta for alleviating the spinal cord ischemia reperfusion injury (SCIRI). METHODS: A total of 36 New Zealand white rabbits were divided randomly into sham-operated group (group S), control group (group C) and gastrodin group (group G), 12 rabbits for each group. Aorta abdominalis infrarenalis blocking method was applied to establish the SCIRI model. The changes of motor evoked potentials (MEPs) before the ischemia and on 30 min, 60 min, 6 h, 12 h and 24 h of reperfusion of the gastrodin were respectively recorded, and the neurologic function score before the ischemia, on the 6 h, 12 h and 24 h of the reperfusion of the gastrodin were assessed. And the changes of the concentration of serum neuron specific enolase (NSE), interleukin (IL)-lß and IL-8 were measured before the ischemia, after 45 min of ischemia, and on 30 min, 60 min, 6 h, 12 h and 24 h of reperfusion of gastrodin. Then the levels of spinal cord nerve cells mitochondrial superoxide dismutase (SOD), reactive oxygen species (ROS), glutathione peroxidase (GSH-PX), malondialdehyde (MDA), total antioxidant capacity (T-AOC) and mitochondrial swelling degree (MSD) were tested and the histopathologic changes in spinal cord tissues were observed. RESULTS: The levels of the NSE, IL-lß, IL-8, ROS, MDA and MSD of group C were all significantly elevated after the ischemia (P < 0.01); the levels of the spinal nerve cell mitochondria SOD, GSH-PX and T-AOC were all significantly reduced (P < 0.01), MEPs and spinal cord tissue pathology were damaged significantly (P < 0.01). The rate of motor neuron abnormalities and the damages of spinal cord tissue pathology of group G were significantly milder than those of group C (P < 0.01); the levels of NSE, IL-lß, IL-8, ROS, MDA and MSD were significantly lower than those of group C (P < 0.01), but the levels of SOD, GSH-PX and T-AOC were all significantly higher than those of group C (P < 0.01), and the recovery of neurologic function score during the reperfusion of gastrodin was significantly faster than group C (P < 0.01). CONCLUSIONS: Perfusion of the gastrodin in abdominal aorta can alleviate the spinal cord ischemia reperfusion injury by promoting the mitochondrial antioxidant capacity and inhibiting the inflammatory reaction.

[Effects of pregnancy and blood components on solubility of fluoride volatile anesthesia].

OBJECTIVE: To determine the effect of pregnancy on blood/gas partition coefficient (B/G) of volatile anesthetics and to evaluate the relation between B/G and blood component concentration. METHODS: Blood samples were obtained from four groups of fasting women: 8 nonpregnancies, 8 first-trimester pregnancies, 12 mid-trimester pregnancies, 12 third-trimester pregnancies. B/G of desflurane, isoflurane and halothane in each subject was measured by double equilibration technique. Red blood cell (RBC), hemoglobin concentration (Hb), hematocrit (HCT) and the serum concentration of cholesterol (Chol), triglyceride (TG), albumen (Alb), globulin (Glob) were measured. RESULTS: 1. There was no significant difference in B/G of desfluraneand and in B/G of halothane among the four groups. There was significant difference in B/G of isoflurane; the lowest B/G was in the mid-trimester and the highest B/G was in the third trimester of pregnancy. The trend direction of halothane among four groups was similar to that of isoflurane, although no significant difference was observed therein. 2. RBC, Hb and HCT showed statistically significant difference among the four groups, which decreased to the lowest level in the mid-trimester and came up slightly in the third trimester. There was statistically significant difference in Alb, A/G, TG and Chol among the four groups. Alb and A/G were the lowest and TG, Chol were the highest in the third-trimester of pregnancy. 3. There was a correlation between the serum TG and the B/G of halothane. The B/G of isoflurane correlated directly with serum TG and Hb. The B/G of desflurane correlated directly with Chol. CONCLUSION: The above findings indicated that pregnancy brought on alterations in the blood components and serum components, thus inducing the difference in B/G between the flaoride volatile anesthetics. During pregnancy, the B/G of isoflurane altered significantly more than that of halothane did, whereas no significant alteration in the B/G of desflurane was noted.

[Expression of HSP70 induced by ketamine in the hippocampus of rat at different ages].

OBJECTIVE: This experiment was designed to explore the possible mechanism of the brain injury caused by ketamine. METHODS: Thirty-five adult SD rats randomly divided into a control group and 6 experiment groups were given intrapertioneal injections of normal saline, 20.0, 40.0, 60.0, 80.0, 100.0, 120.0 mg/kg of ketamine respectively. Another 35 SD rats at 0-10, 11-20, 21-30, 31-45, 46-60, 61-90, 91-120 days old were allocated to 7 corresponding age groups and were given intrapertioneal injection of ketamine 80.0 mg/kg. Immunocytochemistry was used to detect HSP70 expression in rat hippocampus, and MIAS-2000 photography analytic software was chosen to analyze HSP70 expression. RESULTS: Ketamine induced HSP70 expression in adult rat hippocampus. Below the dose of 80.0 mg/kg, ketamine induced higher level of HSP70 expression as the dose increased; however, above the dose of 80.0 mg/kg, ketamine induced lower level of HSP70 expression as the dose increased. Ketamine did not induce HSP70 expression in the rats under 20 days of age; it induced the same HSP70 expression in rats of 90 days and over; and analyses of the rats of 20-90 days revealed that the elder the rat is, the higher the HSP70 expression will be. CONCLUSION: Ketamine injures the neurons of rat hippocampus and induces the expression of HSP70, and the higher the dose is given, the more serious the injury is seen; and ketamine induces higher level of HSP70 expression in adult rats than in infant rats.

[Effect of clonidine on rat's behavior response and spinal nitric oxide in formalin test].

OBJECTIVE: To assess the effect of Clonidine on SD rat's behavior response and spinal nitric oxide in the formalin test. METHODS: The effects of Clonidine (Clo), L-arginine(L-Arg), and NG-nitro-L-arginine (L-NAME) on the flinching and licking time of rats in the formalin test were assessed using the model of formalin-induced hyperalgia. RESULTS: The flinching and licking time of group Clo was shorter (38.60 +/- 17.34) s/5 min than that of group Formalin(155.41 +/- 22.04) s/5 min. Pre-administration of L-Arg could potentiate the Clonidine-induced response; pre-administration of L-NAME could reduce the Clonidine-induced response. CONCLUSION: Spinal nitric oxide release might be one of the antinociception mechanisms of Clonidine in the formalin test.

[The effect of propofol on isolated human pregnant uterine muscles].

OBJECTIVE: To investigate the effects of propofol on spontaneous contractions of isolated human pregnant myometrial smooth muscles. METHODS: Twenty isolated human pregnant myometrial muscle strips with rhythmic spontaneous contraction were randomly divided into two groups: control group (n=10) and propofol group (n=10). In propofol group propofol was added cumulatively. The changes of uterine contraction were monitored. RESULTS: Propofol at concentration of 0. 5 microg/ml and 2 microg/ml had no effect on the spontaneous contraction of isolated human pregnant uterine muscles; propofol at concentration of 5 microg/ml and 10 microg/ml could significantly reduce the spontaneous contraction of isolated human pregnant uterine muscles; the higher the concentration was, the more would be the reduction. The effect could be blocked by oxytocin (140 +/- 50) microU/ml. CONCLUSION: Propofol could significantly reduce the spontaneous rhythmic contractions of isolated human pregnant myometrial smooth muscles in concentration-dependent manner. Oxytocin could antagonize the action.

[Effects of pyrrolidine dithiocarbamate pretreatment on canine myocardial energy metabolism during cardiopulmonary bypass].

OBJECTIVE: To develop a technology for production of recombinant SAG1 of Toxoplasma gondii(T.g) in batches. METHODS: Twelve healthy mongrel dogs undergoing CPB were randomly allocated into control group (group C, n=6) and PDTC pretreatment group (group P, n=6). In group P, the dogs received intravenous injection of PDTC at 30 mg/kg before CPB, while in group C, normal saline was given instead. The myocardial tissues were obtained before CPB, 60 min after aortic cross-clamping (AC) and 60 min after declamping (DC) for determining the myocardial contents of adenine nucleotides (ATP, ADP, AMP, TAN, EC) and malondialdehyde (MDA) and evaluating the total anti-oxidation capacity (T-AOC) and mitochondrial swelling degree (MSD). The heart rate (HR), mean arterial pressure (MAP) and cardiac output (CO) were monitored before CPB, 30 min and 60 min after DC. RESULTS: In both groups, the myocardial contents of ATP, TAN, EC and T-AOC decreased while MDA content and MSD increased after AC as compared to the values before CPB (P<0.01). In group C, ATP, TAN, EC and T-AOC decreased while MDA content and MSD increased after DC as compared to the values before CPB (P<0.01). At 60 min after DC, the dogs in group P showed no significant variation in the contents of ATP, TAN, EC, MDA, T-AOC or MSD (P>0.05). ATP, TAN, EC and T-AOC were significantly lowered while MDA and MSD increased at 60 min after AC and after DC in group P in comparison with the measurements in group C (P<0.01). HR, MAP and CO of group P recovered rapidly at 30 min and 60 min after DC as compared with those in group C (P<0.01). CONCLUSION: CPB can induce serious energy exhaustion and delay in the recovery of energy metabolism. PDTC pretreatment can substantially ameliorate myocardial energy depletion and protect the myocardial mitochondria to attenuate myocardial ischemia/reperfusion injury.