ObjectiveTo investigate the localization G protein couple receptor 30 (GPR30) and its mRNA in submaxillary gland, and to supply theoretic evidence for further studying functional significance of the GPR30 in submaxillary gland of rats. Methods Four male SD rats were sacrificed by cervical dislocation after the intraperitoneal anesthesia, and excised the submaxillary glands. The distribution of GPR30 and its mRNA were studied through immunohistochemistry and in situ hybridization in the experiment. After isolation of the total RNA from the submaxillary gland, RT-PCR was conducted to obtain GPR30 cDNA by using the specific primers. The products of PCR were analyzed by sequencing with Sanger's method. Results The serous acinus epithelial cells and granular convoluted epithelial cells in submaxillary gland of rats showed GPR30 immunoreactivity, which were located in cytoplasm with negative nuclei. GPR30 mRNA hybridized signals were also detected in cytoplasm in the above cells. The products of PCR is identical to that of the GPR30 sequence of rats. Conclusion The serous acinus and granular convoluted epithelial cells not only express GPR30 but also may be a target organ by rapid estrogen signaling pathway in submaxillary gland of rats. This may be involved in the functional regulation of submaxillary gland.

ObjectiveTo compare the effects of dexmedetomidine and propofol for stereotactic brain surgery in patients with intractable psychosis.MethodsThirty male patients with intractable psychosis,aged 22-33 yr,weighing 60-90 kg,scheduled for stereotactic surgery,were randomized to receive either propofol (group P,n =15) or dexmedetomidine (group D,n =15).Anesthesia was induced with iv injection of midazolam 0.05-0.10 mg/kg and fentany 1-2 μg/kg in the two groups,and in addition,dexmedetomidine was infused at 0.3-0.7μg· kg- 1 · h- 1 after a loading dose of 1 μg/kg (duration of infusion ＞ 10 min) and propofol 1-2 mg/kg was injected intravenously before endotracheal intubation in group D and propofol 2-3 mg/kg was injected intravenously and then propofol was infused at a rate of 3-4 mg· kg- 1 · h- 1 in group P.Orotracheal intubation was performed under the guidance of direct laryngoscope.The patients kept spontaneous breathing.The adverse events such as body movement,bucking,apnea,adverse cardiac events and hypoxemia were recorded during location.ResultsThe incidence of body movement,bucking,apnea,tachycardia,hypotension and hypoxemia was significandy lower,while the incidence of bradycardia was significantly higher in group D than in group P ( P ＜ 0.01 ).There was no significant difference in the incidence of hypertension between the two groups (P ＞ 0.05).ConclusionDexmedetomidine provides better anesthesia,exerts less effect on the respiratory and circulatory functions and is safer than propofol for stereotactic surgery in patients with intractable psychosis.

Objective To investigate the effect of recombinant human erythropoietin(rh‐EPO ) on acute cerebral injury and expression of GLT‐1 and GLAST in rat .Methods Sixty SD rats were randomly divided into three groups by weight :control group (n=18) ,acute cerebral injury group(n=22) and rh‐EPO conditioning group(n=20) .Acute cerebral injury models were made by modified Feeney′s method .rh‐EPO was injected in abdominal cavity 15 min after acute cerebral injury in rh‐EPO conditioning group .Rats′brain were removed 48 h after experiments .Rat GLT‐1 and GLAST mRNA expression were determined by RT‐PCR , GLT‐1 and GLAST protein expression were determined by Western blot .Results GLT‐1/GLAST mRNA and protein expression decreased significantly after acute cerebral injury(all P<0 .01) ,but increased significantly in rh‐EPO preconditioning group com‐pared with acute cerebral injury group(all P<0 .01) .Conclusion rh‐EPO preconditioning may protect against acute cerebral injury by up regulating the expression of GLT‐1/GLAST .

Objective To study the distribution and sequence analysis of gonadotropin releasing hormone (GnRH) gene in cultured gastric parietal cells of rats. Methods The distribution of GnRH molecule and GnRH mRNA were observed out through immunohistochemical ABC methods and in situ hybridization methods in cultured gastric parietal cells of rats. After isolation of the total RNA from the parietal cells, RT PCR was conducted to obtain GnRH cDNA. Then, the products of PCR was purified, digested by the restriction enzyme of Hind Ⅲ and EcoR Ⅰ, and DNA fragments interests were cloned into pUC19 vector. The products of PCR were analyzed by sequenceing with Sanger's method after identified by PCR and digestion of restriction enzyme. Results Gastric parietal cells showed GnRH immunoreactivity, positive material was located in cytoplasm with negative nuclei. GnRH mRNA hybridized signals were also detected in cytoplasm with negative nuclei. The specific amplified band of GnRH mRNA was detected through agarose gel electrophoresis and gene sequence is identical to the GnRH which has been reported in rat hypothalamus.Conclusion Our data suggest that GnRH could be produced by gastric parietal cells of rats and may modulate physiological function of gastric parietal cells of rats.\;[

Objective To investigate the effect of isoflurane preconditioning on Toll-like receptor 4 (TLR4)-myeloid differentiation factor 88 (MyD88) signaling pathway in ischemic penumbra following focal cerebral ischemia-reperfusion (I/R) in rats.Methods Fifty-four healthy male SD rats,aged 3 months,weighing 250-280 g,were randomly divided into 3 groups (n =18 each):sham operation group (group S),I/R group and isoflurane preconditioning group (group IP).Focal cerebral I/R was induced by middle cerebral artery occlusion.In groups I/R and IP,a nylon thread with rounded tip was inserted into the right internal jugular vein and threaded cranially until resistance was met.The middle cerebral artery was occluded for 2 h,followed by 24 h reperfusion.In group IP,the animals inhaled 2.0％ isoflurane for 2 h,and middle cerebral artery occlusion was performed at 24 h after the end of preconditioning.Neurological deficit was scored at 24 h of reperfusion and then the rats were sacrificed.Five rats in each group were chosen and the brains removed for measurement of the cerebral infarct volume.The right cerebral ischemic penumbra was removed for detection of the expression of HSP60,TLR4,MyD88 protein and mRNA by Western blot analysis and real time-PCR.Apoptosis was detected in the ischemic penumbra in the left 3 rats in each group using TUNEL.Apoptosis index (AI) was calculated.Results Neurological deficit scores and AI were significantly increased,the cerebral infarct volume was significantly enlarged,and the expression of HSP60,TLR4,MyD88 protein and mRNA was up-regulated in groups I/R and IP as compared with group S ( P ＜ 0.05).Isoflurane preconditioning significantly reduced the cerebral infarct volume and decreased neurological deficit scores and AI,and down-regulated the expression of HSP60,TLR4,MyD88 protein and mRNA (P ＜ 0.05).Conclusion The mechanisn by which isoflurane preconditioning protects ischenic penumbra following focal cerebral I/R may be related to inhibition of TLR4-MyD88 signaling pathway.

Objective To evaluate the effect of isoflurane preconditioning on inflammatory responses during spinal cord injury (SCI ) in rats .Methods Sixty adult male Sprague-Dawley rats ,weighing 250-300 g , were randomly divided into 3 groups ( n= 20 each ) using a random number table :sham operation group (S group) , SCI group , and isoflurane preconditioning group (I group ) . The animals were anesthetized with intraperitoneal pentobarbital sodium 40 mg/kg .SCI was produced by a weight-drop contusion at the T10 level .The rats inhaled 2% isoflurane for 2 h ,and the model was established at 24 h after the end of isoflurane inhalation in I group . Neurological function was assessed and scored by using the the Basso , Beattie , Bresnahan (BBB ) Locomotor Rating Scale on 7 days after SCI .Five rats in each group were then chosen and spinal cord specimens were obtained and cut into sections which were stained with haematoxylin and eosin for determination of the viable neuron count .Fifteen rats in each group were sacrificed and the spinal cord was removed for detection of nuclear factor kappaB (NF-κB ) and interleukin-1β (IL-1β) expression (by Western blot ) .Results Compared with S group ,BBB score and the number of viable neurons were significantly decreased ,and the expression of NF-κB and IL-1βprotein was up-regulated in SCI group ( P<0.05) .Compared with SCI group ,BBB score and the number of viable neurons were significantly increased ,and the expression of NF-κB and IL-1βprotein was down-regulated in group I ( P<0.05 ) .Conclusion The mechanism by which isoflurane preconditioning protects the spinal cord is related to inhibition of inflammatory responses in rats .

Objective To investigate the effect of isoflurane preconditioning on the expression of 5-lipoxy-genase (5-LOX) during focal cerebral ischemia-reperfusion (I/R) in rats.Methods Thirty-nine male adult Sprague-Dawley rats weighing 250-300 g were randomly divided into 3 groups (n =13 each):sham operation group (group S); focal cerebral I/R group (group I/R); isoflurane preconditioning group (group Ⅰ).Focal cerebral I/R was produced by mid-cerebral artery occlusion in anesthetized rats.The rats inhaled 2 h of 2％ isoflurane and focal cerebral I/R was produced 24 h later in group I.The neurological deficits were scored at 24 h of reperfusion.The animals were then sacrificed.The brains were immediately removed for determination of the infarct size.The expression of 5-LOX,myeloid differentiation factor88 (MyD88) and nuclear factor kappa B (NF-κB) protein and mRNA was detected using Western blot and RT-PCR respectively.Results Compared with group S,the neurological deficit score was significantly increased,the infarct size was enlarged in groups I/R and I,the expression of 5-LOX,MyD88 and NF-κB protein and mRNA was up-regulated in group I/R,and the expression of 5-LOX mRNA and MyD88 protein and mRNA was up-regulated in group I (P ＜ 0.05).Compared with group I/R,the neurological deficit score was significantly lower,the infarct size was smaller,and the expression of 5-LOX,MyD88 and NF-κB protein and mRNA was lower in group I (P ＜ 0.05).Conclusion Isoflurane preconditioning can reduce focal cerebral I/R injury by down-regulating the expression of 5-LOX and inhibiting MyD88/NF-κB signaling pathway in rats.

Objectiye To investgate the effects of isoflurane preconditioning on expression of Toll-like receptor 4 (TLR4) and myeloid differentiation factor 88 (MyD88) during focal cerebral ischemia-reperfusion (IR) in rats. Methods Thirty male SD rats weighing 250-300 g were randomly divided into 3 groups ( n = 10 each):sham operation group (group S);focal cerebral IR group and isoflurane preconditioning group (group IP). The animals were anesthetized with intraperitoneal pentobarbital 40 mg/kg. In group IR and IP a nylon thread with rounded tip was inserted into right internal jugular vein and threaded cranially until resistance was met. Mid-cerebral artery was occluded (MCAO) for 2 h followed by 24 h reperfusion. In group IP the animals inhaled 2% isoflurane98 % O2 for 1 h once a day for 5 consecutive days at 24 h before MCAO. Neurologic function was assessed and scored and cerebral infarct volume was measured at 24 h of reperfusion. The animals were sacrificed at 24, 48 and 72 h of reperfusion respectively. The right ischemic frontal lobes were removed for determination of TLR4, MyD88and NF-κB expression by Western blot analysis. Results MCAO significantly worsened neurologic function. The neurologic function deficit scores were significantly increased and the TLR4, MyD88 and NF-κB expression were significantly up-regulated in group IR as compared with group S (P ＜ 0.05). Isoflurane preconditioning significantly decreased cerebral infarct volumes and neurologic function deficit scores and down-regulated the expression of TLR4, MyD88 and NF-κB in group IP as compared with group IR ( P ＜ 0.05). Conclusion Isoflurane preconditioning can reduce inflammatory response and focal cerebral IR injury by down-regulating the expression of TLR4and Myd88.

0.05),the escape latency was longer(P

Objective To evaluate the lung protection of remote limb ischemic preconditioning during one-lung ventilation (OLV) in the patients undergoing esophageal cancer resection.Methods Seventyone patients of both sexes,aged 30-64 yr,with body mass index of 15-28 kg/m2,of American Society of Anesthesiologists physical status Ⅰ or Ⅱ,scheduled for elective esophageal cancer resection,were randomly divided into control group (group C,n =34) and remote limb ischemic preconditioning group (group RLIP,n =37) using a random number table.Patients in group RLIP received three cycles of 5-min ischemia/5-min reperfusion induced by a blood pressure cuff placed on one upper arm before OLV.Before OLV (T0),at 1 and 2 h of OLV (T1,2),at 20 min after re-expansion of the collapsed lung (T3),and at 2 h after operation (T4),blood samples were drawn from the radial artery for blood gas analysis,oxygenation index (PaO2/FiO2) and alveolar-arterial oxygen gradient (A-aDO2) were calculated.At T0,T2,T3 and T4,blood samples were collected from the radial artery for determination of plasma tumor necrosis factor-alpha (TNF-α),interleukin-6 (IL-6),and IL-10 concentrations.Results Compared with group C,PaO2/FiO2 was significantly increased,and A-aDO2was decreased at T1,2,the plasma TNF-α concentrations were decreased at T2-4 (P＜0.05),and no significant change was found in the plasma IL-6 and IL-10 concentrations and rate of abnormal pulmonary function at T1-4 in group RLIP (P＞O.05).Conclusion Although remote limb ischemic preconditioning can produce lung protection during OLV in the patients undergoing esophageal cancer resection,it provides no clinical significance.