A novel track guidance ultrasound facilitates radial arterial cannulation: A prospective randomized controlled trial.

BACKGROUND: Ultrasound guidance for radial arterial cannulation is currently considered a best practice approach despite its clear advantages over the blind and palpation technique, the success rate is related to several factors, including clinician's experience and technical ability. The study aimed to explore the use of a novel track guidance ultrasound that may increase the success rate of radial arterial cannulation. METHODS: A randomized controlled trial was conducted, in which 80 adults scheduled for elective surgery requiring radial arterial cannulation were recruited and randomly assigned to either the experimental group, which utilized novel track ultrasound guidance (group T, n = 40), or the control group, which utilized traditional ultrasound guidance (group U, n = 40). The novel track guidance ultrasound comprises a positioning track and a guided track. The radial artery could be positioned at the center of the positional track on the ultrasound image, and the direction and angle of needle are fixed and toward the center of the positioning track. The primary endpoint of the study was the first-pass cannulation success rate, while the secondary endpoints included the failure rate of cannulation, the number of radial artery punctures, the time of cannulation, and the incidence of hematoma. RESULTS: The success rate of cannulation at the first attempt in group T (35 of 40 (87.5%)) was significantly higher than that in group U (23 of 40 (57.5%); p = 0.003). Although seven patients in Group U (7 of 40 (17.5%)) experienced failed cannulation compared to one in Group T (1 of 40 (2.5%)), the difference in failure rate between the two groups did not reach statistical significance (p = 0.06). CONCLUSIONS: The implementation of novel track ultrasound guidance has demonstrated a notable improvement in the success rates at the first attempt while reducing the frequency of punctures and cannulation times.

Roles for c-Abl in postoperative neurodegeneration.

The nonreceptor tyrosine kinase c-Abl is inactive under normal conditions. Upon activation, c-Abl regulates signaling pathways related to cytoskeletal reorganization. It plays a vital role in modulating cell protrusion, cell migration, morphogenesis, adhesion, endocytosis and phagocytosis. A large number of studies have also found that abnormally activated c-Abl plays an important role in a variety of pathologies, including various inflammatory diseases and neurodegenerative diseases. c-Abl also plays a crucial role in neurodevelopment and neurodegenerative diseases, mainly through mechanisms such as neuroinflammation, oxidative stress (OS), and Tau protein phosphorylation. Inhibiting expression or activity of this kinase has certain neuroprotective and anti-inflammatory effects and can also improve cognition and behavior. Blockers of this kinase may have good preventive and treatment effects on neurodegenerative diseases. Cognitive dysfunction after anesthesia is also closely related to the abovementioned mechanisms. We infer that alterations in the expression and activity of c-Abl may underlie postoperative cognitive dysfunction (POCD). This article summarizes the current understanding and research progress on the mechanisms by which c-Abl may be related to postoperative neurodegeneration.

Sevoflurane induces microRNA-18a to delay rat neurodevelopment via suppression of the RUNX1/Wnt/ß-catenin axis.

Sevoflurane anesthesia is reported to repress neurogenesis of neural stem cells (NSCs), thereby affecting the brain development, but the underlying mechanism of sevoflurane on the proliferation of NSCs remains unclear. Thus, this study aims to discern the relationship between sevoflurane and NSC proliferation. Bioinformatics tools were employed to predict the expression of microRNA-18a (miR-18a) in 9-day-old neonatal rat hippocampal tissues after sevoflurane treatment and the downstream genes of miR-18a, followed by a series of assays to explore the relationship among miR-18a, runt related transcription factor 1 (RUNX1), and ß-catenin in the hippocampal tissues. NSCs were isolated from the hippocampal tissues and subjected to gain-/loss-of-function assays to investigate the interactions among miR-18a, RUNX1, and ß-catenin in NSCs and their roles in NSC development. Bioinformatics analysis and experimental results confirmed high expression of miR-18a in rat hippocampal tissues and NSCs after sevoflurane treatment. Next, we found that miR-18a downregulated RUNX1 expression, while RUNX1 promoted NSC proliferation by activating the Wnt/ß-catenin signaling pathway. The behavioral experiments also showed that sevoflurane caused nerve injury in rats, whilst RUNX1 overexpression protected rat neurodevelopment. Our findings uncovered that sevoflurane attenuated NSC proliferation via the miR-18a-meidated RUNX1/Wnt/ß-catenin pathway, thereby impairing rat neurodevelopment.

Preoperative malnutrition as an independent risk factor for the postoperative mortality in elderly Chinese individuals undergoing hip surgery: a single-center observational study.

Objective: Malnutrition is prevalent in elderly with hip fracture and higher than in community-dwelling older adults. Scarce studies have examined the association between preoperative malnutrition and postoperative mortality in elderly Chinese individuals with hip fracture. This study was designed to explore the effect of preoperative malnutrition on the postoperative long-term mortality in elderly Chinese individuals undergoing hip surgery. Methods: As a single-center observational study, this study included 263 consecutive patients above 70 years old with hip fracture and elective surgery. Preoperative nutritional status was evaluated by prognostic nutritional index (PNI). Patients were divided into one group with malnutrition (26 patients with PNI ⩽ 38) and the other group without malnutrition (169 patients with PNI > 38), respectively. Results: The overall malnutrition rate was 13.3% (26 patients). The postoperative long-term mortality rates of patients with and without malnutrition had statistically significant difference [10 patients (38.5%) and 32 patients (18.9%), p < 0.05]. Cox regression analysis showed that malnutrition (hazard ratio: 0.269, 95% confidence interval: 0.085-0.859, p < 0.05) and partial pressure of carbon dioxide (hazard ratio: 0.873, 95% confidence interval: 0.790-0.964, p < 0.05) were independent risk factors for the postoperative long-term mortality. Conclusion: This study demonstrated that preoperative malnutrition was an independent risk factor for the postoperative long-term mortality and resulted in a more than 2.5-fold increase of the postoperative long-term mortality in elderly Chinese individuals undergoing hip surgery.

Delayed Recovery After Deep Brain Stimulation Surgery for Parkinson's Disease Under General Anesthesia-Cases Report.

Objective: Parkinson's disease (PD) is a neurodegenerative syndrome, and deep-brain stimulation (DBS) is an effective therapy for carefully screened patients with PD. However, delayed recovery after anesthesia, which occurs after taking prolonged general anesthesia for such patients, has been reported less frequently in literature. This report explores the possible causes of postoperative awakening delay in patients undergoing DBS surgery due to general anesthesia and provides a reference for anesthesia management of similar operations in the future. Case Presentation: Three patients with PD elective underwent DBS surgery. The first patients demonstrated walking disability, gait deficits, unstable posture, limb stiffness, and imbalance. The second demonstrated left limb static tremor, stiffness, and bradykinesia. The third demonstrated bradykinesia, rigidity, walking deficits, and decreased facial expression. These included two males and one female with a mean patient age of 60.7 ± 6.7year, weight of 63.7 ± 11 kg, the height of 163.3 ± 7.6 cm, and preoperative American Society of Anesthesiology rating of 2.3 ± 0.6. The preoperative Glasgow Coma Scale mean score was 15. All patients completed the operation under general anesthesia (the mean anesthesia time was 5.3 ± 1.1 h). The mean operation time was 252 ± 60 min. The mean bleeding volume was 50 ml, and the urine volume was 867 ± 569 ml. However, all the patients showed unconsciousness after 95 ± 22 min after stopping the anesthetic, and the respiratory function was in good condition, but they could not cooperate with anesthesiologists and had no response to the anesthesiologist's instructions. The mean hospital stay was 17 ± 7 days. All patients were discharged uneventfully. The average number of days patients followed up postoperatively was 171 ± 28.5 days. Motor and speech were improved significantly postoperatively in three patients compared with preoperatively. Taking anti-Parkinson medication was markedly reduced. There were no complications during postoperative follow-up. Conclusions: To prevent delayed recovery occurring after DBS surgery in Parkinson's disease, it is recommended to take scalp nerve block + general anesthesia to complete the procedure while avoiding general anesthesia.

Comparison of propofol-nalbuphine and propofol-fentanyl sedation for patients undergoing endoscopic retrograde cholangiopancreatography: a double-blind, randomized controlled trial.

BACKGROUND: Endoscopic retrograde cholangiopancreatography (ERCP) has been increasingly used to treat patients with biliary/pancreatic duct obstruction or stricture outside the operating room. Effective and safe sedation techniques are needed because of painful stimuli and the long duration of the ERCP procedure.Nalbuphine has been shown to cause less respiratory depression during sedation than similar cases without nalbuphine. This study compared the effects of propofol-nalbuphine (PN) and propofol-fentanyl (PF) sedation in patients undergoing ERCP. METHODS: Four hundred patients scheduled for ERCP procedures were divided into two groups: the PF group (receiving PF sedation,n = 199) and the PN group (receiving PN sedation,n = 201). Vital signs, adverse events during surgery, patient movement scores, pain scores, and adverse events one day post-ERCP were recorded. RESULTS: Stable haemodynamics were observed in both groups.Compared to the PF group, the PN group showed significantly decreased respiratory depression (P < 0.0001) and surgical interruptions (P = 0.048).Nalbuphine decreased patient movement by reducing pain from ERCP. CONCLUSION: Nalbuphine, instead of fentanyl, precipitated less respiratory depression while permitting adequate/equivalent sedation for ERCP and therefore provides more efficient and safer sedation. Trial registration ChiCTR, ChiCTR1800016018, Registered 7 May 2018, http://www.chictr.org.cn/showproj.aspx?proj=27085.

The TRPA1 Channel Mediates Mechanical Allodynia and Thermal Hyperalgesia in a Rat Bone Cancer Pain Model.

Background: Bone cancer pain (BCP) significantly affects patient quality of life, results in great bodily and emotional pain, and creates difficulties in follow-up treatment and normal life. Transient receptor potential ankyrin 1 (TRPA1) is an essential transduction ion channel related to neuropathic and inflammatory pain. However, the role of TRPA1 in BCP remains poorly understood. This study aimed to explore the relationship between TRPA1 and BCP. Methods: A BCP model was induced by Walker256 cells to the left tibia. The sham group was induced by normal saline to the left tibia. Thereafter, pain behaviors and TRPA1 expression between the BCP group and the sham group were observed on the 14th day of modeling. The TRPA1 antagonist A967079 (10 mg/kg) was injected via tail vein. TRPA1 antisense oligodeoxynucleotide (AS-ODN, 5 nmol/10 µl) and missense oligodeoxynucleotide (MS-ODN, 5 nmol/10 µl) were intrathecally delivered via a mini-osmotic pump for 5 consecutive days to assess the effect of TRPA1 on BCP. Behavioral tests were assessed preoperatively and postoperatively. Real-time quantitative PCR and western blot analyses were used to measure TRPA1 levels among the different groups. Results: The BCP model was successfully established via X-ray and pathological sections at 14 days. Compared to the sham group, the BCP group was more sensitive to mechanical stimuli, cool stimuli and hot stimuli. Intravenously injected A967079 can relieve paw mechanical withdrawal threshold and paw withdrawal thermal latency in rats with BCP. Moreover, AS-ODN can relieve paw mechanical withdrawal threshold and paw withdrawal thermal latency in rats with BCP. Additionally, relative mRNA and protein expression of TRPA1 in the BCP group were much higher than those in the sham group (14.55 ± 1.97 vs. 1 ± 0.04, P < 0.01). Compared to the BCP group, the relative mRNA and protein expression of TRPA1 in the BCP+AS-ODN group was reduced (14.55 ± 1.97 vs. 2.59 ± 0.34, P < 0.01). Conclusions: The TRPA1 channel mediates mechanical allodynia and thermal hyperalgesia in a rat BCP model.

Corrigendum to "Dexmedetomidine Postconditioning Alleviates Hypoxia/Reoxygenation Injury in Senescent Myocardial Cells by Regulating lncRNA H19 and m6A Modification".

[This corrects the article DOI: 10.1155/2020/9250512.].

Propofol inhibits the expression of Abelson nonreceptor tyrosine kinase without affecting learning or memory function in neonatal rats.

OBJECTIVE: Propofol is one of the most commonly used intravenous drugs to induce and maintain general anesthesia. In vivo and in vitro studies have shown that propofol can affect neuronal growth, leading to apoptosis and impairing cognitive function. The Abelson nonreceptor tyrosine kinase (c-Abl) is associated with both neuritic plaques and neurofibrillary tangles in the brains of patients with Alzheimer's disease and other neurodegenerative diseases. This study aimed to explore the effect of propofol on apoptosis and neurocognition through its regulation of c-Abl expression in vivo and in vitro. MATERIALS AND METHODS: In this study, primary hippocampal neurons were cultured and exposed to propofol at different concentrations. Protein expression was measured by Western blotting and coimmunoprecipitation. The c-Abl transcription level was verified by fluorescence quantitative PCR. Reactive oxygen species (ROS) levels were detected by flow cytometry. In addition, an animal experiment was conducted to assess neuronal apoptosis by immunofluorescence staining for caspase-3 and to evaluate behavioral changes by the Morris water maze (MWM) test. RESULTS: The in vitro experiment showed that propofol significantly decreased c-Abl expression and ROS levels. In addition, propofol has no cytotoxic effect and does not affect cell activity. Moreover, in the animal experiment, intraperitoneal injection of 50 mg/kg propofol for 5 days obviously decreased the expression of c-Abl in the neonatal rat brain (p < .05) but did not significantly increase the number of caspase-3-positive cells. Propofol treatment did not significantly reduce the number of platform crossings (p > .05) or prolong the escape latency of neonatal rats (p > .05) in the MWM test. CONCLUSIONS: The present data suggest that reduced expression of this nonreceptor tyrosine kinase through consecutive daily administration of propofol did not impair learning or memory function in neonatal rats.

Preoperative anemia and total hospitalization time are the independent factors of preoperative deep venous thromboembolism in Chinese elderly undergoing hip surgery.

BACKGROUND: This study was designed to explore the prevalence and risk factors of preoperative deep venous thromboembolism (DVT) in Chinese elderly with hip fracture. METHODS: From January 1, 2012, to December 31, 2018, 273 elderly patients over 70 years old with elective hip surgery were collected from the electronic medical records. Collected data included demographic characteristics, comorbidities, ASA classification, types of previous operations, types of anesthesia, operation time, fracture to operation time, preoperative hemoglobin level, anemia, blood-gas analysis, cardiac function, whether transfusion, preoperative hospitalization, postoperative hospitalization, electrocardiograph, lower limb venous ultrasonography and total hospitalization time. RESULTS: In these 273 patients, 15(5.6%) had ultrasonography evidence of DVT in affected limbs before surgery. Three of all patients received an temporary inferior vena cave filter placement preoperatively. Fracture to surgery time, preoperative hemoglobin level, anemia, preoperative hospitalization, pulmonary disease and total hospitalization time were statistically different between DVT group and non-DVT group (P < 0.05 for all). Moreover, preoperative anemia (OR: 0.144, 95%CI: 0.026-0.799, P = 0.027) and total hospitalization time (OR: 1.135; 95%CI: 1.023-1.259, P = 0.017) were the two independent risk factors for preoperative DVT. CONCLUSION: Preoperative anemia and total hospitalization time were independent risk factors for venous DVT in Chinese elderly with hip fracture.

The lncRNA, H19 Mediates the Protective Effect of Hypoxia Postconditioning Against Hypoxia-Reoxygenation Injury to Senescent Cardiomyocytes by Targeting microRNA-29b-3p.

BACKGROUND: Ischemic postconditioning (I/Post) is an endogenous protection mechanism that reduces injury induced by ischemia-reperfusion (I/R). It remains controversial whether I/Post protects against I/R injury to the aging heart. The long non-coding RNA, H19 protects H9c2 cells against hypoxia-induced injury. This study aimed to elucidate the role of H19 in the hypoxic postconditioning (H/Post) of aged cardiomyocytes. METHODS: Senescence induced by D-galactose in primary cardiomyocytes from neonatal Sprague-Dawley rats was measured by senescence-associated ß-galactosidase staining. Hypoxic injury was evaluated by cell viability and apoptosis assays. H19 expression before and after hypoxia-reoxygenation (H/R) and H/Post was evaluated by real-time polymerase chain reactions. miR-29b-3p-binding sites in H19 and the cellular inhibitor of apoptosis protein 1 (cIAP1) were predicted by bioinformatics analysis, and interaction was verified by luciferase assay. The effects of altered H19, miR-29b-3p, and cIAP1 expression on the viability and apoptosis of senescent cardiomyocytes following H/Post were determined. RESULTS: H/Post prevented H/R injury in normal but not senescent cardiomyocytes. H19 expression was remarkably down-regulated after H/Post in senescent compared with normal cardiomyocytes. Small interfering RNA-mediated knockdown of H19 in senescent cardiomyocytes increased H/Post-induced injury. miR-29b-3p was regulated by H19 and led to a greater injury. miR-29b-3p directly targeted the 3'-untranslated region of cIAP1 and suppressed its expression. Furthermore, knockdown of cIAP1 damaged senescent cardiomyocytes following H/Post. CONCLUSIONS: These findings suggest that H19 mediated the antiapoptotic effect of H/Post against H/R-induced injury to aged cardiomyocytes by inhibiting miR-29b-3p expression.

Analgesic effects of TLR4/NF-κB signaling pathway inhibition on chronic neuropathic pain in rats following chronic constriction injury of the sciatic nerve.

OBJECTIVE: Chronic neuropathic pain (CNP) is attributed to a lesion or disease of the somatosensory system, may be derived from the peripheral and central system. Recent study revealed that spinal cord stimulation attenuated CNP by inhibiting TLR4/NF-κB signaling pathway. The present study focuses on the potential analgesic effects of TLR4/NF-κB signaling pathway on CNP in a rat model of chronic constriction injury (CCI). METHODS: We successfully established the rat model of CCI by Bennett method, and then inhibited the TLR4/NF-κB signaling pathway in rat models. Next, we measured the mechanical withdrawal threshold (MWT) and thermal withdrawal latency (TWL) 0D, 2D, 6D, 8D and 12D after operation respectively. MTS510 100 mg/kg, an inhibitor of TLR4, was intrathecal injected into rats after 6D, 8D and 12D after operation. The experiment lasted for 12 days, and then the rats were sacrificed to collect the spinal cord tissues. Protein and mRNA expression levels of toll-like receptor 4 (TLR4), nuclear factor-kappaB (NF-κB), glial cell line-derived neurotrophic factor (GDNF), glial fibrillary acidic protein (GFAP) and nerve growth factor (NGF) were detected by western blot analysis and RT-qPCR, respectively. Immunohistochemistry was performed to detect GDNF, GFAP and NGF expression. RESULTS: With the prolongation of MTS510 treatment time, MWT and TWL were increased and finally, the MWT and TWL were close to the baseline level. The levels of TLR4, NF-κB, GDNF, and GFAP as well as NGF increased in rats treated with CCI + Immunoglobulin G1 (IgG1) or CCI + MTS510, suggesting the model establishment was successful. Besides, with the prolongation of MTS510 treatment time, the protein level and mRNA expression of NF-kB, GDNF, GFAP and NGF decreased in rats treated with CCI + IgG1 or CCI + MTS510. Moreover, the GDNF, GFAP and NGF expression in spinal cord tissue in rats treated with CCI + IgG1 or CCI + MTS510 increased obviously, while the GDNF, GFAP and NGF expression decreased in spinal cord tissue in rats treated with CCI + IgG1 or CCI + MTS510 after MTS510 treatment. CONCLUSIONS: Collectively, this study defines the role of TLR4 and NF-κB, and inhibition of TLR4/NF-κB signaling pathway might contribute to the alleviation of CNP and improvement of MWT and TWL in a rat model of CCI. Additionally, the results obtained from the study provided a promising basis that could aid as an experimental basis for the potential treatment of TLR4/NF-κB signaling pathway.

Propofol postconditioning protects H9c2 cells from hypoxia/reoxygenation injury by inducing autophagy via the SAPK/JNK pathway.

Propofol postconditioning (P­PostC) offers cardioprotection in mice, and the upregulation of autophagy protects cardiac cells against ischemia/reperfusion injury. The present study aimed to examine the effects of P­PostC on the induction of autophagy and its potential roles in hypoxia/reoxygenation (H/R) injury. Rat heart­derived H9c2 cells were exposed to H/R, comprising 6 h of hypoxia followed by 4 h of reoxygenation, as well as postconditioning with various concentrations of propofol at the onset of reperfusion. Lactate dehydrogenase (LDH) activity and the rate of cell apoptosis were measured to evaluate the degree of cardiomyocyte H/R injury. The induction of autophagy in myocytes subjected to H/R injury and P­PostC was detected by western blotting and immunofluorescence. Furthermore, the activation of c­Jun N­terminal kinase (JNK) in cells treated with P­PostC with or without co­treatment with SP600125, an inhibitor of JNK, was also determined by western blotting. P­PostC reduced the activity of LDH in the culture medium and the percentage of apoptotic cells compared with cells in the untreated H/R group. In addition, P­PostC induced autophagy and promoted survival signaling in H9c2 cardiac myoblast cells. The inhibition of autophagy by 3­methyladenine treatment diminished the cardioprotective effects of P­PostC. These results indicated that propofol postconditioning promoted cell survival through the induction of autophagy in H9c2 cardiac cells, and that the stress­activated protein kinase/JNK survival pathway may be partly involved in P­PostC­induced autophagy.

n-Dodecyl ß-D-maltoside specifically competes with general anesthetics for anesthetic binding sites.

We recently demonstrated that the anionic detergent sodium dodecyl sulfate (SDS) specifically interacts with the anesthetic binding site in horse spleen apoferritin, a soluble protein which models anesthetic binding sites in receptors. This raises the possibility of other detergents similarly interacting with and occluding such sites from anesthetics, thereby preventing the proper identification of novel anesthetic binding sites. n-Dodecyl ß-D-maltoside (DDM) is a non-ionic detergent commonly used during protein-anesthetic studies because of its mild and non-denaturing properties. In this study, we demonstrate that SDS and DDM occupy anesthetic binding sites in the model proteins human serum albumin (HSA) and horse spleen apoferritin and thereby inhibit the binding of the general anesthetics propofol and isoflurane. DDM specifically interacts with HSA (Kd = 40 µM) with a lower affinity than SDS (Kd = 2 µM). DDM exerts all these effects while not perturbing the native structures of either model protein. Computational calculations corroborated the experimental results by demonstrating that the binding sites for DDM and both anesthetics on the model proteins overlapped. Collectively, our results indicate that DDM and SDS specifically interact with anesthetic binding sites and may thus prevent the identification of novel anesthetic sites. Special precaution should be taken when undertaking and interpreting results from protein-anesthetic investigations utilizing detergents like SDS and DDM.

Synthesis and fungicidal activities of novel indene-substituted oxime ether strobilurins.

Nineteen novel indene-substituted oxime ether strobilurins, which used an indene group to stabilize the ( E)-styryl group in SYP-Z071 (an unsaturated oxime strobilurin fungicide under development by the Shenyang Research Institute of Chemical Industry), were designed and synthesized. The biological assay results showed that all compounds possessed good or excellent fungicidal activities. It was found that most of the compounds showed higher fungicidal activities against Pyricularia oryzae, Phytophthora infestans, Erysiphe graminis, and Colletotrichum lagenarium than SYP-Z071 at the tested concentration. The biological assay results also indicated that most of the compounds exhibited higher in vivo fungicidal activities against cucumber Pseudoperonospora cubensis and C. lagenarium than the commercial fungicides trifloxystrobin and kresoxim-methyl at a concentration of 6.25 mg/L. Furthermore, it was found that alpha-(methoxyimino)- N-methylphenylacetamide oxime ethers 6m- s exhibited a broad spectrum and remarkably higher activities against all tested fungi. Especially, the 6-methylindene-substituted compound 6p was identified as the most promising candidate for further study.

[Studies of potassium channel in pulmonary artery smooth muscle cells derived from renal hypertensive rat].

AIM: To investigate the differences of membrane capacitance, membrane current, current density and I-V curves between smooth muscle cells isolated from RHR and NTR pulmonary arteries. METHODS: Under antiseptic conditions, the left renal artery was exposed through a retroperitoneal flank incision and carefully dissected free of the left renal vein. A silver clip with an internal diameter of 0.2-0.3 mm was placed around the left renal artery, resulting in partial occlusion of renal perfusion. SBP was observed by tail blood pressure. Whole cell recordings were made from smooth muscle cells freshly isolated from pulmonary arteries derived from RHR or NTR. RESULTS: The average membrane capacitance was (3.43 +/- 1.16) pF, decreased by 31.1%; membrane current was (0.54 +/- 0.26) nA, decreased by 68.2%; current density was (180 +/- 90) pA/pF, decreased by 48.6%; membrane potential was (-26.96 +/- 7.23) mV, decreased by 2.5%, all compared with that of NTR respectively. Iptakalim hydrochloride at the concentration of 0.1-100 micromol/L can significantly increased NTR potassium currents. Iptakalim hydrochloride 1-100 micromol/L can significantly increased RHR potassium currents. CONCLUSION: Membrane capacitance, membrane current, membrane potential were decreased, I-V curves were shift downward, compared with that of NTR. Iptakalim hydrochloride might significantly increase NTR and RHR potassium currents.

[Expression and significance of enkephalin and dopamine in experimental rat cerebral concussion tissue].

AIM: To explore the expression and significance of enkephalin and dopamine in rat cerebral concussion tissue. METHODS: 80 Wistar male rats were used to make animal model of cerebral concussion, which were sacrificed on 1,3,7,14 and 30 days after postconcussion and the brain tissues were taken out. The expression patterns of enkephalin and dopamine were studied in the course of cerebral concussion by immunohistochemical staining. RESULTS: The clinical manifestation with typical cerebral concussion character was seen in rat group with 100 g body weight. The mainly pathologic changes were cerebral vascular constriction and dilatation, congestion and edema of cerebral tissue, and neuronal degeneration and necrosis. Expression of enkephalin was increased on day 1 after injury and the enkephalin positive area was in the plasma of endothelial cells in cerebral cortex, hippocamp and cerebellum. The expression of enkephalin reached the peak on day 7 after injury, and the positive area was also seen in the plasma of neurons in cerebral cortex, hippocamp and cerebellum. From 14 days after injury, the expression of enkephalin decreased gradually, but until 30 days after injury it was still higher than that of controls. Expression of dopamine increased in 7 days after injury and the positive area was seen in the plasma of endothelial cells and in the vessel wall in cerebral cortex, hippocamp, thalamus and cerebellum, and had no notable changes at other time points. CONCLUSION: The mainly pathologic changes after cerebral concussion were blood circulatory disorder and denaturation and necrosis of parenchymal cells. Enkephalin and dopamine may participate in the pathophysiological course of cerebral injury after cerebral concussion, and play an important role in the blood vessel injury, regulation of blood-brain barrier and the denaturation and necrosis of nerve cells.