Relationship between sevoflurane-induced cognitive impairment and α1B and α1D adrenoceptors in cerebral cortex of rats / 中华麻醉学杂志

Objective To evaluate the relationship between sevoflurane-induced cognitive impairment and α1B adrenoceptors (ADRA1B) and ADRA1D in the cerebral cortex of rats.Methods Forty-eight SPF adult Sprague-Dawley rats (half male,half female),weighing 220-260 g,were divided into control group (C group,n =24) and sevoflurane group (S group,n =24) using a random number table method.Group C and group S inhaled air and 3％ sevoflurane,respectively,for 5 h.Eight rats in each group were sacrificed immediately after anesthesia,and the cerebral cortex was removed.Eight rats in each group were selected on days 1 and 7 after anesthesia and underwent Barnes maze test.The rats were then sacrificed,and the cerebral cortex was removed.The expression of ADRA1B and ADRA1D protein and mRNA in cerebral cortex tissues was detected by Western blot and fluorescent quantitative real-time polymerase chain reaction,respectively.Results Compared with group C,the number of entering incorrect holes was significantly increased at 1 and 7 days after anesthesia,the latency and total distance to enter the target hole were prolonged,and the expression of ADRA1B and ADRA1D protein and mRNA in cerebral cortex was down-regulated immediately after anesthesia and at 1 and 7 days after anesthesia in group S (P＜0.05).Conclusion The mechanism underlying sevoflurane-induced cognitive impairment may be related to the down-regulated expression of ADRA1B and ADRA1D in cerebral cortex of rats.

Role of α2A adrenergic receptors in dexmedetomidine-induced inhibition of TLR4/NF-κB signaling pathway activation during hypoxia-reoxygenation-caused injury to alveolar type Ⅱ epithelial cells / 中华麻醉学杂志

Objective To evaluate the role of α2A adrenergic receptor (α2AAR) in dexmedetomidine-induced inhibition of TLR4/NF-κB signaling pathway activation during hypoxia-reoxygenation (H/R)caused injury to alveolar type Ⅱ epithelial cells.Methods Type Ⅱ] alveolar epithelial cells of rats RLE6TN cells cultured in vitro were divided into 4 groups (n =6 each) using a random number table method:control group (group C),H/R injury group (group H/R),dexmedetomidine group (group D) and α2A AR small interfering RNA (siRNA) plus dexmedetomidine group (group α2AAR-siRNA+D).H/R was produced by exposing cells to 1％ O2-5％ CO2-94％ N2 for 24 h followed by 4-h reoxygenation.Cells were incubated for 1 h with dexmedetomidine at the final concentration of 1 nmol/L,and then H/R model was established in group D.In group α2AAR-siRNA+D,cells were transfected with 50 nmol/L α2AAR-siRNA,48 h later dexmedetomidine at the final concentration of 1 nmol/L was added,cells were incubated for 1 h,and then H/R model was established.The cell viability was measured using CCK-8 method,cell apoptosis rate was determined by flow cytometry,and the expression of TLR4 and NF-κB was detected by immunofluorescence.Results Compared with group C,the cell viability was significantly decreased,the apoptosis rate was increased,and the expression of TLR4 and NF-κB was up-regulated in group H/R (P＜0.05),and no significant change was found in the parameters mentioned above in group D (P＞0.05).Compared with group H/R,the cell viability was significantly increased,the apoptosis rate was decreased,and the expression of TLR4 and NF-κB was down-regulated in group D (P＜0.05),and no significant change was found in the parameters mentioned above in group α2AAR-siRNA+D (P＞0.05).Compared with group D,the cell viability was significantly decreased,the apoptosis rate was increased,and the expression of TLR4 and NF-κB was up-regulated in group α2AAR-siRNA+D (P＜0.05).Conclusion The mechanism by which dexmedetomidine inhibits TLR4/NF-κB signaling pathway activation may be related to activating α2AAR during H/R-caused injury to alveolar type Ⅱ epithelial cells.

Relationship between sevoflurane-induced cognitive decline and α1A norepinephrine receptor in cerebral cortex of rats / 中华麻醉学杂志

Objective To evaluate the relationship between sevoflurane-induced cognitive decline and α1A norepinephrine receptor (ADRA1A) in the cerebral cortex of rats.Methods Forty-eight cleangrade healthy adult Sprague-Dawley rats (24 male,24 female),weighing 220-260 g,aged 3-4 months old,were divided into 2 groups (n =24 each) using a random number table method:control group (group C) and sevoflurane group (S group).Group S inhaled 3％ sevoflurane for 5 h.Rats underwent the Barnes maze test on days 1 and 7 after anesthesia.Rats were sacrificed immediately after anesthesia and on days 1 and 7 after anesthesia,and the cerebral cortex was removed for determination of the expression of ADRA1A protein and mRNA (by Western blot or fluorescent quantitative real-time polymerase chain reaction).Results Compared with group C,the number of entering incorrect holes was significantly increased,and the latency of entering the target hole and the distance were prolonged,and the expression of ADRA1A protein and mRNA in cerebral cortex was down-regulated at each time point in group S (P＜0.05).Conclusion The mechanism of sevoflurane-induced cognitive decline is related to down-regulated expression of ADRA1A in the cerebral cortex of rats.

Effect of dexmedetomidine on visceral pain in rats: the role of a2 adrenergic receptors in locus coeruleus / 中华麻醉学杂志

Objective To evaluate the effect of dexmedetomidine on visceral pain in rats and the role of α2 adrenergic receptors in locus coeruleus (LC).Methods Thirty-two healthy adult male SpragueDawley rats,weighing 250-300 g,were divided into 4 groups (n=8 each) using a random number table method:control group (group C),visceral pain group (group VP),dexmedetomidine group (group DEX) and α2-adrenergic receptor antagonist atipamezole group (group AP).α2-adrenergic receptor antagonist atipamezole 522 μg/kg was intramuscularly injected in group AP,and the equal volume of normal saline was given instead in C,VP and DEX groups.At 10 min after intramuscular injection,dexmedetomidine 10 μg/kg was injected via the tail vein in DEX and AP groups,and the equal volume of normal saline was given instead in C and VP groups.VP,DEX and AP groups received intraperitoneal injection of 0.9％ acetic acid 10 ml/kg to make the visceral pain model at 15 min after injection via the tail vein.The cumulative visceral pain score was recorded within 60 min after acetic acid injection.The number of c-fos positive cells in LC was detected by immunohistochemistry,and the content of norepinephrine (NA) in the spinal cord were detected by enzyme-linked immunosorbent assay at 2 h after acetic acid injection.Results Compared with group C,the cumulative visceral pain scores,the number of c-fos positive cells in LC and content of NA in the spinal cord were significantly increased in VP,DEX and AP groups (P＜0.05).Compared with group VP,the cumulative visceral pain scores,the number of c-fos positive cells in LC and content of NA in the spinal cord were significantly decreased in DEX and AP groups (P＜0.05).Compared with group DEX,the cumulative visceral pain scores,the number of c-fos positive cells in LC and content of NA in the spinal cord were significantly increased in group AP (P＜0.05).Conclusion Dexmedetomidine can alleviate visceral pain in rats,and the mechanism is partially related to activating α2 adrenergic receptors in LC.

Effect of dexmedetomidine on long-term anxiety state after sevoflurane anesthesia in neonatal rats:the role of different central subtypes of α2 receptors / 中华麻醉学杂志

Objective To evaluate the effect of dexmedetomidine on the long-term anxiety state after sevoflurane anesthesia in neonatal rats and the role of different central subtypes of α2 receptors.Methods A total of 216 clean-grade healthy male Sprague-Dawley rats,aged 4-6 days,weighing 8-15 g,were divided into 6 groups (n =36 each) using a random number table method:control group (group C),sevoflurane group (group S),dexmedetomidine + sevoflurane group (group D+S),dexmedetomidine + α2 receptor antagonist atipamezole + sevoflurane group (group D+A+S),dexmedetomidine + α2A receptor antagonist BRL44408 + sevoflurane group (group D+B+S),and dexmedetomidine + α2C receptor antagonist JP1302 + sevoflurane group (group D+J+S).Anesthesia was induced by inhaling 6％ sevoflurane for 3 min and maintained by inhaling 2.1％ sevoflurane for 6 h.At 30 min before anesthesia induction,dexmedetomidine 25 μg/kg was intraperitoneally injected in group D+S,dexmedetomidine 25 μg/kg and atipamezole 250 μg/kg were intraperitoneally injected in group D + A + S,dexmedetomidine and α2A receptor antagonist BRL44408 1.5 mg/kg were intraperitoneally injected in group D+B+S,and dexmedetomidine 25 μg/kg and α2C receptor antagonist JP1302 3 mg/kgwere intraperitoneally injected in group D+J+S.Twelve rats in each group were randomly selected and sacrificed after the end of anesthesia,blood samples were collected for blood gas analysis,and the serum corticosterone concentration was measured by enzyme-linked immunosorbent assay.The elevated plus maze was performed when the left rats in each group were 60 days old,and 12 rats were selected when the they were 80 days old to perform the restraint stress test.Results Compared with group C,the percentage of time of staying at the open arm was significantly decreased,the total motion distance was shortened,and the serum corticosterone concentration was increased after the end of anesthesia and during the restraint stress test in S,D+A+S and D+B+S groups (P＜0.05),and no significant change was found in the parameters mentioned above in D+S and D+J+S groups (P＞0.05).Compared with group S,the percentage of time of staying at the open arm was significantly increased,the total motion distance was prolonged,and the serum corticosterone concentration was decreased after the end of anesthesia and during the restraint stress test in group D+S and group D+J+S (P＜0.05),and no significant change was found in the parameters mentioned above in group D+A+S and group D+B+S (P ＞0.05).Compared with group D+S,the percentage of time of staying at the open arm was significantly decreased,the total motion distance was shortened,and the serum corticosterone concentration was increased after the end of anesthesia and during the restraint stress test in D+A+S and D+B+S groups (P＜0.05),and no significant change was found in the parameters mentioned above in group D+J +S (P＞ 0.05).Conclusion Dexmedetomidine can reduce the long-term anxiety state after sevoflurane anesthesia in neonatal rats,and the mechanism may be related to activating central α2A receptors and improving hypothalamic-pituitary-adrenocortical axis hyperfunction.

Intoxicación por amitraz. Un reporte de caso / Amitrazpoisoning: case report

Resumen El amitraz es un compuesto insecticida utilizado a nivel mundial para el control de plagas, en especial en áreas rurales agrícolas y ganaderas. La intoxicación por amitraz es infrecuente en Colombia. Se presenta el caso de una paciente de 18 años de edad, quien ingresa al servicio de urgencias 3 horas después de la ingesta de Triatox® (amitraz) en cantidad desconocida. La mujer llega con depresión del estado de conciencia, dificultad respiratoria, hipotensión, bradicardia, miosis y acidosis metabólica compensada con alcalosis respiratoria, por lo que se le suministra tratamiento inicial con medidas de soporte vital en el servicio de urgencias, con posterior necesidad de traslado y soporte en la unidad de cuidados intensivos, siendo dada de alta de la misma unidad 24 horas después del ingreso. El caso pone en consideración la similitud clínica entre la intoxicación por amitraz y la debida a otros compuestos tóxicos más frecuentes como carbamatos, organofosforados y opioides, los cuales requieren un manejo distinto.

Abstract Amitraz is an insecticide compound used worldwide for controlling pests, especially in agricultural and livestock areas. However, amitraz poisoning in Colombia is rare. This article reports the case of an 18-year-old female patient who was admitted in the emergency service 3 hours after the intake of an unknown amount of Triatox® (amitraz). The patient presented with a depressed level of consciousness, respiratory distress, hypotension, bradycardia, myosis and metabolic acidosis compensated with respiratory alkalosis. Initial treatment was provided using life support measures in the emergency ward, and subsequent transfer and support in the intensive care unit. She was discharged 24 hours after admission. This case considers the clinical similarity between amitraz poisoning and poisoning caused by other more frequent toxic compounds such as carbamates, organophosphates and opioids, which require different management.

Effect of median nerve electrical stimulation on expression of α1-adrenergic receptor in prefrontal cortex of coma rats induced by traumatic brain injury / 重庆医学

Objective To investigate the wake-promoting action of median nerve electrical stimulation(MNES) in coma rats induced by traumatic brain injury(TBI) and its influence on the expression of α1-adrenergic receptor(α1 R) in the prefrontal contex (PFC).Methods Seventy-two healthy Sprague Dawley(SD) rats were randomly divided into the control group,sham-stimulated group(TBI),stimulated group (TBI+ MNES) and antagonist group(TBI+ OX1R antagonist +MNES).The control group had no any treatment.The TBI coma rat models were prepared in the other 3 groups.The sham stimulated group had no treatment.The antagonist group was injected with orexin receptor-l(OX1R) antagonist SB334867 into lateral ventricle,and both the antagonist group and stimulated group received MNES treatment.Then the behavior changes of rats in each group were observed and the α1 R expression level in PFC was detected by using the immunohistochemistry technique.Results Thirteen rats in the stimulated group and 8 rats in the antagonist group revived,while only 4 rats in the TBI group.The α1R levels from low to high were the blank control group,sham-stimulated group,antagonist group and stimulated group,showing the increasing trend,and the difference was statistically significant(P＜0.05).Conclusion MNES can improve the rat consciousness level after TBI coma,and its mechanism may be related with up-regulating the α1 R expression level in PFC area,moreover Orexin-A participates in this regulation process.

Role of α2 adrenergic receptors in dexmedetomidine-induced inhibition of lipid peroxidation during lung ischemia-reperfusion injury in rats / 中华麻醉学杂志

Objective To evaluate the role of α2 adrenergic receptors in dexmedetomidine-induced inhibition of lipid peroxidation during lung ischemia-reperfusion (I/R) injury in rats.Methods Thirty-two isolated rat lungs in which the model of isolated lung perfusion was successfully established,were divided into 4 groups (n=8 each) using a random number table:control group (C group),I/R group,dexmedetomidine group (D group) and dexmedetomidine plus yohimbine group (DY group).The isolated lungs were subjected to 60 min of ischemia and apnea followed by 75 min of reperfusion and ventilation to establish the model of isolated lung I/R injury.From the beginning of reperfusion,2.3 ng/ml dexmedetomidine was added to the perfusion fluid in D group,and 2.3 ng/ml dexmedetomidine and 0.4 μg/ml yohimbine (an α2 adrenergic receptor blocker) were added to the perfusion fluid in DY group.Lung specimens were obtained immediately after the end of reperfusion for determination of the wet/dry weight ratio (W/D ratio),superoxide dismutase (SOD) activity (by using modified pyrogallol autoxidation method) and malondialdehyde (MDA) content (by thiobarbituric acid method) and for examination of the pathological changes (using haematoxylin and eosin staining).Results Compared with C group,the W/D ratio and MDA content were significantly increased,and the SOD activity was decreased in I/R,D and DY groups (P＜0.05).Compared with I/R group,the W/D ratio and MDA content were significantly decreased,and the SOD activity was increased in D group (P＜0.05).Compared with DY group,the W/D ratio and MDA content were significantly decreased,and the SOD activity was increased in group D (P＜0.05).The pathological changes of lung tissues were significantly attenuated in D group as compared with I/R and DY groups.Conclusion The mechanism by which dexmedetomidine inhibits lipid peroxidation is related to activating α2 adrenergic receptors during lung I/R injury in rats.

Influence of Panax ginseng on Alpha-Adrenergic Receptor of Benign Prostatic Hyperplasia / 대한배뇨장애요실금학회지

PURPOSE: Benign prostatic hyperplasia (BPH) is the most common prostate problem in older men. The present study aimed to investigate the inhibitory effect of Panax ginseng C.A. Meyer (P. ginseng) on a rat model of testosterone-induced BPH. METHODS: The rats were divided into 3 groups (each group, n=10): control, testosterone-induced BPH (20 mg/kg, subcutaneous injection), and P. ginseng (200 mg/kg, orally) groups. After 4 weeks, all animals were sacrificed to examine the blood biochemical profiles, prostate volume, weight, histopathological changes, alpha-1D adrenergic receptor (Adra1d) mRNA expression, and epidermal growth factor receptor (EGFR) and B-cell CLL/lymphoma 2 (BCL2) protein expression. RESULTS: The group treated with P. ginseng showed significantly lesser prostate size and weight than the testosterone-induced BPH group. In addition, P. ginseng decreased the mRNA expression of Adra1d as well as the expression of EGFR and BCL2 in prostate tissue. CONCLUSIONS: These results suggest that P. ginseng may inhibit the alpha-1-adrenergic receptor to suppress the development of BPH.

Influence of propofol on spinal cord transected rat vascular reactivity / 解放军医学杂志

Objective To observe the reactivity of spinal cord transection (SCT) rat abdominal aorta to ?-AR agonists and the infuence of propofol on vascular reactivity, so as to explore the mechanism of autunomic dysreflxia. Methods The rats were divided into sham-operated group and SCT group. 4 weeks after transection of the fourth thoracic spinal cord, the rats were killed, then abdominal aorta rings were adopted to assay their sensitivity to noradrenaline, phenylephrine, clonidine and propofol in isolated organ perfusion system. Results Compared with the rats in sham-operated group, the abdominal aorta reactivity of SCT rats to noradrenaline and clonidine was significantly higher (P

An experimental study on ADRA2A gene polymorphism of the servicemen of Han ethnic in PLA / 解放军医学杂志

Objective To explore the features of polymorphism in ADRA2A gene phenotypes and their relationship to oxygen endurance in the Han servicemen in PLA.Methods One hundred and eight healthy recruits of Han ethnic were subjected to a 5000-meter race program for 18 weeks,and then the tests were done after a 5000-meter race.The ADRA2A allelic variant and genotype were analyzed by polymerase chain reaction and sequencing,and the features of polymorphism in three sites,G6412C,T6623A and C6645C,were determined with biochemical technique.The relationship between the results after the 5000-meter race,and the polymorphism of ADRA2A was then analyzed.Results The genotype distribution at all the three locations was consistent with the Hardy-Weinberg equilibrium.The genotype frequency in T6623A of A/G(50%)was higher than that of G/G(26%)and A/A(24%).The allele frequency of A(51%)was higher than that of G(49%).The time for completing 5000-meter running was significantly longer in recruits carrying A/G(20.95?0.82min)than those carrying A/A(18.97?0.65min,P0.05).There was no significant association between the oxygen endurance capacity and the polymorphism of G6412C and C6645C.Conclusion The T6623A of ADRA2A was the ideal gene marker for predicting endurance capacity,but G6412C and C6645C polymorphism is not ideal gene marker for oxygen endurance.

Analysis of the autoantibodies against ?_1 and ?_1-adrenergic receptor in patients of hypertension with renal failure / 中国医师杂志

Objective To explore the role of the autoantibodies against ?_1 and ?_1-adrenergic receptor(?_1-receptor)in the development of hypertension with renal failure.Methods The epitopes of the second extracellular loop of ?_1-receptor(197-222) and ?_1-receptor(192-218) were synthesized and used respectively to screen sera autoantibodies in patients with hypertension and renal failure(n=61),hypertension without renal failure(n=60) and healthy blood donors(n=40,control) by ELISA.Results The positive rates of the autoantibodies against ?_1-receptor(62.3%)and ?_1 receptor(50.8%) in patients with hypertension with renal failure were higher than those of patients with hypertension without renal failure(13.3% and10.0%)(P

Effects of antioxidant on the gene expression of ?_1-adrenergic receptors during endotoxic shock in rats / 中华麻醉学杂志

Objective To investigate the effects of antioxidant on the gene expression of ?1-adrenergic receptors (AR) during endotoxic shock. Methods Forty male SD rats weighing 200-250 g were anesthetized with intraperitoneal (i.p.) pentobarbital. The animals kept spontaneous breathing. Femoral artery and vein were cannulated for BP monitoring and drug administration. The animals were randomly divided into 5 groups ( n = 8 each) : (1) control group; (2) LPS group received IPS 15 mg?kg-1 i.v. ; (3) LPS + propofol group received at 1h after LPS a bolus of propofol 10mg?kg-1 i.v. followed by continuous infusion of propofol at 10 mg?kg-1?h-1; (4) LPS + uric acid (UA) group received uric acid 200 mg i.p. 1 h after LPS and (5) LPS + melatonin (MLT) group received MLT 10 mg?kg-1 i.p. 1h after LPS. The animals were killed at 6 h after LPS. Total RNA was extracted from the heart, aorta, vein, lung, liver and kidney. ?1A-,?1B-,?1D- AR mRNA and ?-actin mRNA were measured using reverse transcription polymerase chain reaction (RT-PCR) .Results The expression of ?1A-AR and ?1B-AR mRNA in all the organs and the ?1D-AR mRNA expression in aorta, liver, lung and kidney were strongly down-regulated in LPS group. In group 3 (LPS + propofol) the expression of ?1A-AR mRNA in the lung and kidney, the ?1B-AR mRNA expression in all of the organs and ?1D-AR mRNA expression in aorta, liver, lung and kidney were significantly increased as compared with LPS group. There was no significant difference in ?1-AR mRNA expression between LPS group and LPS + MLT group. The expression of ?1A-AR mRNA in kidney, the ?1B-AR mRNA expression in all of the organs except the lung and the ?1D-AR mRNA expression in aorta, liver, lung and kidney were significantly higher in LPS + UA group than in LPS group. Conclusion Circulatory failure induced by endotoxic shock is related to the down-regulation of ?1-AR gene expression. The therapeutic effects of antioxidant on the endotoxic shock is partly due to up-regulation of ?1-AR gene expression.

Effect of nitrotyrosine on ?-adrenergic receptor-mediated vascular reactivity in rats / 中华麻醉学杂志

Objective3-nitro-L-tyrosine(3-NT)has been shown to be the marker of ONOO-productionin the tissue during septic shock.We aimed to investigate the effects of 3-NT on adrenergic receptor-mediatedvascular reactivity and the possible mechanism.Methods The experiment consisted of two parts.In part Ⅰ twenty-four male SD rats weighing 200-300g were anesthetized with intraperitoneal pentobarbital 40 mg?kg~(-1).Spontaneousbreathing was maintained.The animals were randomly divided into 2 groups:A control group received normalsaline i.v.(n=12)and B 3-NT group received 3-NT 2.5 ?mol?kg~(-1) i.v.(n=12).30 min and 90 min after 3-NT/N.S.administration the animals received i.v.phenylephrine(PE)0.5,1.0,1.5,2.0,2.5 ?g?kg~(-1)(subgroup Ⅰ)or vasopressin 1.3,2.6,3.9,5.2 ?g?kg~(-1)(subgroup Ⅱ)at 15 min intervals.The percentageincrease in MAP was recorded.In part Ⅱ six male SD rats were anesthetized and killed.The thoracic aorta wasimmediately removed and aortic rings of 3 cm in length were prepared and suspended in Krebs-Hensleit solutionmaintained at 37℃ and aerated with 95% O_2 and 5% CO_2 and prestretched with a load of 2g.Before theexperiment the response of the aortic tings to cumulative addition of PE(1?10~(-9)-3?10~(-5)mol)was prelimarilymeasured.Alter five washes the aortic rings were randomly divided into 2 groups:control group(KH solution)and 3-NT group(KH solution containing 3-NT 250 ?mol?L~(-1)).After 60 min incubation,response to PE wasmeasured in both groups and concentration-response curve was obtained and Emax and CE_50 were calculated.Results PE increased MAP in a dose-dependent manner.PE 2.5 ?g?kg~(-1) increased MAP by 20% of thebaseline value.30 and 90 min after 3-NT 2.5 ?mol?kg~(-1) the hypertensive response of the animal to PE wassignificantly inhibited but 3-NT did not affect the increase in MAP induced by vasopressin.In the isolated SD rataortic ring experiment there was no significant difference in the concentration-response curve and Emax and EC50values of PE between the 3-NT and control group.Conclusion 3-NT selectively inhibits ?-adrenoceptor mediatedhemodynamic response through mechanisms other than competitively antagonizing ?-adrenoceptor.

Changes in peripheral ?_1-adrenergic receptor sensitivity after high spinal cord injury in rats / 中华麻醉学杂志

Objective To evaluate the changes in peripheral?1-adrenergic receptor sensitivity in a rat model of chronic high spinal cord injury (SCI)Methods Thirty male 18-week-old Wistar rats weighing 290-310g were randomly divided into 2 groups: SCI group (n=24) and control group (C n=6) . The animals were anesthetized with intraperitoneal 2 % pentobartital 50 mg?kg-1 and subjected to spinal cord injury (SCI) at T4 according to modified Allen's method. Successful high SCI was confirmed by bilateral hindlimb flaccid paralysis. Three weeks after SCI the animals were further divided into 4 subgroups (n=6) receiving 4 different doses of phenylephrine 1, 2, 3 and 4 ?g?kg-1 i.v. Femoral artery was connulated for BP (SBP and DBP) and HR monitoring. HR and SBP and DBP were recorded before and after i.v. phenylephrine injection. In control group phenylephrine (PE) 1,2,3 and 4 ?g?kg-1 were injected i.v. successively at an 1h interval. % changes in HR, SBP and DBP were calculated: % change = (post-injection value- baseline value) / baseline value. Results The animals lost weight and HR was significantly slower and SBP and DBP were significantly lower 3 weeks after SCI as compared with control group. In both group C and SCI, HR was significantly decreased and SBP and DBP were significantly increased after i.v. PE injection as compared to the baseline value before PE. The % changes in HR, SBP and DBP were significantly greater in group SCI than in group C. Conclusion In a rat model of chronic high SCI, peripheral?1-adrenergic receptor sensitivity is significantly increased 3 weeks after high SCI.

Effect of nitrotyrosine on the expression of ?1D-adrenoceptor mRNA in vascular smooth muscle of rat / 中华麻醉学杂志

Objective To investigate the effect of nitrotyrosine (3-NT) on the expression of ?1D adrenoceptor (?1D-AR) mRNA in cultured vascular smooth muscle cells (SMCS) .Methods SMCS were obtained from the tunica media of thoracic aorta of 1 month old SD rats and cultured in DMEM medium. The experiment consisted of two parts. In part Ⅰ SMCS were incubated with 0,1, 10, 100 or 200 ?mol?L-1 3-NT for 24 h and in part Ⅱ SMCS were incubated with 100 ?mol?L-1 3-NT forO,12, 24, 48 or 72 h. The total RNA was isolated by using Trizol reagent. The expression of ?1D-AR mRNA was determined by RT-PCR and agarose gel electrophoresis. Results In part I incubation with 1 and 10 ?mol?L- 3-NT for 24 h had no significant effect on the expression of ?1D-AR mRNA while incubation with 100 or 200 ?mol?L-1 3-NT for 24 h decreased the expression of ?1D-AR mRNA compared with 0?mol?L-1 3-NT (P

Changes of pulmonary ?_1-and ?-adrenergic receptors during endotoxin-induced acute lung injury in rats / 中国病理生理杂志

Changes of pulmonary ?_1-and ?-adrenergic receptor (?_1-AR and ?-AR)during endotoxin-induced acute lung injury in rates were oberved to find out the rela-tionship between them and the mechanism of change. Results showed that there was amarked decrease of B_max of both ?_1-AR and ?-AR by 35% and 43% respectively, dur-ing acute lung injury. The down regulation of ?-AR might be one of causes of acutelung injury while that of ?_1-AR seems to be a protective response. Active oxygen playedan important role in endotoxin-induced down regulation of AR in the rat lungs. The increa-sed level of norepinephrine and epinephrine was not the main factor that initiate the downregulation of AR. Intravenous injection of tumor necrosis factor (5?10~6U/kg ) exerts noiafluence on the changes of pulmonary AR in rats.

The changes of ?_1-adrenoceptor in ischeamic rabbit myocardium / 中国病理生理杂志

We used (H~3)-prazosin on rabbits to determine the changes of ?_1-adrenoceptor number (Bmax) and affinity (k_D) before and after ischemia, Within 15min of ischemia, we demonstrated that Bmax increased to twfold in ischeamic regions. The increase persisted for 30 min of ischemla and then began to fall at 45 min of ischemia. At the same time, in the nonischemic regions Bmax did not change. The results also showed that ischemia did not alter K_D markedly in both nonischeamic and ischeamic regions.

Studies on mechanism of myocardial injury induced by adrenergic alpha receptors and catecholamines / 中国病理生理杂志

Seventy eight New Zealand rabbits were divided into 8 groups. NE, M, and control group were given norepinephrine (1mg/kg), methoxamine or saline, respectively. The other 5 groups were given regitine (R group), propranolol (P group), metaprolol (MP group), yohimbine (Y group) and prazosine (PR group) respectively before NE infusion.Myocardial injury was estimated with a semi-quantitative histological scoring system, and 11 intermediate metabolites in glycolysis and ATP, ADP, AMP, CP in myocardium were measured. Results showed that myocardial injury was observed in NE group (P

Relationship between renal hypertension and cardiac ?_1-adrenoceptor autoantibodies in rats / 中国病理生理杂志

AIM: To examine the autoantibody against ? 1-adrenoceptor and its biologic activities during the development of renal hypertension. METHODS: Renal hypertension of rat was achieved by clipped renal artery, the titre of autoantibody to ? 1-adrenoceptor was detected using ELISA immunoassay. Furthermore, the biological offects of these autoantibodies on cultured cardiomyocytes were also examined. RESULTS: After two weeks of clipping renal arteries, both the frequency of occurrence and the titre of autoantibodies to cardiac ? 1-adrenergic receptor were significantly increased as compared with the control of pre-treatment. The increased autoantibodies lasted for several weeks and then automatically decreased gradually to the pre-clipping level at 12 weeks. The biological effects of these autoantibodies displayed an "agonistic-like" activities on the beating frequency of cultured neonatal cardiomyocytes. CONCLUSION: Autoantibodies against ? 1-adrenoceptor may play a role in the elevation of peripheral vascular resistance and in the development of cardiac hypertrophy in rats with renal hypertension.