Comparison of hyperalgesia induced by capsaicin injection and controlled heat injury: effect on temporal summation

The relationship between induction of central sensitization and facilitation of temporal summation to repetitive stimulation is still unclear. The aim of this study was to investigate temporal summation before and after the induction of secondary hyperalgesia by two different experimental methods: capsaicin injection and controlled heat injury. The effect of each injury model was assessed on a separate day with an interval of at least 5 days. Twelve healthy volunteers participated. Each experiment was performed using electrical, radiant heat, mechanical impact, and punctuate stimuli consecutively. The pain threshold (PT) to a single stimulus and the summation threshold to five repetitive stimuli for electrical (2 Hz) and radiant heat (0.83 Hz) were assessed within the secondary hyperalgesic area. The degree of temporal summation for stimulus intensities of 0.8, 1.0, and 1.2 times the baseline pain thresholds were evaluated by the increase in visual analogue scale (VAS) scores from the first to the fifth stimulus of the train. Further, the degrees of temporal summation were assessed for mechanical impact and punctuate stimuli within the primary and secondary hyperalgesic areas. The contra-lateral forearm served as control (no injury). The pain threshold and the summation threshold to electrical and heat stimuli decreased significantly within the secondary hyperalgesic area after the injury induced by both heat injury or capsaicin injection. However, there was no temporal summation for heat and electrical stimuli in either model. In contrast, for the mechanical impact and punctuate mechanical stimuli the degree of temporal summation was significantly facilitated in the secondary hyperalgesic areas compared with the baseline and the control arm in both models. In the primary hyperalgesic area, the degree of temporal summation was facilitated to mechanical impact and punctuate stimuli but only following the capsaicin injection. In conclusion, the temporal summation mechanism for mechanical stimuli was facilitated in the secondary hyperalgesic area.     

Modulation of oral heat and cold pain by irritant chemicals

Common food irritants elicit oral heat or cool sensations via actions at thermosensitive transient receptor potential (TRP) channels. We used a half-tongue, 2-alternative forced-choice procedure coupled with bilateral pain intensity ratings to investigate irritant effects on heat and cold pain. The method was validated in a bilateral thermal difference detection task. Capsaicin, mustard oil, and cinnamaldehyde enhanced lingual heat pain elicited by a 49 degrees C stimulus. Mustard oil and cinnamaldehyde weakly enhanced lingual cold pain (9.5 degrees C), whereas capsaicin had no effect. Menthol significantly enhanced cold pain and weakly reduced heat pain. To address if capsaicin's effect was due to summation of perceptually similar thermal and chemical sensations, one-half of the tongue was desensitized by application of capsaicin. Upon reapplication, capsaicin elicited little or no irritant sensation yet still significantly enhanced heat pain on the capsaicin-treated side, ruling out summation. In a third experiment, capsaicin significantly enhanced pain ratings to graded heat stimuli (47 degrees C to 50 degrees C) resulting in an upward shift of the stimulus-response function. Menthol may induce cold hyperalgesia via enhanced thermal gating of TRPM8 in peripheral fibers. Capsaicin, mustard oil, and cinnamaldehyde may induce heat hyperalgesia via enhanced thermal gating of TRPV1 that is coexpressed with TRPA1 in peripheral nociceptors.     

鸡矢藤注射液和野木瓜注射液对大鼠足底皮下化学组织损伤诱致自发痛、痛敏和炎症的作用

研究市售中药制剂鸡矢藤注射液和野木瓜注射液有无抗伤害及抗炎作用。采用两种持续性痛动物实验模型——蜜蜂毒(bee venom,BV)模型和福尔马林(formalin,F)模型,评价鸡矢藤注射液和野木瓜注射液系统给药对持续性自发痛反应、原发性热和机械痛敏及炎症反应的作用效果。成年清醒大鼠足底皮下注射BV(0．2％,50μl)不仅可诱发注射侧长达1h以上的、持续的、单相性的自发痛反应(其表现为自发缩足反射行为)和之后出现的持续3—4d的原发性热和机械痛敏现象,而且注射爪出现明显的红、肿等炎症反应。皮下注射F(2．5％,50μl)则产生双相性自发痛反应。与盐水组比较,致痛前系统给予0．32、1．6和9．0ml／kg三个剂量的500％鸡矢藤注射液或250％野木瓜注射液,对BV或F诱致的1h自发缩足反射次数具有剂量依赖性抑制作用;致痛5min后分别给予鸡矢藤或野木瓜注射液对BV或F诱发的自发痛反应也产生显著的抑制作用。然而,致痛前或致痛后静脉注射鸡矢藤注射液或野木瓜注射液对BV诱致的原发性热／机械痛敏及炎症反应均无明显的抑制作用。纳洛酮(一种非选择性的阿片受体拮抗剂)不能翻转鸡矢藤或野木瓜注射液对BV产生的自发痛反应的镇痛作用,提示其镇痛作用不是由内源性阿片受体介导。本研究结果证实鸡矢藤或野木瓜注射液能预防和缓解临床持续性自发痛,但是对原发性热／机械痛敏及炎症反应均无抗伤害效应和抗炎作用。在中药镇痛抗炎有效成分的筛选和评价中,BV模型是一个理想的实验动物模型。     

热激处理对冷藏枇杷果实冷害的生理作用

枇杷(Eriobotrya japonica Lindl.)果实采后经48～52℃、10 min的热激处理,然后2～5℃贮藏,通过对贮藏期间果实冷害级别、呼吸速率、过氧化物酶、过氧化氢酶、苯丙氨酸解氨酶活性和质膜相对透性变化的分析,研究贮前热激处理对冷藏枇杷果实冷害的生理作用.结果表明,2～5℃低温可诱导枇杷果实呼吸速率和苯丙氨酸解氨酶活性异常升高,果实冷害程度与苯丙氨酸解氨酶活性之间呈正相关,相关系数r=0.926.热激处理能降低冷藏条件下(2～5℃)枇杷果实呼吸速率的异常升高,减轻由于低温胁迫造成的果肉细胞膜损伤,提高枇杷果实的过氧化物酶和过氧化氢酶活性,降低苯丙氨酸解氨酶的活性.贮前热激处理有推迟和减轻枇杷果实冷害症状发生、降低果肉低温劣变的作用.贮前热激处理结合低温冷藏是延长枇杷果实贮藏寿命的有效措施之一.     

The effect of in vivo heat treatments on blowfly flight muscle mitochondrial function: Effects on partial reactions of the respiratory chain

1. 1. The development of thermotolerance has been shown to protect blowfly flight muscle mitochondrial function from damage resulting from an LD₅₀ in vivo heat dose.

2. 2. The principal sites of the damage have been studied using specific inhibitors of the respiratory chain, rotenone and antimycin A, together with substrates that stimulate respiration through the different complexes.

3. 3. Complex I was identified as the primary site for heat damage. State III respiration was inhibited following the LD₅₀ in vivo heat dose, and uncoupling with FCCP did not restore respiration to control levels, indicating that the respiratory enzymes were inactivated. The development of thermotolerance protected this site from heat damage.

4. 4. In contrast, G3-P stimulated respiration was the same in control, LD₅₀ in vivo treated controls and LD₅₀, in vivo treated thermotolerant mitochondria, and significantly higher than state III respiration of LD₅₀ in vivo treated controls. This suggested that respiration through G3-P dehydrogenase, Co enzyme Q and Complex III is not damaged. However, as G3-P stimulated respiration of coupled mitochondria from LD₅₀ in-vivo treated flies was markedly reduced (El-Wadawi and Bowler, 1995. J. exp. Biol. 198: 2413–2421), phosphorylation at complex III may be inhibited also.

5. 5. Ferrocyanide stimulated respiration through cytochrome c-Complex IV was also inhibited in LD₅₀ in vivo treated flies, as compared with unheated control mitochondria. However, thermotolerance protected this site also from heat damage.

     

注射硫代乙酰胺及饲喂不同油脂水平饲料建立草鱼肝损伤实验模型

目的通过注射硫代乙酰胺(TAA)及饲喂不同油脂水平饲料建立草鱼肝损伤实验模型。方法 实验草鱼分模型组和对照组,每组分别投喂2.8%油脂组、4.8%油脂组和6.8%油脂组,模型组腹腔注射TAA 300mg/kg,1次/日,注射1 d,共计6个实验组,饲养10周。养殖过程中,于2周、4周和6周对每组实验鱼采血,测定天门冬酸氨基转移酶(AST)、丙氨酸氨基转移酶(ALT)和AST/ALT。结果①模型组特定生长率显著降低了30.5%(P<0.01),成活率平均为73.33%。模型组草鱼肌肉粗脂肪含量显著降低了17.6%,而肝胰脏粗脂肪含量显著增高了13.38%(P<0.01)。②模型组2周、4周和6周时,模型组血清AST/ALT分别为对照组的1.94倍、1.38倍和1.31倍。10周时,模型组草鱼血清AST/ALT增高了10.10%(P>0.05),而血清胆碱酯酶(CHE)降低了6.38%(P>0.05)。模型组草鱼血清超氧化物歧化酶(SOD)活力显著低于对照组8.56%(P<0.05)。③与对照组相比,模型组肝细胞肿胀且边界模糊,肝细胞部分脂肪病变,有部分炎症浸润,并均出现肝纤维化。结论注射TAA及饲喂不同油脂水平饲料可以诱导草鱼肝损伤实验模型,实验模型具备脂肪肝和肝纤维化病理特征。     

牛磺酸对失血性休克再灌注肺损伤的防护作用及其机制探讨

目的:探讨失血性休克再灌注肺损伤与一氧化氮的关系及牛磺酸对其的影响.方法:健康家兔24只随机分为三组:对照组、单纯休克组、牛磺酸治疗组.采用失血性休克再灌注后肺损伤模型.测定肺组织及血浆中一氧化氮合酶(NOS)活性、一氧化氮代谢产物(NO2-/NO3-)含量、超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量、肺湿重/肺干重、肺水含量、肺通透指数(LPI)、肺泡灌洗液(PALF)中蛋白含量等指标的变化,并常规留取肺标本进行病理形态观察.结果:①再灌注3 h时肺组织及血浆中SOD活性显著下降,而上述其它指标均显著升高,与对照组相比差异有显著性(均P<0.01).②血浆、肺组织中NO2-/NO3-含量与MDA含量均呈正相关,且肺组织中NO2-/NO3-含量和肺损伤指标呈显著正相关.③牛磺酸(40 mg*kg-1,iv)可减轻上述指标的变化.结论:NO在休克再灌注肺损伤中起重要作用,牛磺酸可减少NO的生成、增强自由基的清除从而使肺组织损伤减轻.     

Absence or presence of glucose in growth medium and its effect on heat injury inStaphylococcus aureus

Summary Staphylococcus aureus 196E, when grown in a glucose (0.25% wt./vol.)-containing medium, produced cells that would undergo injury when subjected to sublethal heat conditions (45 min at 50°C); however, if glucose was omitted from the growth medium, the extent of injury was greatly reduced. Media containing glucose sterilized by filtration or by separate autoclaving produced cells equal in injury susceptibility to medium in which glucose was autoclaved as part of the medium components. Injury also occurred when other sugars such as fructose, mannose, maltose, or lactose were substituted for glucose. Sugar-containing media that producedStaphylococcus aureus of maximal susceptibility to heat injury reached a pH of approximately 6 or lower during growth of the cells. Incubation of staphylococci in growth medium acidified with acetic or lactic acids or HCl did not lead to cells that would undergo injury under the stated conditions. The stimulatory effect of glucose on injury appears to be related to the metabolism of the sugar byStaphylococcus aureus.Agricultural Research Service, U.S. Department of Agriculture. Reference to brand or firm name does not constitute endorsement by the U.S. Department of Agriculture over others of a similar nature not mentioned.     

鞘内注射孤啡肽对大鼠足底注入蜜蜂毒诱致长时程自发痛、痛敏和炎症的不同效果

为进一步了解孤啡肽在脊髓水平是否具有抗伤害及抗炎作用,本实验在具有多种痛行为表现的蜜蜂毒模型上观察了鞘内注射孤啡肽对大鼠一侧后足底注入蜜蜂毒所诱致的同侧自发缩足反射、原发热和机械性痛敏以及注射部位炎症反应的影响,同时观察了新的高选择性孤啡肽受体拮抗剂CompB的作用.结果表明与生理盐水对照组比较,鞘内注射孤啡肽(3、10、30 nmol/10μl)对蜜蜂毒诱发的自发缩足反射次数的抑制作用随剂量提高而增大,抑制率分别为37±7,43±6and57±11%(三个剂量vs对照,P＜0.05);而对蜜蜂毒诱发的注射部位炎症反应(爪体积、爪背腹厚度和蛋白渗出的增加)无显著影响.CompB(30 nmo1)可完全翻转10 nmol孤啡肽对自发缩足反射的抑制作用.鞘内单次或重复注射孤啡肽(10 nmol/10μl)对蜜蜂毒诱致的原发性热和机械性痛敏的发生和维持均无作用.本实验结果提示,外源性孤啡肽在脊髓通过孤啡肽受体的介导产生一定的镇痛作用,但是它可能仅对持续性自发痛有抑制作用,而对热和机械性痛敏及炎症反应均无影响.     

内源性一氧化氮在内毒素引起的肺动脉高压和肺损伤中的作用

本实验观察了家兔静脉内注入内毒素的主要成分脂多糖(LPS)后平均动脉血压(MAP)、肺动脉压(PAP)及入、出肺血NO含量的变化,并观察了静脉内预注入NO生成抑制剂Nω-硝基-L-精氨酸(L-NNA)及诱生型NO生成抑制剂氨基胍(AG)后PAP和肺损伤的变化.结果观察到:家兔LPS注入后,MAP均明显下降,LPS注入后0.5、1、1.5、2h PAP明显增高(P<0.05).LPS注入后PAP的高峰期(1h)入肺血NO含量明显降低,出肺血NO无明显变化.与对照组相比,LPS注入后3h出肺血NO含量和5h入、出肺血NO含量均明显增多.相关分析表明,兔LPS注入前和LPS注入后1h PAP与入肺血NO含量呈明显的负相关,而LPS注入后 3h和5h两者相关不明显.静脉预注入L-NNA后,LPS处理组的动物PAP明显增高,入、出肺血丙二醛(MDA)含量也明显增高,动物生存率明显降低.肺组织光镜下可见肺萎陷和小血管淤血加重,白细胞明显增加.静脉预注入AG后,LPS处理组的动物MAP在3～5h明显增高,此时PAP无明显改变,但5h时血中MDA含量明显减低,5h时与LPS组相比肺萎陷和小血管淤血减轻,白细胞也明显减少.以上结果提示,内毒素入血后较早期阶段可出现PAP的升高,此时入肺血NO的减少是参与肺动脉压增高(PAH)的机制之一.家兔内毒素进入血后较早期阶段NO对减轻内毒素引起的PAH和肺损伤起重要作用,而较晚的时期当诱生型NO合酶(iNOS)诱生后释放的NO则参与内毒素引起的肺组织炎症反应和肺损伤.     

Protective effect of aescin from the seeds of Aesculus hippocastanum on liver injury induced by endotoxin in mice

To investigate the effect and underlying mechanism of aescin on acute liver injury induced by endotoxin, liver injury was established by injecting lipopolysaccharide (LPS) in mice. Animals were assigned to seven groups: the control group and groups treated with LPS (40 mg/kg), aescin (3.6 mg/kg), LPS plus dexamethasone (4 mg/kg) and LPS plus aescin (0.9, 1.8 or 3.6 mg/kg). Hepatic histopathological changes were examined under a light microscope. Activities of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in serum were determined. Levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), nitric oxide (NO) and antioxidative parameters in liver homogenate were measured. Glucocorticoid receptor (GR), 11 beta-hydroxysteroid dehydrogenase type 1 (11β-HSD1) and 11 beta-hydroxysteroid dehydrogenase type 2 (11β-HSD2) expressions in liver were determined by western blotting. Treatment with escin could inhibit immigration of inflammatory cells, alleviate the degree of necrosis, and decrease serum ALT and AST activities. Aescin also down-regulated levels of inflammation mediators (TNF-α, IL-1β and NO) and 11β-HSD2 expression in liver, up-regulated GR expression, enhanced endogenous antioxidative capacity, but have no obvious effect on 11β-HSD1 expression in liver. The findings suggest aescin has protective effects on endotoxin-induced liver injury, and the underlying mechanisms were associated with its anti-inflammatory effects, up-regulating GR expression, down-regulating 11β-HSD2 experssion, and antixoidation.     

L-Arg对LPS诱导的急性肺损伤大鼠肺表面活性物质和肺泡巨噬细胞功能的影响

目的:探讨L-精氨酸(L-Arg)对脂多糖(LPS)诱导的急性肺损伤大鼠肺表面活性物质和肺泡巨噬细胞功能的影响。方法:舌下静脉注射脂多糖(LPS)复制肺损伤模型。健康雄性SD大鼠48只,随机分为对照组、模型组(LPS组)和L-Arg治疗组(L-Arg组)(n=16)。分别于给予LPS 3 h或6 h后给予生理盐水(对照组及LPS组,ip)和L-Arg(500 mg/kg ip)(L-Arg治疗组),治疗3 h。原位杂交法(ISH)检测肺组织中肺表面活性蛋白A(SP-A)mRNA的表达;测定肺泡灌洗液(BALF)中的总蛋白(TP)。体外分离培养大鼠肺泡巨噬细胞,以LPS(终浓度10 mg/L)处理巨噬细胞,观察L-Arg对肺泡巨噬细胞的影响。结果:与对照组比较,大鼠肺损伤后SP-A mRNA表达减弱,BALF中TP增多(P<0.01)。肺损伤3 h用L-Arg治疗3 h后,SP-A mRNA阳性细胞表达明显增强,BALF中TP较LPS组相同时间点明显降低(P<0.05,P<0.01),肺损伤减轻。体外实验中,与正常对照组相比,LPS组细胞培养上清中乳酸脱氢酶(LDH)、一氧化氮(NO)、肿瘤坏死因子-α(TNFα-)和白细胞介素-6(IL-6)浓度明显增高(P<0.01);L-Arg明显减少LPS所致的LDH的释放,降低TNFα-和IL-6浓度。结论:L-Arg可减轻内毒素性肺损伤,此机制可能与增强SP-AmRNA表达有关;LPS可刺激巨噬细胞分泌促炎因子和NO,L-Arg可抑制LPS对巨噬细胞的作用。     

Up-regulation of interleukin-6 induced by prostaglandin E from invading macrophages following nerve injury: an in vivo and in vitro study

The mechanisms underlying neuropathic pain caused by nerve injury are not well understood. Inflammatory responses in injured nerves are likely to be key contributing factors in the generation and maintenance of neuropathic pain. The pro-inflammatory cytokine interleukin-6 (IL-6) is up-regulated in invading macrophages and has been implicated in the development of neuropathic pain. We previously demonstrated that invading macrophages up-regulate cyclooxygenase 2 (COX2) and prostaglandin E2 (PGE2) receptors EP1 and EP4, suggesting that PGE2 may affect macrophage function via autocrine or paracrine mechanisms. This study was undertaken to determine whether PGE2 is involved in the up-regulation of IL-6 in invading macrophages. Two weeks following partial sciatic nerve ligation, numerous IL-6 immunoreactive (IR) cell profiles were present in injured nerves. Colocalization of IL-6 with the invading macrophage marker ED1 or with COX2 was frequently observed. IL-6-IR, COX2-IR and ED1-IR cells were present only in cultures derived from injured nerve segments. PGE2 and IL-6 release from cultured cells derived from injured nerves was increased significantly compared with uninjured nerves. Non-selective and selective COX2 inhibitors suppressed PGE2 and IL-6 release. Treatment with PGE2 further enhanced IL-6 release in a concentration- and time-dependent manner. A selective EP4 receptor antagonist L-161982 was able to suppress IL-6 release, whereas an EP1 receptor antagonist, SC19220, was ineffective. Moreover, a protein kinase C inhibitor, calphostin C, dramatically suppressed IL-6 release, whereas a protein kinase A inhibitor H-89 and a Ca2+ chelator EGTA failed. Taken together, our data suggest that PGE2 is involved in mediating the up-regulation of IL-6 occurring in invading macrophages. This action is mediated through an EP4 receptor and the protein kinase C signaling pathway.     

Effects of intraplantar injections of nociceptin and its N-terminal fragments on nociceptive and desensitized responses induced by capsaicin in mice

Injection of capsaicin into the hindpaw has been employed as a model of chemogenic nociception in mice. Intraplantar injection of nociceptin (30–240 pmol) produced a significant and dose-dependent antinociceptive activity in the capsaicin test. The nociceptin N-terminal fragments, (1–11) and (1–13), were also active with a potency higher than nociceptin and comparable to nociceptin, respectively. Intraplantar injection of the nociceptin (1–7) fragment had no effect on capsaicin-induced nociception. Antinociception induced by nociceptin or nociceptin (1–13) was reversed significantly by intraplantar co-injection of [Nphe¹]nociceptin (1–13)NH₂, an orphan opioid receptor-like 1 (ORL1) receptor antagonist, whereas local injection of the antagonist did not interfere with the action of nociceptin (1–11). Nociceptin (1–11) was approximately 2.0-fold more potent than naturally occurring peptide nociceptin, and 10-fold more active than intraplantar morphine. Nociceptive licking/biting response to intraplantar injection of capsaicin was desensitized by repeated injections of capsaicin at the interval of 15 min. Desensitization induced by capsaicin was attenuated significantly by co-injection of nociceptin at much lower doses than antinociceptive ED₅₀ for nociceptin. Capsaicin desensitization was also decreased by co-injection of nociceptin (1–11) and (1–13) to a similar extent. The present results indicate that not only nociceptin but also the N-terminal fragment (1–13) possesses a local peripheral antinociceptive action, which may be mediated by peripheral ORL1 receptors. In addition, the difference of the effective doses suggests that the antinociceptive action and inhibition of capsaicin-induced desenitization by nociceptin, nociceptin (1–11) and (1–13), may involve distinct mechanisms at the level of the peripheral nerve terminal.     

Effects of heat stress on antioxidant defense system,inflammatory injury,and heat shock proteins of Muscovy and Pekin ducks: evidence for differential thermal sensitivities

Rising temperatures are severely affecting the mortality, laying performance, and meat quality of duck. Our aim was to investigate the effect of acute heat stress on the expression of heat shock proteins (HSPs: HSP90, 70, 60, 40, and 10) and inflammatory factors (nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2)) and antioxidant enzyme activity (superoxide dismutase (SOD), malondialdehybe (MDA), catalase (CAT), total antioxidant capacity (T-AOC)) in livers of ducks and to compare the thermal tolerance of Pekin and Muscovy ducks exposed to acute heat stress. Ducks were exposed to heat at 39 ± 0.5 °C for 1 h and then returned to 20 °C for 1 h followed by a 3-h recovery period. The liver and other tissues were collected from each individual for analysis. The mRNA levels of HSPs (70, 60, and 40) increased in both species, except for HSP10, which was upregulated in Muscovy ducks and had no difference in Pekin ducks after heat stress. Simultaneously, the mRNA level of HSP90 decreased in the stress group in both species. Morphological analysis indicated that heat stress induced tissue injury in both species, and the liver of Pekin ducks was severely damaged. The activities of several antioxidant enzymes increased in Muscovy duck liver, but decreased in Pekin duck. The mRNA levels of inflammatory factors were increased after heat stress in both duck species. These results suggested that heat stress could influence HSPs, inflammatory factors expression, and the activities of antioxidant enzymes. Moreover, the differential response to heat stress indicated that the Muscovy duck has a better thermal tolerance than does the Pekin duck.     

Thermal substitution and aerobic efficiency: measuring and predicting effects of heat balance on endotherm diving energetics

For diving endotherms, modelling costs of locomotion as a function of prey dispersion requires estimates of the costs of diving to different depths. One approach is to estimate the physical costs of locomotion (Pmech) with biomechanical models and to convert those estimates to chemical energy needs by an aerobic efficiency (eta=Pmech/Vo2) based on oxygen consumption (Vo2) in captive animals. Variations in eta with temperature depend partly on thermal substitution, whereby heat from the inefficiency of exercising muscles or the heat increment of feeding (HIF) can substitute for thermogenesis. However, measurements of substitution have ranged from lack of detection to nearly complete use of exercise heat or HIF. This inconsistency may reflect (i) problems in methods of calculating substitution, (ii) confounding mechanisms of thermoregulatory control, or (iii) varying conditions that affect heat balance and allow substitution to be expressed. At present, understanding of how heat generation is regulated, and how heat is transported among tissues during exercise, digestion, thermal challenge and breath holding, is inadequate for predicting substitution and aerobic efficiencies without direct measurements for conditions of interest. Confirming that work rates during exercise are generally conserved, and identifying temperatures at those work rates below which shivering begins, may allow better prediction of aerobic efficiencies for ecological models.     

外源性硫化氢对大鼠内毒素性肺损伤的影响及机制研究

目的：应用H2S供体硫氢化钠（NaHS）,观察外源性H2S对中性粒细胞（PMN）在脂多糖（LPS）刺激大鼠肺内聚集的影响及其机制。方法：采用尾静脉注射致Sprague-Dawley（SD）大鼠内毒素急性肺损伤（ALI）模型,将大鼠随机分为4组（n=8～12）。对照组：由尾静脉注射无菌生理盐水（0.5ml/kg）;LPS组：由尾静脉注射LPS（1mg/kg）;LPS＋NaHS组：注射LPS前10min腹腔注射NaHS（28μmol/kg）;NaHS组：腹腔注射NaHS（28μmol/kg）。6h后光镜下观察各组大鼠肺组织学变化并计数肺泡间隔中PMN数目（number/HP）;脱氧核苷酸末端转移酶介导的原位末端标记技术（TUNEL）测定支气管肺泡灌洗液（BALF）中PMN凋亡百分率及应用Western blot检测肺组织细胞间黏附分子（ICAM）-1和核转录因子（NF）-κB表达的变化。结果：注射LPS后动物肺组织出现出血、水肿及PMN聚集等病理征象。LPS组大鼠肺组织中PMN数目较对照组显著增加,PMN凋亡百分率下降,ICAM-1、NF-κB表达显著增高;应用NaHS后每高倍镜PMN数目显著减少,PMN凋亡百分率明显增高,ICAM-1、NF-κB表达显著降低,肺组织损伤减轻。单独应用NaHS组大鼠上述各项指标与对照组大鼠相比无显著差异。结论：NaHS可减少PMN在肺内聚集,其机制与其抑制NF-κB通路,从而下调ICAM-1表达、促进PMN凋亡有关。     

Galls induced by Calophya latiforceps (Hemiptera: Calophyidae) reduce leaf performance and growth of Brazilian peppertree

Schinus terebinthifolia Raddi (Anacardiaceae) (Brazilian peppertree) is one of the most serious terrestrial invasive plants in Florida. The leaf galling psyllid, Calophya latiforceps Burckhardt (Hemiptera: Calophyidae), was discovered feeding on the Brazilian peppertree in Bahia, Brazil, in 2010, and is being evaluated for release as a biological control agent. In order to understand how this candidate biological control agent affects the growth of S. terebinthifolia, we measured the effect of the psyllid on photosynthesis, leaf chlorophyll content and plant growth. Infested plants had lower photosynthesis compared to uninfested plants 30 and 45 days after gall initiation, and chlorophyll content was lower over a 70-d period. Plant height was reduced 31% and biomass 11% after three months of infestation. Results of these studies suggest that C. latiforceps will negatively affect the growth of the Brazilian peppertree if released in Florida.     

Antinoceptive effect of triterpenoid α,β-amyrin in rats on orofacial pain induced by formalin and capsaicin

The effects of α,β-amyrin, a pentacyclic triterpene isolated from Protium heptaphylum was investigated on rat model of orofacial pain induced by formalin or capsaicin. Rats were pretreated with α,β-amyrin (10, 30, and 100 mg/kg, i.p.), morphine (5 mg/kg, s.c.) or vehicle (3% Tween 80), before formalin (20 μl, 1.5%) or capsaicin (20 μl, 1.5 μg) injection into the right vibrissa. In vehicle-treated controls, formalin induced a biphasic nociceptive face-rubbing behavioral response with an early first phase (0–5 min) and a late second phase (10–20 min) appearance, whereas capsaicin produced an immediate face-rubbing (grooming) behavior that was maximal at 10–20 min. Treatment with α,β-amyrin or morphine significantly inhibited the face-rubbing response in both test models. While morphine produced significant antinociception in both phases of formalin test, α,β-amyrin inhibited only the second phase response, more prominently at 30 mg/kg, in a naloxone-sensitive manner. In contrast, α,β-amyrin produced much greater antinociceptive effect at 100 mg/kg in the capsaicin test, which was also naloxone-sensitive. These results provide first time evidence to show that α,β-amyrin attenuates orofacial pain atleast, in part, through a peripheral opioid mechanism but warrants further detailed study for its utility in painful orofacial pathologies.