慢性非细菌性前列腺炎SD大鼠前列腺平滑肌细胞内钙离子浓度的变化

目的:探讨SD大鼠慢性非细菌性前列腺炎(CAP)炎症组与正常对照组前列腺平滑肌细胞(PSMCs)内游离钙离子浓度([Ca2+]i)的差异及其在CAP中的意义。方法:利用SD大鼠前列腺蛋白提取液与弗氏完全佐剂(FCA)诱导出CAP模型,体外贴壁培养并纯化炎症组与正常对照组PSMCs,细胞经钙离子荧光探针FLUO-3AM孵育后在激光共聚焦显微镜(LSCM)下连续动态扫描。结果:CAP组与对照组的PSMCs钙离子荧光强度分别为80.39±9.00和27.95±10.04,差异具有显著性(P<0.01)。结论:CAP SD大鼠PSMCs[Ca2+]i明显升高,其升高可能增强了PSMCs的收缩作用,从而引起CAP的一系列如对疼痛敏感性增强、下腹部疼痛不适的症状。     

瑞芬太尼对人肠系膜小动脉平滑肌细胞大电导钙激活钾通道的影响

目的 观察瑞芬太尼对人肠系膜小动脉平滑肌细胞大电导钙激活钾通道(BKCa)的影响,探讨其扩张血管的机制.方法 酶消化法急性分离人肠系膜小动脉平滑肌细胞,采用全细胞膜片钳技术,+80 mV钳制电压下记录不同浓度瑞芬太尼(1.2、4.8、19.4、77.4和310.0 nmol/L)给药后人肠系膜小动脉平滑肌细胞BKCa电流及达峰时间,计算BKCa激活率.结果 瑞芬太尼可激活BKCa,使电流密度-电压曲线上移,激活电压不变;随瑞芬太尼浓度升高,BKCa激活率逐渐升高(P＜0.01),19.4 nmol/L时BKCa激活率趋于稳定;各浓度瑞芬太尼给药后BKCa电流达峰时间比较差异无统计学意义(P＞0.05);瑞芬太尼浓度与BKCa激活率成对数曲线关系,其半数最大激活效应浓度为(118±7)nmol/L.结论 瑞芬太尼浓度依赖性地激活人肠系膜小动脉平滑肌细胞BKCa,该作用可能是其产生扩张血管作用的机制.     

雌二醇诱导的慢性非细菌性前列腺炎大鼠前列腺平滑肌细胞电压依赖钙离子通道的定量表达

目的:建立慢性非细菌性前列腺炎大鼠模型,探讨炎症组与正常对照组大鼠前列腺平滑肌细胞电压依赖钙离子通道定量表达的差异性。方法:采用雌二醇诱导大鼠前列腺炎,体外培养纯化前列腺平滑肌细胞(PSMCs),用Trizol提取总RNA,经逆转录,SYBR Green I实时定量PCR测定各亚型钙离子通道α1亚基的mRNA相对表达水平,比较两组间的差异。结果:炎症组和对照组均见L、T、P/Q型钙通道表达,炎症组L型钙通道CaV1.2相对对照组表达量增多,分别为0.048±0.024和0.031±0.015,差异具有显著性(t=2.846,P=0.007),T、P/Q型两组间无统计学差异。结论:慢性前列腺炎PSMCs细胞膜L型钙通道CaV1.2数目上调,钙内流增多,在发病机制中可能具有一定作用。     

BKCa和PKG在氯胺酮舒张哮喘大鼠离体气管平滑肌中的作用

目的 评价大电导钙激活钾通道(BKCa)和蛋白激酶G(PKG)在氯胺酮舒张哮喘大鼠离体气管平滑肌中的作用.方法 健康SD大鼠,体重250 ～ 300 g,采用卵蛋白致敏法建立哮喘模型,取哮喘大鼠15只,每只大鼠制备2～3条离体气管环.取哮喘大鼠离体气管环36条,采用随机数字表法,将其分为3组(n=12):氯胺酮处理组(AK组)、BKCa阻断剂IBTX+氯胺酮处理组(AKI组)和PKG抑制剂KT-58232+氯胺酮处理组(AKK组);AK组采用0.1 mmol/L乙酰胆碱预收缩大鼠气管环达稳态后,用0.4 g/L氯胺酮孵育15 min; AKI组用乙酰胆碱和氯胺酮孵育前,用3 μmol/L IBTX孵育30 min;AKK组用入乙酰胆碱和氯胺酮孵育前,用2μmol/L KT-5823孵育30 min;采用气管环相连的力-位移换能器测定气管环舒张幅度.结果 与AK组比较,AKI组和AKK组大鼠离体气管平滑肌舒张幅度降低(P＜0.05).结论 氯胺酮可通过激活BKCa和PKG信号通路舒张哮喘大鼠离体气管平滑肌.     

异丙酚对人动脉平滑肌细胞膜大电导钙激活钾通道的影响

异丙酚引起低血压的电生理机制有两种可能，一种可能是抑制交感神经肌接头活动，降低血浆儿茶酚胺的浓度，从而降低血管外周阻力；另一种可能是对内皮的影响和对血管平滑肌细胞的直接作用，Wanersted等在器官水平上证实了异丙酚扩张血管可能与大电导钙激活钾通道（BKCa）有关。本研究拟观察不同浓度异丙酚对人肠系膜动脉血管平滑肌细胞膜BKCa的影响，从分子水平探讨其扩张血管的机制。     

瑞芬太尼对正常和高血压大鼠基底动脉平滑肌细胞的不同作用

目的评价瑞芬太尼对正常和高血压大鼠基底动脉平滑肌细胞上大电导钙激活钾通道(BKCa)和电压门控钾通道(Kv)激活电流的影响。方法自发性高血压大鼠(spontaneously hypertensive rats,SHR)和同源正常血压(wistar-kyoto,WKY)大鼠,采用酶消化法急性分离基底动脉平滑肌细胞,每种大鼠选择6个基底动脉平滑肌细胞,采用全细胞膜片钳技术记录外向电流幅度。加入瑞芬太尼3×10-7mol/L,分别记录所设置的方波刺激(step刺激)方案中所有刺激电压下给药前(基础水平)和给药后电流幅度,并计算净电流=给药后电流幅度-基础值;采用浓度累积法给药,分别记录+60 m V刺激电压下给药前(基础值)和给予10-10、10-9、10-8、10-7、10-6、10-5mol/L瑞芬太尼后电流幅度,计算电流增加率和瑞芬太尼增加基底动脉平滑肌细胞电流幅度的半数有效浓度(EC50);另取每种大鼠6个基底动脉平滑肌细胞,加入瑞芬太尼3×10-7mol/L后分别给予BKCa阻滞剂四乙胺(tetraethylammonium,TEA)和Kv阻滞剂4-氨基吡啶(4-aminopyridine,4-AP),再分别加入其相应的瑞芬太尼混合液,记录每一次给药后的电流幅度。结果两种大鼠基底动脉平滑肌细胞给瑞芬太尼后在0、+20、+40和+60 m V刺激电压下产生的净电流依次明显增大(P0.05);10-10、10-9、10-8、10-7mol/L瑞芬太尼作用下,两种大鼠基底动脉平滑肌细胞外向电流增加率依次明显升高(P0.05);与WKY大鼠比较,瑞芬太尼增加SHR基底动脉平滑肌细胞电流幅度的(EC50)明显升高(P0.05);与基础值比较,两种大鼠基底动脉平滑肌细胞瑞芬太尼给药后电流幅度明显升高,TEA给药后或4-AP给药后电流幅度明显降低(P0.05);与TEA给药后或4-AP给药后比较,TEA+瑞芬太尼给药后或4-AP+瑞芬太尼给药后两种大鼠基底动脉平滑肌细胞电流幅度明显升高(P0.05)。结论瑞芬太尼呈电压依赖性和浓度依赖性激活两种大鼠基底动脉平滑肌细胞BKCa和Kv电流,瑞芬太尼对SHR基底动脉平滑肌细胞上BKCa和Kv激活电流的作用较WKY大鼠弱。     

肝硬化大鼠小肠Cajal间质细胞超微结构及平滑肌细胞线粒体膜电位的变化

目的研究肝硬化大鼠小肠Cajal间质细胞超微结构的改变及平滑肌细胞线粒体膜电位的变化,探讨肝硬化胃肠动力障碍的相关机制。方法 20只Wister大鼠随机分为肝硬化模型组和对照组,每组10只,采用CCl4溶剂大腿根部皮下注射法制作肝硬化模型,用葡聚糖蓝-2000作为胃肠内标记物,观察大鼠肠道传输,透射电镜观察小肠Cajal间质细胞超微结构的改变,激光共聚焦显微镜检测小肠平滑肌细胞线粒体膜电位的改变。结果与对照组比较,肝硬化组大鼠小肠动力明显减弱(P0.01),透射电镜观察显示空肠Cajal间质细胞的超微结构发生明显改变,线粒体等细胞器明显减少(P0.01)。小肠平滑肌线粒体膜电位显著低于对照组(P0.01)。结论肝硬化大鼠肠道传输减弱与肠道Cajal间质细胞超微结构改变,细胞器减少及线粒体膜电位的降低有关。     

大电导钙激活钾通道与心血管保护

背景 大电导钙激活钾通道(large conductance Ca2+-activated K+ channels,BKCa)可能是各类心脏疾病的重要治疗靶点. 目的 主要阐述如何通过调节心肌及血管平滑肌的BKCa通道而发挥保护心肌作用及其相关机制. 内容 在心肌细胞的线粒体上,BKCa通道能够有效地调节线粒体的活性氧、Ca2+和呼吸作用.在血管平滑肌细胞,BKCa通道能调节血管紧张度,促进血管扩张. 趋向 BKCa通道在心肌缺血/再灌注(ischemia/reperfusion,I/R)损伤中有着重要的作用,包括改善心肌功能和减少梗死面积.     

风湿性瓣膜病心房颤动患者右心房超极化激活电流密度及其通道表达的变化

目的 比较风湿性心脏瓣膜病心房颤动患者和窦性心律患者右心房单个心肌细胞超极化激活电流(If)密度及超极化激活的环核苷酸门控(HCN)通道表达的变化.方法 应用全细胞膜片钳技术记录25例房颤患者和16例窦性心律患者右心耳单个心房肌细胞If的变化,并用Westernblot法检测两组患者右心耳组织HCN通道的表达水平.结果 相同激活电位时,房颤组患者右心耳单个心房肌细胞If电流密度明显大于窦性心律组,且随电位增加激活更快,尤其在-70 mV时,房颤组和窦性心律组If电流密度分别为(-43.74±2.87)和(-26.81 ±1.41)pA/pF,此时两组比较差异有统计学意义(P＜0.01).房颤组HCN2、HCN4通道表达水平分别为0.44±0.20和0.53±0.20,与窦性心律组的0.23±0.13和0.36 ±0.18比较均明显增高(P＜0.01).结论 心房组织If电流密度增大及HCN通道表达上调参与了心房电重构,在房颤发生和维持中发挥作用.     

膀胱间质细胞起搏机制的研究进展

膀胱间质细胞(IC)是区别于神经细胞和平滑肌细胞(SMC)的一类细胞。目前对IC的研究多聚焦于Cajal间质细胞(ICC)初始的起搏机制中,可认为IC中ICC表面存在产生超极化激活的内向电流的超极化激活环核苷酸门控阳离子通道,使得ICC成为膀胱起搏细胞成为可能。而成纤维样细胞和端粒细胞与膀胱平滑肌细胞和神经纤维之间存在...     

Modulation of Ca2+-activated K+ channel in renal artery endothelium in situ by nitric oxide and reactive oxygen species

BACKGROUND: Endothelium-derived nitric oxide and reactive oxygen species (ROS) have been proposed to regulate vascular tone by complex mechanisms, including the modulation of ion channel function. In endothelial function itself, activation of Ca2+-activated K+ channels (KCa) plays a crucial role by inducing hyperpolarization, which promotes membrane potential-driven Ca2+ influx and Ca2+-dependent synthesis of vasodilatory factors. In the present study, we tested whether nitric oxide and ROS modulate endothelial KCa function. METHODS: By employing the patch-clamp technique in endothelium of porcine renal arteries in situ, we identified a large-conductance Ca2+-activated K+ channel (big K+ channel, BKCa) with a conductance of 297 +/- 6 pS. RESULTS: Channel activity was strongly controlled by the membrane potential and the cytosolic Ca2+ concentration (EC50 3.1 +/- 0.5 micromol/L Ca2+ at 0 mV). Channel activity was inhibited by Ba2+ and iberiotoxin. At submicromolar [Ca2+]i, nitric oxide induced a dose-dependent stimulation of BKCa activity with a 10-fold increase at the highest dose tested (1 micromol/L). A similar stimulation was achieved by the nitric oxide donors, sodium nitroprusside (SNP), and diethylamine nitric oxide complex (DEA-NO). In contrast, ROS and, in particular, hydrogen peroxide (H2O2) led to dose-dependent inactivation of BKCa with an IC50 of 80 +/- 6 nmol/L and 1.1 +/- 0.4 micromol/L, respectively. In isolated porcine renal arteries, bradykinin-induced vasodilation was significantly reduced by either iberiotoxin or H2O2. CONCLUSION: Direct stimulation of endothelial BKCa by nitric oxide might represent a novel mechanism of autocrine regulation of endothelial function and points to a positive feedback mechanism by promoting hyperpolarization and nitric oxide production itself. The ROS-induced inhibition of BKCa could be part of the cellular mechanisms by which ROS impairs endothelium-dependent vasodilation.     

Potassium channel openers as potential therapeutic weapons in ion channel disease

The opening of potassium (K+) channels, causing hyperpolarization of the cell membrane, is a physiological means of decreasing cell excitability. Thus, drugs with this property will demonstrate a broad clinical potential. The identification of synthetic molecules that evoke physiological responses (for example smooth muscle relaxation) by the opening of K+ channels led to a new direction in the pharmacology of ion channels. The term "potassium channel openers" was initially associated with a group of chemically diverse agents (for example, cromakalim, pinacidil, nicorandil) that evoke K+ efflux through adenosine 5'-triphosphate (ATP)-sensitive K+ channels (KATP). This finding initiated a search to identify molecules that specifically open other K+ channel subtypes (for example large conductance calcium-activated K+ channels [BKCa]). K+ channel opening properties have been demonstrated in a diverse range of synthetic chemical structures and endogenous substances. Second generation KATP channel openers (KATPCOs) demonstrate heterogeneous pharmacology indicative of independent sites of action for the different agents. Successful cloning of the KATP channel has shed light on the heterogeneity of the structure targeted by KATPCOs. Expression of the actions of KATPCOs involves three isoforms of the sulfonylurea (SUR) receptor (which forms the beta subunit of the KATP channel). The distribution of the SUR isoforms (and potential of identifying new isoforms) provides unique targets for the development of selective KATPCOs giving focused therapeutic approaches to clinical conditions for example cardiac ischemia, urinary incontinence, neurodegeneration, obesity and autoimmune diseases. BKCa channels are found in a diverse array of tissues and due to voltage and Ca sensitivity may work as a negative feedback process. A variety of small synthetic molecules (for example, NS004, fenamates) and natural product-derived compounds (DHS-I, maxikdiol) have been identified as selective BKCa channel openers which should have a profound impact in controlling diseases. The discovery of numerous variants of the alpha subunit (ion conductance pore) and beta subunit (contributes biophysical and pharmacological properties) complex of the BKCa channel gives potential to target specific tissues with selective openers. Little is known, however, about the site(s) of interaction of openers of these channels. The discovery of K+ channel subtype-specific openers and their evaluation in different diseases will determine the degree to which these channels (KATP, BKCa), or their isoforms, represent realistic therapeutic targets. Drugs already marketed that open K+ channels were discovered empirically, and most have serious safety and efficacy problems. New scientific methods, utilizing molecular insight, are implicating K+ channel dysfunction in numerous disease states and are identifying new targets for the future generation of K+ channel opening drugs.     

Captopril reduces the proteinuric effect of human growth hormone in adriamycin nephrosis

 Developing male Sprague-Dawley rats (125 g) with adriamycin (doxorubicin hydrochloride) nephrosis (AN) were treated with growth hormone (GH) which may induce hyperfiltration potentiating glomerulosclerosis. Since captopril (CAP) reduces hyperfiltration, we studied its effects in GH-treated rats with AN. After 41, 76, and 90 days of therapy, urine protein excretion was significantly (P<0.05) reduced in GH-treated AN plus CAP compared with AN rats receiving GH alone. After 90 days, urine protein, creatinine ratio was significantly (P<0.05) increased in GH-treated AN (95.2±13.9) compared with untreated AN (64.8±7.8) and GH-treated AN rats plus CAP (41.8±8.8). The mean serum cholesterol level was significantly (P<0.05) reduced in GH-treated AN rats receiving CAP compared with AN rats receiving GH alone and untreated AN controls. Histologically tubular dilation was significantly (P<0.05) reduced in GH-treated AN rats plus CAP compared with AN rats receiving GH alone. Tubular atrophy and scarring were significantly (P<0.05) increased in AN rats treated with GH compared with untreated AN rats, and normalized in GH-treated AN rats plus CAP. We conclude that CAP reduces the proteinuric response of GH in rats with AN and ameliorates tubular injury. Received: 5 March 1997 / Revised: 7 October 1998 / Accepted: 9 October 1998     

Ionic currents in single smooth muscle cells of the human vas deferens

PURPOSE: Smooth muscle cells of the vas deferens have an important role in carrying sperms to the exterior but little is known of their electrophysiological properties. We characterized the voltage-gated ion channel currents in single smooth muscle cells of the human vas deferens (HVSMCs). MATERIALS AND METHODS: We observed contractile responses of 8 circular smooth muscle strips of the human vas deferens to a high concentration (10 mM) of tetraethylammonium. HVSMCs were isolated using proteolytic enzymes (collagenase and papain), and were used for an electro-physiological study using whole cell and inside-out patch clamp configurations. RESULTS: The application of 10 mM tetraethylammonium induced rhythmic contractions of the strips. When HVSMCs were dialyzed with a KCl solution, step depolarizations of membrane potential evoked oscillatory outward K currents that were not inactivated. The large conductance Ca activated K (BKCa) and delayed rectifier components of the outward current were identified. The BKCa channel showed a large single channel conductance (162.7 +/- 13.2 pS with 5 mM K in the patch pipette). Two types of Ca currents were identified in the whole cell configuration. With a cell held at -50 mV an L-type Ca current was present during a depolarizing step pulse. From a holding potential of -90mV L-type and T-type Ca currents were elicited by depolarizing step pulses. CONCLUSIONS: HVSMCs have 2 (L and T) types of Ca channels and 2 types of K (BKCa and delayed rectifier) channels. Voltage dependent changes of these ion channels and their interactions may be important in regulating vas contractility.     

Involvement of adenosine triphosphate-sensitive potassium channels in the response of membrane potential to hyperosmolality in cultured human aorta endothelial cells

The membrane potential of endothelial cells is an important determinant of endothelial functions, including regulation of vascular tone. We investigated whether adenosine triphosphate-sensitive potassium (K(ATP)) channels were involved in the response of membrane potential to hyperosmolality in cultured human aorta endothelial cells. The voltage-sensitive fluorescent dye, bis-(1,3-diethylthiobarbiturate)trimethine oxonol, was used to assess relative changes in membrane potential semiquantitatively. To investigate the effect of mannitol-, sucrose-, and NaCl-induced hyperosmolality on membrane potential, cells were continuously perfused with Earle's balanced salt solution (285 mOsm/kg H(2)O) containing 200 nM bis-(1,3-diethylthiobarbiturate)trimethine oxonol and exposed to 315 and 345 mOsm/kg H(2)O hyperosmotic medium sequentially in the presence and absence of 1 muM glibenclamide, a well-known K(ATP) channel blocker. Hyperosmotic mannitol significantly induced hyperpolarization of the endothelial cells, which was prevented by 1 microM glibenclamide (n = 6). Estimated changes of membrane potential at 315 and 345 mOsm/kg H(2)O were 13 +/- 8 and 21 +/- 8 mV, respectively. Hypertonic sucrose induced similar changes. However, although hypertonic saline also significantly induced hyperpolarization of the endothelial cells (n = 6), the hyperpolarization was not prevented by 1 muM glibenclamide. In conclusion, K(ATP) channels may participate in hyperosmotic mannitol- and sucrose-induced hyperpolarization, but not in hypertonic saline-induced hyperpolarization in cultured human aorta endothelial cells.     

Nitric Oxide and Endothelium‐Derived Hyperpolarizing Factor in Human Arteries and Veins

Abstract Background: We have investigated and compared nitric oxide (NO) release and endothelium‐derived hyperpolarizing factor (EDHF)‐mediated hyperpolarization in the human internal mammary artery (IMA), radial artery (RA), saphenous vein (SV), and coronary artery. Materials and Methods: Vessel segments taken from coronary artery bypass grafting or heart transplantation patients were placed in an organ chamber. NO‐sensitive electrode or intracellular glass microelectrode was used to study NO or EDHF in response to acetylcholine (ACh) and bradykinin (BK). Results: The resting membrane potential of the smooth muscle cells of IMA, RA, and SV was‐58 ± 0.84 (n # 61),‐61 ± 1.3mV (n # 46, p # 0.03), and‐62 ± 0.9 mV (n # 23, p = 0.0001) respectively. BK‐(10–⁷M) induced EDHF‐mediated hyperpolarization (‐10.9 ± 1.5 mV, n # 7) in the IMA was significantly greater than that in RA (‐5.8 ± 0.9 mV, n # 6, p # 0.04) and SV (‐5.1 ± 0.5 mV, n = 8, p < 0.01). The basal release of NO in IMA (16.8 ± 1.9 nM) was significantly higher than that in RA (11.1 ± 1.0 nM, n # 12, p # 0.02) and in SV (9.9 ± 2.8 nM, n # 13, p < 0.001). The stimulated release of NO to BK in IMA was significantly greater than that in RA (44.3 ± 4.0 vs 25.8 ± 3.6 nM, n # 8, p # 0.004). The duration of NO release was longer in IMA than in RA or in SV. Conclusions: The basal and stimulated release of NO and EDHF‐mediated hyperpolarization in the IMA are significantly greater than that in the RA and SV. EDHF exists in all these human vessels. This study reveals the differences among human vessels regarding the endothelial function that have implications in vasospasm, coronary protection, or long‐term graft patency.     

Remifentanil-induced mechanical responses and membrane potential changes in human umbilical arteries

BACKGROUND: The aim of this study was to evaluate the characteristic features of the mechanical responses and membrane potential changes induced by remifentanil in human umbilical arteries (HUAs). The ionic mechanisms underlying the electrophysiological responses were pharmacologically assessed using two K(+) channel blockers. METHODS: Thirty-eight HUAs were obtained. Contraction-relaxation, membrane potential changes and electrical responses of the HUAs were recorded. RESULTS: Remifentanil produced concentration-dependent relaxation in both endothelium-intact and endothelium-denuded HUA rings. Remifentanil produced a significantly greater relaxation response in intact than in denuded HUA rings. In endothelium-intact rings, pre-treatment with L-nitroarginine [N(w)-NITRO-(L)-ARGININE (L-NO-ARG)] or indomethacin decreased the degree of remifentanil-induced relaxation. Remifentanil (10(-9)-10(-6) mol/l) produced a transient concentration-dependent membrane hyperpolarization, which was not decreased by pre-treatment with L-NO-ARG or indomethacin. It also produced a small concentration-dependent hyperpolarization in the presence of charybdotoxin or tetraethylammonium. CONCLUSION: In both endothelium-intact and endothelium-denuded HUAs, remifentanil induces concentration-dependent vasorelaxation and simultaneously releases nitric oxide, prostaglandins and possibly an endothelium-derived hyperpolarizing factor. In addition, it produces hyperpolarization in a dose-dependent manner. Hyperpolarization induced by remifentanil involves the activation of Ca(2+)-dependent and Ca(2+)-independent potassium channels regulated by intracellular Ca(2+).     

The ATP—sensitive K^＋ channel and membrane potential in the pathogenesis of vascular hyporeactivity in severe hemorrhagic shock

Objective:To elucidate the mechanism of vascular hyporeactivity following severe hemorrhagic shock(HS) by studying the changes of ATP-sensitive potassium channels‘(KATP) groperties and membrane potential of mesenteric arteriolar smooth muscle cells.Methods:single channel currents were studied on cell-attached and indide-out patches of enzymatically isolated mesenteric arteriolar smooth muscle cells (ASMCs).Membrane potentials of arteriolar strips and ASMCs were recorded by intracellular membrane potential recording method and confocal microscopy,respectively.Results:KATP channels in ASMCs were activated,which induced smooth muscle hyperpolarization following vascular hyporeactivity in HS.Conclusions:Hyperpolarizing effect of KATP channel activation plays an important role in low vasoreactivity during severe hemorrhagic shock.     

CO_2气腹对大鼠重症急性胰腺炎胰腺病理变化及白介素1、2、6、10表达的影响

目的:探讨腹腔镜手术时CO2气腹对SD大鼠重症急性胰腺炎(severe acute pancreatitis,SAP)胰腺局部病变及血淀粉酶、炎症细胞因子白细胞介素1、2、6、10的影响。方法:随机将雄性SD大鼠50只分为3组:Ⅰ组20只(CO2组),胰胆管逆行注射5%牛磺胆酸钠,制备SAP动物模型,用气腹机向大鼠腹腔内注入CO2,压力12mm Hg,维持30min;Ⅱ组20只建立SAP模型后关腹,不充入CO2;Ⅲ组10只(对照组)开腹翻动胰腺后关腹。各组均于术后2.5h处死动物,对胰腺组织行病理学检查,并测定血淀粉酶、IL-1、IL-2、IL-6及IL-10的变化。结果:Ⅰ、Ⅱ、Ⅲ组的病理组织学评分分别为(1.900±0.370)、(1.750±0.259)及(0.000±0.000);淀粉酶(U/L)为(6 769±2 216)、(5 241±2 048)及(1 610±414);IL-1(pg/ml)为(0.241±0.052)、(0.320±0.067)及(0.143±0.057);IL-2(pg/ml)为(4.480±1.582)、(5.288±0.973)及(4.762±0.812);IL-6(pg/ml)为(176.39±41.75)、(206.10±37.29)及(115.14±24.96);IL-10(pg/ml)为(171.10±28.73)、(182.26±28.09)及(97.79±20.65)。与Ⅱ组相比,Ⅰ组的IL-1及IL-6表达明显降低(P<0.05),血清淀粉酶、IL-2、IL-10及胰腺病理组织学评分差异无统计学意义(P>0.05)。结论:CO2气腹对SD大鼠SAP胰腺病理变化及白介素1、2、6、10表达改变无不利影响。