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1.
M. I. Harhun A. E. Belevich Ya. D. Tsytsuyra I. B. Filyppov M. F. Shuba 《Neurophysiology》2000,32(4):260-265
Using the standard voltage-clamp technique in the whole-cell mode, we studied the characteristics of barium currents (I
Ba; Ba2+ concentration in the external solution was 5 mM) carried through L-type Ca2+ channels in the membrane of myocytes of the resistive mesenteric artery from normotensive and genetically hypertensive rats (NR and GHR, respectively). To perforate the membrane, we used amphotericin B. The arbitrary density of I
Ba through the plasma membrane of GHR myocytes significantly exceeded this parameter in the NR group. For both animal groups, activation curves plotted as the dependence of the membrane conductance (G
Ba) on the membrane potential were not significantly different: the membrane potential for half activation (V
0.5) of I
Ba in the NR myocytes was equal to 1.0 ± 0.3 mV with slope factor k = 6.3 ± 0.4 mV, whereas in the GHR myocytes V
0.5 = -1.6 ± 0.2 mV and k = 6.2 ± 0.5 mV. The stationary inactivation curves for I
Ba differed significantly: in the NR myocytes, V
0.5 = -24.2 ± 0.4 mV and k = 8.3 ± 0.2 mV, whereas in the GHR myocytes such parameters were, respectively, -21.4 ± 0.4 and 8.7 ± 0.3 mV. The pattern of intersection of stationary activation and stationary inactivation curves for I
Ba was indicative of the existence of a window current, i.e., the non-inactivating component of I
Ba within the -40 to ±20 mV range; the phenomenon was clearly pronounced in the GHR myocytes. Differences in the arbitrary density of integral I
Ba and window current were observed. These differences can cause an increased tone of the blood vessels in hypertensive animals. 相似文献
2.
David Ortiz Lindsay Gossack Ulrich Quast Joseph Bryan 《The Journal of biological chemistry》2013,288(26):18894-18902
Neuroendocrine-type KATP channels, (SUR1/Kir6.2)4, couple the transmembrane flux of K+, and thus membrane potential, with cellular metabolism in various cell types including insulin-secreting β-cells. Mutant channels with reduced activity are a cause of congenital hyperinsulinism, whereas hyperactive channels are a cause of neonatal diabetes. A current regulatory model proposes that ATP hydrolysis is required to switch SUR1 into post-hydrolytic conformations able to antagonize the inhibitory action of nucleotide binding at the Kir6.2 pore, thus coupling enzymatic and channel activities. Alterations in SUR1 ATPase activity are proposed to contribute to neonatal diabetes and type 2 diabetes risk. The regulatory model is partly based on the reduced ability of ATP analogs such as adenosine 5′-(β,γ-imino)triphosphate (AMP-PNP) and adenosine 5′-O-(thiotriphosphate) (ATPγS) to stimulate channel activity, presumably by reducing hydrolysis. This study uses a substitution at the catalytic glutamate, SUR1E1507Q, with a significantly increased affinity for ATP, to probe the action of these ATP analogs on conformational switching. ATPγS, a slowly hydrolyzable analog, switches SUR1 conformations, albeit with reduced affinity. Nonhydrolyzable AMP-PNP and adenosine 5′-(β,γ-methylenetriphosphate) (AMP-PCP) alone fail to switch SUR1, but do reverse ATP-induced switching. AMP-PCP displaces 8-azido-[32P]ATP from the noncanonical NBD1 of SUR1. This is consistent with structural data on an asymmetric bacterial ABC protein that shows that AMP-PNP binds selectively to the noncanonical NBD to prevent conformational switching. The results imply that MgAMP-PNP and MgAMP-PCP (AMP-PxP) fail to activate KATP channels because they do not support NBD dimerization and conformational switching, rather than by limiting enzymatic activity. 相似文献
3.
Marcella Maddaluno Gianluca Grassia Maria Vittoria Di Lauro Antonio Parisi Francesco Maione Carla Cicala Daniele De Filippis Teresa Iuvone Angelo Guglielmotti Pasquale Maffia Nicola Mascolo Armando Ialenti 《PloS one》2012,7(10)
Bindarit, a selective inhibitor of monocyte chemotactic proteins (MCPs) synthesis, reduces neointimal formation in animal models of vascular injury and recently has been shown to inhibit in-stent late loss in a placebo-controlled phase II clinical trial. However, the mechanisms underlying the efficacy of bindarit in controlling neointimal formation/restenosis have not been fully elucidated. Therefore, we investigated the effect of bindarit on human coronary smooth muscle cells activation, drawing attention to the phenotypic modulation process, focusing on contractile proteins expression as well as proliferation and migration. The expression of contractile proteins was evaluated by western blot analysis on cultured human coronary smooth muscle cells stimulated with TNF-α (30 ng/mL) or fetal bovine serum (5%). Bindarit (100–300 µM) reduced the embryonic form of smooth muscle myosin heavy chain while increased smooth muscle α-actin and calponin in both TNF-α- and fetal bovine serum-stimulated cells. These effects were associated with the inhibition of human coronary smooth muscle cell proliferation/migration and both MCP-1 and MCP-3 production. The effect of bindarit on smooth muscle cells phenotypic switching was confirmed in vivo in the rat balloon angioplasty model. Bindarit (200 mg/Kg/day) significantly reduced the expression of the embryonic form of smooth muscle myosin heavy chain, and increased smooth muscle α-actin and calponin in the rat carodid arteries subjected to endothelial denudation. Our results demonstrate that bindarit induces the differentiated state of human coronary smooth muscle cells, suggesting a novel underlying mechanisms by which this drug inhibits neointimal formation. 相似文献
4.
David W. Ferguson Allan P. Farwell William A. Bradley Robert C. Rollings 《The Western journal of medicine》1988,148(6):664-669
A 17-year-old boy had a 2-day prodrome of fever and mild sore throat followed by 2 episodes of severe anginal chest discomfort and substantial transient ST-segment elevations in the anterior leads of the electrocardiogram. A subsequent evaluation showed the 2 episodes were most likely coronary vasospasm complicating acute viral myocarditis. 相似文献
5.
Samantha Hover Barnabas King Bradley Hall Eleni-Anna Loundras Hussah Taqi Janet Daly Mark Dallas Chris Peers Esther Schnettler Clive McKimmie Alain Kohl John N. Barr Jamel Mankouri 《The Journal of biological chemistry》2016,291(7):3411-3422
Bunyaviruses are considered to be emerging pathogens facilitated by the segmented nature of their genome that allows reassortment between different species to generate novel viruses with altered pathogenicity. Bunyaviruses are transmitted via a diverse range of arthropod vectors, as well as rodents, and have established a global disease range with massive importance in healthcare, animal welfare, and economics. There are no vaccines or anti-viral therapies available to treat human bunyavirus infections and so development of new anti-viral strategies is urgently required. Bunyamwera virus (BUNV; genus Orthobunyavirus) is the model bunyavirus, sharing aspects of its molecular and cellular biology with all Bunyaviridae family members. Here, we show for the first time that BUNV activates and requires cellular potassium (K+) channels to infect cells. Time of addition assays using K+ channel modulating agents demonstrated that K+ channel function is critical to events shortly after virus entry but prior to viral RNA synthesis/replication. A similar K+ channel dependence was identified for other bunyaviruses namely Schmallenberg virus (Orthobunyavirus) as well as the more distantly related Hazara virus (Nairovirus). Using a rational pharmacological screening regimen, two-pore domain K+ channels (K2P) were identified as the K+ channel family mediating BUNV K+ channel dependence. As several K2P channel modulators are currently in clinical use, our work suggests they may represent a new and safe drug class for the treatment of potentially lethal bunyavirus disease. 相似文献
6.
目的:研究腹型肥胖对急性冠脉综合征(ACS)患者冠状动脉病变严重程度的影响。方法:选择2012年4月至2013年4月在我院接受治疗的ACS患者120例,根据腰围身高比(RWH)将患者分为无腹型肥胖者60例(对照组,RWH0.5)及腹型肥胖者60例(观察组,RWH0.5)。测量所有患者的基本参数,计算RWH,利用冠脉造影判断冠脉病变的支数和程度,根据Gensini评分法对冠脉造影结果进行评价,分析冠脉病变范围、Gensini积分和RWH的相关性。结果:观察组的收缩压(SBP)、空腹血糖(FPG)、总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白(LDL-C)及Gensini积分水平均显著高于对照组,差异均有统计学意义(均P0.05)。观察组的高密度脂蛋白(HDL-C)水平显著低于对照组,差异有统计学意义(P0.05)。双支病变的RWH及Gensini积分水平显著高于单支病变,三支病变的RWH及Gensini积分水平显著高于单支病变及双支病变,差异均有统计学意义(均P0.05)。根据Spearman法分析相关性可知,冠脉病变范围、Gensini积分和RWH均呈正相关(r=0.635,0.739;P=0.000,0.000)。结论:ACS患者RWH水平增高与冠脉病变的严重程度关系密切,有效控制腹型肥胖对于降低心血管类疾病发病率以及降低冠脉病变的程度具有重要意义。 相似文献
7.
目的:探讨N末端脑钠肽原(NT-pro BNP)与急性冠脉综合征(ACS)患者冠脉病变程度及预后的关系。方法:选择2012年1月至2015年6月我院收治的ACS患者400例为研究对象,根据病情症状的不同将患者分为不稳定心绞痛(UA)组和急性心肌梗死(AMI)组,各200例,另选同期200例非ACS患者作为对照组,比较各组患者的NT-pro BNP水平及ACS患者的心功能情况,并比较ACS患者的冠脉造影结果,通过Syntax评分系统评价冠脉病变,随访6-12个月,对比各组患者的主要心血管不良事件(MACE)发生率,通过上述比较及分析,研究ACS患者NT-pro BNP与冠脉病变程度及预后的关系。结果:AMI组及UA组患者的NT-pro BNP水平明显高于对照组,且AMI组患者的NT-pro BNP水平明显高于UA组,差异有统计学意义(P0.05);AMI组患者的冠脉病变Syntax积分高于UA组,差异有统计学意义(P0.05);冠脉病变Syntax积分≥33分的ACS患者的NT-pro BNP水平高于Syntax积分0-22分的患者,差异有统计学意义(P0.05);同时双支病变和三支病变患者的Syntax积分及NT-pro BNP水平高于单支病变患者,差异有统计学意义(P0.05);随访6-12个月发生MACE患者的NT-pro BNP水平明显高于未发生MACE者,差异有统计学意义(P0.05)。Pearson相关性分析显示,患者的冠脉病变程度与NT-pro BNP及Syntas积分均呈正相关(r=0.667,0.842;P0.05)。患者随访6-12个月MACE发生率与NT-pro BNP及Syntas积分也呈正相关(r=0.708,0.821;P0.05)。结论:ACS患者的冠脉病变程度及预后与其NT-pro BNP水平具有较好的相关性,值得临床关注。 相似文献
8.
Xuxia Liu Haixia Huang Wei Wang Jun Wang Frederick Sachs Weizhen Niu 《The Journal of membrane biology》2008,226(1-3):17-25
Stress in the lipids of the cell membrane may be responsible for activating stretch-activated channels (SACs) in nonspecialized sensory cells such as cardiac myocytes, where they are likely to play a role in cardiac mechanoelectric feedback. We examined the influence of the mechanical microenvironment on the gating of stretch-activated potassium channels (SAKCs) in rat atrial myocytes. The goal was to examine the role of the cytoskeleton in the gating process. We recorded from blebs that have minimal cytoskeleton and cells treated with cytochalasin B (cyto-B) to disrupt filamentous actin. Histochemical and electron microscopic techniques confirmed that the bleb membrane was largely free of F-actin. Channel currents showed mechanosensitivity and potassium selectivity and were activated by low pH and arachidonic acid, similar to properties of TREK-1. Some patches showed a time-dependent decrease in current that may be adaptation or inactivation, and since this decrease appeared in control cells and blebs, it is probably not the result of adaptation in the cytoskeleton. Cyto-B treatment and blebbing caused an increase in background channel activity, suggesting a transfer of stress from actin to bilayer and then to the channel. The slope sensitivity of gating before and after cyto-B treatment was similar to that of blebs, implying the characteristic change of dimensions associated with channel gating was the same in the three mechanical environments. The mechanosensitivity of SAKCs appears to be the result of interaction with membrane lipids and not of direct involvement of the cytoskeleton. 相似文献
9.
Do Young Kim Mohammed G. Abdelwahab Soo Han Lee Derek O’Neill Roger J. Thompson Henry J. Duff Patrick G. Sullivan Jong M. Rho 《PloS one》2015,10(4)
Dietary and metabolic therapies are increasingly being considered for a variety of neurological disorders, based in part on growing evidence for the neuroprotective properties of the ketogenic diet (KD) and ketones. Earlier, we demonstrated that ketones afford hippocampal synaptic protection against exogenous oxidative stress, but the mechanisms underlying these actions remain unclear. Recent studies have shown that ketones may modulate neuronal firing through interactions with ATP-sensitive potassium (KATP) channels. Here, we used a combination of electrophysiological, pharmacological, and biochemical assays to determine whether hippocampal synaptic protection by ketones is a consequence of KATP channel activation. Ketones dose-dependently reversed oxidative impairment of hippocampal synaptic integrity, neuronal viability, and bioenergetic capacity, and this action was mirrored by the KATP channel activator diazoxide. Inhibition of KATP channels reversed ketone-evoked hippocampal protection, and genetic ablation of the inwardly rectifying K+ channel subunit Kir6.2, a critical component of KATP channels, partially negated the synaptic protection afforded by ketones. This partial protection was completely reversed by co-application of the KATP blocker, 5-hydoxydecanoate (5HD). We conclude that, under conditions of oxidative injury, ketones induce synaptic protection in part through activation of KATP channels. 相似文献
10.
P. Light Y. Shimoni S. Harbison W. Giles R.J. French 《The Journal of membrane biology》1998,162(3):217-223
The effects of thyroid status on the properties of ATP-sensitive potassium channels were investigated. Single-channel recordings
were made using excised inside-out membrane patches from enzymatically dissociated ventricular myocytes from hearts of control
and thyroidectomized rats and each group was studied with and without administration of thyroid hormone.
In patches excised from hypothyroid myocytes the IC50 for ATP inhibition of KATP channels was 110 μm. This value was 3-fold higher than the IC50 in control myocytes (43 μm). Treatment of hypothyroid rats to restore physiological levels of thyroid hormone (tri-iodothyronine, T3), resulted in a return to normal ATP-sensitivity (IC50= 46 μm). In patches from animals rendered hyperthyroid, the IC50 for ATP was 50 μm and this value was not significantly different from the control. There was no difference in the cooperativity of ATP-binding
(Hill coefficient, nH) among control (nH= 2.2), hypothyroid (nH= 2.1), T3-treated (nH= 2.0) and hyperthyroid groups (nH= 2.4). The unitary conductance was unchanged and there was no apparent change in intraburst kinetics between examples of
single KATP channels from control and hypothyroid rats. Action potentials recorded in myocytes from hypothyroid rats were significantly
shortened by 50 μm levcromakalim, a KATP channel opener (P < 0.001) but unchanged in control myocytes.
We conclude that hypothyroidism significantly decreased the ATP-sensitivity of KATP channels, whereas the induction of hyperthyroid conditions did not alter the ATP-sensitivity of these channels. Thus, hypothyroidism
is likely to have important physiological consequences under circumstances in which KATP channels are activated, such as during ischemia.
Received: 1 July 1997/Revised: 24 December 1997 相似文献
11.
目的观察开胸结扎冠状动脉与闭胸明胶海绵栓塞法制备急性心肌梗死(AMI)动物模型的特点。方法分别经开胸结扎犬冠状动脉左前降支主干及闭胸冠脉栓塞的方法阻断冠脉血流;采用单级肢体导联和胸导联方式,在阻断前后监测心电图波形变化;造模72h后取心肌组织行病理切片染色。结果经心电图和病理验证,两种方法均可成功制备犬心梗模型,开胸冠脉结扎犬死亡率较高,而冠脉栓塞成活率高。结论相较开胸冠脉结扎法,闭胸栓塞法制备心梗模型对动物损伤小,成活率高,具推广价值。 相似文献
12.
目的应用心导管介入方法封堵冠状动脉制备兔急性心肌梗死模型。方法选择雄性新西兰兔,先行冠状动脉造影,利用导引钢丝将微导管置于左前降支远端,将高分子栓塞剂与碘油混合配制成封闭胶,经微导管注入血管,造成急性心肌梗死。术前、术中和术后l周记录心电图变化。实验终点切取心肌组织标本分别行苏木素一伊红(H.E)染色、氯化硝基四氮唑蓝(NBT)染色、免疫组化染色。结果造模动物20只,存活16只。冠脉造影显示封闭胶持续滞留于左前降支远端,提示血管完全堵塞。心电图提示存在动态变化,ST段抬高,病理性Q波逐渐形成。心脏大体观测提示左心室前侧壁呈灰白色为梗死区。E染色提示梗死区局部纤维组织增生、疤痕形成、钙盐沉积,缺血区肌束变性、炎症细胞浸润,符合典型心肌梗死的病理变化。NBT染色后测定梗死面积为28.32%±5.21%。免疫组化染色提示缺血区CD34阳性面积和血管新生密度明显高于梗死区及正常组织区(P〈0.05)。结论通过心导管介入方法制备兔急性心肌梗死模型成功,避免了开胸损伤对实验结果的影响,更符合临床急性心肌梗死的病理特点。 相似文献
13.
Harper AA Catacuzzeno L Trequattrini C Petris A Franciolini F 《The Journal of membrane biology》2001,179(2):103-111
The effects of verapamil on the large conductance Ca-activated K (BK) channel from rat aortic smooth muscle cells were examined
at the single channel level. Micromolar concentrations of verapamil produced a reversible flickering block of the BK channel
activity. Kinetic analysis showed that verapamil decreased markedly the time constants of the open states, without any significant
change in the time constants of the closed states. The appearance of an additional closed state — specifically, a nonconducting,
open-blocked state — was also observed, whose time constant would reflect the mean residence time of verapamil on the channel.
These observations are indicative of a state-dependent, open-channel block mechanism. Dedicated kinetic (group) analysis confirmed
the state-dependent block exerted by verapamil. D600 (gallopamil), the methoxy derivative of verapamil, was also tested and
found to exert a similar type of block, but with a higher affinity than verapamil. The permanently charged and membrane impermeant
verapamil analogue D890 was used to address other important features of verapamil block, such as the sidedness of action and
the location of the binding site on the channel protein. D890 induced a flickering block of BK channels similar to that observed
with verapamil only when applied to the internal side of the membrane, indicating that D890 binds to a site accessible from
the cytoplasmic side. Finally, the voltage dependence of D890 block was assessed. The experimental data fitted with a Langmuir
equation incorporating the Woodhull model for charged blockers confirms that the D890-binding site is accessed from the internal
mouth of the BK channel, and locates it approximately 40% of the membrane voltage drop along the permeation pathway.
Received: 11 April 2000/Revised: 17 October 2000 相似文献
14.
为研究视黄醇结合蛋白4(retinol binding protein 4,RBP4)对猪前体脂肪细胞分化的影响,实验构建了RBP4重组腺病毒表达载体,包装并感染猪前体细胞,采用油红O染色和Real-time PCR等方法,检测了过表达RBP4对成脂分化的作用. 研究结果显示,重组腺病毒RBP4载体构建成功,转染猪前体脂肪细胞后,使RBP4的mRNA水平和蛋白水平分别增加了约400倍和20倍. 过表达RBP4能减少脂肪细胞的脂质积累,降低成脂关键基因过氧化物酶体增生物激活受体γ (peroxisome proliferator-activated receptor gamma, PPARγ)和脂肪酸结合蛋白2 (adipocyte protein 2, aP2)的表达. 结果表明,RBP4对猪前体脂肪细胞分化有抑制作用,为进一步研究RBP4对猪前体脂肪细胞分化的作用机制奠定基础. 相似文献
15.
Single inward rectifier K+ channels were studied in Xenopus laevis embryonic myocytes. We have characterized in detail the channel which is most frequently observed (Kir) although we routinely
observe three other smaller current levels with the properties of inward rectifier K+ channels (Kir(0.3), Kir(0.5) and Kir(0.7)). For Kir, slope conductances of inward currents were 10.3, 20.3, and 27.9 pS, in 60, 120 and 200 mM [K+]
o
respectively. Extracellular Ba2+ blocked the normally high channel activity in a concentration-dependent manner (K
A
= 7.8 μm, −90 mV). In whole-cell recordings of inward rectifier K+ current, marked voltage dependence of Ba2+ block over the physiological range of potentials was observed. We also examined current rectification. Following step depolarizations
to voltages positive to E
K
, outward currents through Kir channels were not observed even when the cytoplasmic face of excised patches were exposed to
Mg2+-free solution at pH 9.1. This was probably also true for Kir(0.3), Kir(0.5) and Kir(0.7) channels. We then examined the possibility of modulation of Kir channel activity and found neither ATP nor GTP-γS had any
effect on Kir channel activity when added to the solution perfusing the cytoplasmic face of a patch. Kinetic analysis revealed
Kir channels with a single open state (mean dwell time 72 msec) and two closed states (time constants 1.4, 79 msec). These
results suggest that the native Kir channels of Xenopus myocytes have similar properties to the cloned strong inward rectifier K+ channels, in terms of conductance, kinetics and barium block but does show some differences in the effects of modulators
of channel activity. Furthermore, skeletal muscle may contain either different inward rectifier channels or a single-channel
type which can exist in stable subconductance states.
Received: 16 September 1996/Revised: 14 March 1997 相似文献
16.
A.E. Alekseev L.A. Gomez L.A. Aleksandrova P.A. Brady A. Terzic 《The Journal of membrane biology》1997,157(2):203-214
Opening of ATP-sensitive K+ (KATP) channels by the uncoupler of oxidative phosphorylation, 2,4 dinitrophenol (DNP), has been assumed to be secondary to metabolic
inhibition and reduced intracellular ATP levels. Herein, we present data which show that DNP (200 μm) can induce opening of cardiac KATP channels, under whole-cell and inside-out conditions, despite millimolar concentrations of ATP (1–2.5 mm). DNP-induced currents had a single channel conductance (71 pS), inward rectification, reversal potential, and intraburst
kinetic properties (open time constant, τopen: 4.8 msec; fast closed time constant, τclosed(f): 0.33 msec) characteristic of KATP channels suggesting that DNP did not affect the pore region of the channel, but may have altered the functional coupling
of the ATP-dependent channel gating. A DNP analogue, with the pH-titrable hydroxyl replaced by a methyl group, could not open
KATP channels. The pH-dependence of the effect of DNP on channel opening under whole-cell, cell-attached, and inside-out conditions
suggested that transfer of protonated DNP across the sarcolemma is essential for activation of KATP channels in the presence of ATP. We conclude that the use of DNP for metabolic stress-induced KATP channel opening should be reevaluated.
Received: 10 September 1996/Revised: 27 December 1996 相似文献
17.
目的:研究血清肌酐(serum creatinine,SCr)与非ST段抬高急性冠脉综合征(non-ST-elevation acute coronary syndrome,NSTE-ACS)患者冠脉病变程度及其预后的关系。方法:对293例患者进行回顾性分析,依据冠脉造影结果分为NSTE-ACS组和非冠心病组。根据Gensini积分系统,评价NSTE-ACS患者冠脉病变程度,并将患者分为轻度病变组、中度病变组和重度病变组。检测患者SCr水平,应用SPSS16.0分析SCr与NSTE-ACS患者冠脉病变程度及其预后关系。结果:(1)与非冠心病组相比,NSTE-ACS患者SCr较高(P0.05);其中,重度冠脉病变NSTE-ACS患者SCr水平尤高(P0.001)。(2)SCr是NSTE-ACS冠脉病变的危险因子;SCr与NSTE-ACS冠脉病变程度呈正相关(r=0.263,P0.000);SCr与NSTE-ACS主要心血管不良事件(Major Adverse Cardiovascular Events,MACE)呈正相关(r=0.183,P0.01)。结论:SCr是NSTE-ACS患者冠脉病变的独立危险因子,且与NSTE-ACS患者预后相关。SCr对于NSTE-ACS的诊疗有潜在临床价值。 相似文献
18.
目的:探讨辛伐他汀对早期急性冠状动脉综合症患者血浆及vWF水平的影响。方法:将120例性冠状动脉综合症患者随机分为常规治疗组(60例)与辛伐他汀治疗组(60例),常规治疗组采用拜阿司匹林、硝酸酯类、血管紧张素转换酶抑制剂等,辛伐他汀组在常规治疗基础上加用辛伐他汀;疗程8周。检测患者治疗前后的hs-CRP、LDL-C、HDL-C、TC、TG与vWF等因子水平的变化。选取60例健康人作为对照组。结果:常规治疗组中患者的hs-CRP、TC与vWF的水平明显下降(P〈0.05);辛伐他汀组中患者的hs-CRP、LDL-C、TC、TG与vWF的水平明显下降(P〈0.01)、而HDL-C的水平明显升高(P〈0.05)。与常规治疗组相比,辛伐他汀组中患者的hs-CRP、LDL-C、TG与vWF的的水平变化差异均有统计学意义(P〈0.05)。结论:常规药物联合辛伐他汀治疗早期急性冠状动脉综合症可获得较好的疗效。 相似文献
19.
目的探讨建立急性心功能不全动物模型的可行性。方法完全结扎犬前降支,进行快速右室起搏,使心输出量(CCO)较基础状态稳定地下降50%,分别测定基础及心输出量下降状态下的血压(AP)、血氧(SaO2)、平均右房压(mRAP)、平均肺毛压(mPCWP)、系统血管阻力(SVR)、心腔大小、左室射血分数(LVEF)、血浆肾素活性(PRA)、内皮素(ET)、尿量(UO)、血肌酐(Scr)、肌酐清除率(Ccr)。结果结扎LAD和快速右室起搏后,CCO较基础状态均稳定地下降50%,CCO降低后,AP、SaO2显著下降,mRAP、mPCWP、SVR显著升高;心脏各腔室明显扩大,LVEF显著降低;PRA、ET、Scr明显升高,UO、Ccr明显下降。结论结扎冠状动脉前降支及快速右心室起搏可成功制作急性心功能不全的动物模型。 相似文献
20.
R. Barrett-Jolley A. Comtois N.W. Davies P.R. Stanfield N.B. Standen 《The Journal of membrane biology》1996,152(2):111-116
We investigated the action of adenosine and GTP on KATP channels, using inside-out patch clamp recordings from dissociated single fibers of rat flexor digitorum brevis (FDB) skeletal
muscle. In excised patches, KATP channels could be activated by a combination of an extracellular adenosine agonist and intracellular Mg2+-ATP and GTP or GTP-γ-S. The activation required hydrolyzable ATP and could be partially reversed with Mg2+, suggesting that it may involve a G-protein dependent phosphorylation of KATP channels. We found that KATP channels of the rat FDB could not be activated by Mg2+-ATP alone or by Mg2+-ATP in the presence of extracellular adenosine. Patches whose channel activity had been `rundown' by Ca2+ could not be recovered by adenosine, GTP or Mg2+-ATP. KATP channels activated by adenosine receptor agonists had a similar ATP sensitivity to those under control conditions; but adenosine
appears to be able to switch these KATP channels from an inactive to an active mode.
Received: 29 December 1995/Revised: 22 March 1996 相似文献