小型猪急性心肌梗死后心力衰竭模型的构建

目的应用选择性冠状动脉前降支(LAD)球囊闭塞结合微血栓微球混悬液灌注方法造成心肌缺血坏死,探索建立稳定存活的小型猪急性心肌梗死(AMI)后心力衰竭(HF)动物模型。方法选择中国五指山小型猪18头,行冠脉造影后沿血管送球囊至LAD中段,依次扩张球囊阻断前向血流1、2、5 min,每次间隔60 s,然后扩张球囊堵闭血流120 min。再以4F导管超选LAD,行微血栓微球混悬液分次注入,间隔10 min重复注射,TIMI心肌灌注分级(TMPG)2级和左室舒张末压(LVEDP)15 mm Hg时停止注射,同时监测心电图及应用漂浮导管监测有创血流动力学参数。并行pigtail导管测量(LVEDP)的变化,待LVEDP稳定在15~18 mm Hg之间后结扎血管,并加压包扎。监测心肌坏死标志物(cTnI和CK-MB)变化。分别于制模前,制模后第1天、7天、14天行心脏超声检查,制模第14天复查有创血流动力学检查,并行心脏病理检查,认定和评价模型的成功率、稳定性和可重复性。结果制模14 d后共有15头小型猪成活,心电图、心肌坏死标记物、病理检查均符合AMI病理生理过程。其中14头小型猪达到动物模型标准【肺毛细血管楔压(PCWP)18 mmHg和心输出量(CO)下降30%以上】,模型成功率为77.78%。制模后第14天PCWP明显升高(P0.01),CO平均下降50.76%;左室射血分数(LVEF)明显降低(P0.01)。病理检查显示心肌梗死面积占左心室面积的25.4%~34.9%。结论球囊闭塞结合微血栓微球混悬液灌注构建小型猪急性心肌梗死后心力衰竭模型具有闭胸、高成功率、稳定和重复性好等优点,较药物、冠状动脉结扎和起搏诱导的心力衰竭模型更接近临床病理生理学特点。     

猪冠状动脉前降支结扎位点和左室功能的线性回归

目的探讨猪冠状动脉前降支(LAD)结扎百分位点和心梗体积、左室射血分数的关系,以期指导研究者能够根据急性心肌梗死模型的心功能要求选择合适的LAD结扎百分位点。方法将47只小型猪开胸结扎心脏LAD中远段约30%~75%的不同百分位点,分别于术前、术后1 h心脏超声检查左室射血分数(LVEF),术后3 d进行常规冠状动脉造影,4周处死测量前降支结扎位点和梗死体积,最后用简单直线回归模型分析LAD结扎百分位点和心梗体积、左室射血分数回归方程和相关系数。结果47例动物手术过程中死亡8只,剩余39只存活动物冠状动脉造影均显示LAD中远段结扎部位处完全闭塞,表明手术成功。LAD结扎百分位点和术后1 h LVEF、术后1 hLVEF下降值、梗死心肌体积均明显相关(相关系数r分别为0.87、0.78和0.90,P均<0.001),其回归方程分别为:术后LVEF(%)=65.88-0.55x结扎百分位点;术后LVEF下降值(%)=0.12 0.59x结扎百分位点;心肌梗死体积(%)=0.53x结扎百分位点-5.43。结论猪LAD结扎百分位点和术后左室功能、梗死心肌体积均存在显著的相关性,可根据实验目的和对心功能的要求选择合适的结扎百分位点。     

心肌声学造影视觉评估兔急性心肌梗死后的微循环

目的在兔急性心肌梗死模型上应用心肌声学造影视觉评估方法评价急性心肌梗死后梗死节段的血流灌注状况。方法将20只清洁级日本大耳兔随机分组,建立急性心肌梗死模型组(A组)和假手术对照组(S组)。采集术前及术后10、45 min心电图,并在术前及术后20 min、2 h、6 h进行常规超声及超声造影,综合评估分析兔急性心肌梗死后造模节段血流灌注情况。实验结束后取出造模节段心肌组织进行病理学检查。结果常规超声心动图均表明缺血后不同时间点造模节段运动幅度显著改变,心肌组织学有显著改变,表明成功建立了日本大耳兔急性心肌梗死模型;同时心肌声学造影视觉评估表明A组造模节段心肌血容量及灌注速度均显著低于非梗死节段及S组对应节段,与常规超声心动图和病理组织学的检查结果一致。结论心肌声学造影的视觉评估能够准确判定急性心肌梗死后梗死心肌节段的血流灌注的状况,是一种有效的诊断手段。     

经股动脉明胶海绵栓塞介入法建立犬精确局灶急性心梗模型

目的:探讨自制明胶海绵栓子经股动脉栓塞介入术制作稳定的犬精确局灶急性心肌梗死模型的可行性.方法:在数字减影血管造影(DSA)引导下,对12只杂种犬用明胶海绵颗粒经微导管栓塞左前降支(LAD)第二对角支远端分支,致前室壁或下壁缺血/梗死;于术前、术后行冠脉造影、心电图、99mTcN-MPO单光子发射型计算机断层(SPECT)心肌灌注显像,术前2h及术后1、3、6、12、24h检测肌酸激酶(CK)、肌酸激酶同工酶(CK-MB)、乳酸脱氢酶(LDH)、谷草转氨酶(AST)、肌钙蛋白I(cTnI);4W后动物处死,苏木素-伊红(HE)染色病理学确认梗死.结果:介入栓塞LAD远端分支后,2只犬由于出现室性纤颤而死亡,10只犬心梗后24h存活,连续观察28d后依然存活良好.与自身对照相比,心梗后冠脉造影示LAD远端分支闭塞;心电图VI-V3,Ⅱ,Ⅲ,aVF表现为S-T段抬高;99mTcN-MPO SPECT心肌断层显像示心梗区放射性核素摄取明显减低或缺损;AST、CK、CK.MB、LDH、cTnl均于术后升高;HE染色示心肌细胞核消失、碎裂,胞质均质红染,间质水肿.结论:微创介入法制作犬精确局灶心梗模型,具有良好的可重复性与安全性,可以为临床研究急性心肌梗死提供可靠的技术平台.     

超声心动图对缺血性二尖瓣反流血流动力学的研究

目的:应用超声心动图研究缺血性二尖瓣反流(IMR)所致左室、二尖瓣环动力学变化。方法:超声心动图检测86例缺血性二尖瓣反流患者(前壁心肌梗死49例,下壁心肌梗死37例)和30例正常人的心脏,测量左室参数及二尖瓣环形态参数。结果:IMR组左室EDV、ESV增加,LVEF减低,但与对照组无显著差异;二尖瓣环面积及位移与对照组有显著差异;不同部位心肌梗死均发生明显左室重构;下壁梗死组PPM-AMP明显延长。结论:超声心动图作为心肌梗死患者的常规检查,可以针对不同患者进行不同的参数检查,这也为临床医生选择个性化治疗方案和疗效评价提供了依据。     

改良左旋支结扎法微创小型猪急性心肌梗死模型建立与评估

目的应用改良的左冠状动脉回旋支结扎方法联合微创手术,制备小型猪急性心肌梗死模型,评估其有效性和稳定性,并探讨其在科研应用中的意义。方法选择3月龄巴马香猪25头,麻醉下行气管插管呼吸机辅助通气,微创开胸结扎左旋支中段,建立急性心肌梗死模型。并于术前、术后1 h、4周行心脏超声评估模型动物的心脏功能,术后4周处死动物,取心脏行TTC染色评估梗死面积及病理变化,统计死亡率和死亡原因。结果结扎术后1 h和4周后心脏功能较术前均明显降低,EF值由(64.2±4.6)%分别降至(48.2±5.3)%和(49.7±6.1)%(P0.01),左心室侧壁室壁厚度变薄,胶原增生。梗死后1 h室颤率17.3%,梗死面积为(19.2±3)%。结论应用改良的左冠状动脉回旋支结扎方法联合微创手术能够建立稳定的猪心肌梗死模型,具有手术创伤小、模型稳定和死亡率低等特点,为相关研究提供了经济、理想的动物模型。     

急性心肌梗死患者脑钠肽水平与血管病变的关系

目的:探讨急性心肌梗死患者血浆脑钠肽(BNP)水平与梗死相关动脉及病变血管的关系。方法:选取2010.7-2011.7于上海市第一人民医院诊断为急性心肌梗死的患者。分为ST抬高型心梗患者和非ST抬高型心梗患者两组,比较BNP水平与血管病变的关系。结果:(1)两组患者的年龄、男女比例、高血压病与糖尿病患病率、吸烟患者比例之间无显著差异。NSTEMI患者中,既往心梗和既往经皮冠状动脉成形术(PTCA)的比例和左室射血分数明显高于STEMI患者。(2)NSTEMI患者多支血管病变比例显著高于STEMI患者并且梗死相关动脉为左回旋支(LCX)的比例显著高于STEMI患者。(3)病变血管支数与心梗患者BNP水平无关,STEMI患者左冠状动脉前降支(LAD)为IRA的患者BNP水平显著高于LCX和右冠状动脉(RCA)分别为IRA的患者。NSTEMI患者LAD、LCX和RCA分别为IRA的患者其BNP水平无显著差异。结论:STEMI患者前壁心梗BNP水平较高,NSTEMI患者BNP水平对血管病变支数和IRA无预测价值。     

小型猪急性心肌梗死模型的建立及其评价

目的探索结扎小型猪冠状动脉左前降支（LAD）建立急性心肌梗死模型及进行血流评价的方法。方法小型猪20头全麻下开胸暴露心脏,预阻断LAD（第二对角支）15min,后予结扎,术中心电图动态监测,术后进行冠状动脉造影,心肌酶学监测以确定模型建立情况,冠状动脉造影以及^13N-NH3 PET心肌血流测定评价手术后血流改变。结果20头小型猪中有16头存活4周,成活率80％,开胸手术中1头因麻醉意外死亡,3头死于术后呼吸不畅。结扎后心电图呈动态变化,24h后血清心肌酶谱（CK,CK—MB,cTnI）较术前明显增高,差异有统计学意义（P〈0．05）,冠状动脉造影显示LAD血流中断,TIMI分级为0级,^13N—NH3 PET检查显示手术后缺损面积百分比（27．0±5．0）较手术前（4．0±3．2）有显著性差异,证实心梗模型建立成功。结论本实验中开胸手术成功率高,术后血流评价方法可用于手术前后冠脉血流和心肌血流的比较以及对心肌梗死后治疗效果进行评价。     

大鼠自主呼吸下建立急性心肌梗死模型

目的大鼠自主呼吸情况下,快捷、简便地建立大鼠急性心肌梗死模型。方法 180～220gSD大鼠60只,于胸骨左缘第4-5肋间隙切开皮层作荷包缝合,逐层钝性分离肌肉,挤出心脏,快速结扎左冠状动脉前降支(LAD)后,送回心脏同时挤压胸廓,拉紧荷包以建立心肌梗死模型。记录结扎前、结扎后3h心电图;结扎3h后取出心脏,冰冻切片TTC染色。结果 50只大鼠成功建立心肌梗死模型,模型成功率为83.33%。心电图显示结扎冠脉后出现R波峰降低,ST段拱背抬高及ST-T融合,TTC染色后左心室出现明显灰白色梗死区。结论本方法可在大鼠自主呼吸情况下,较短的时间内以简便的手术、较小的创伤建立大鼠急性心肌梗死模型。     

猪急性心肌梗死模型发生心室颤动的相关因素分析

目的探讨猪冠状动脉前降支(LAD)结扎后发生室颤的特点及其相关因素,以期提高猪急性心肌梗死模型的成活率。方法57只小型猪开胸结扎心脏LAD不同位点,对室颤和体重、性别、术前心率、术前左室射血分数(LVEF)、开胸径路(旁正中/肋间)、手术时间、结扎百分位点、术后心率、术后发生室早或短阵室速等因素进行单因素相关分析和Logistic回归分析,进而对室颤的发生时间、室颤前心电图特点等进行评价。结果57例动物手术过程发生室颤18例,死亡11例。室颤均发生在结扎冠脉后35 min内,高峰时间为结扎冠脉后5 min和20 min;心率快于160 bpm或慢于60 bpm时容易诱发室颤。与非室颤组动物比较,室颤组动物的结扎位点高,术后最快心率>60 bpm的动物较多,短阵室速发生率高(P<0.01)。Logistic回归分析显示结扎位点过高是急性心肌梗死后发生室颤唯一的独立危险因素。结论结扎位点过高是猪急性心肌梗死后发生室颤的最重要危险因素;冠脉结扎后30 min内应该严密心电监护,特别注意结扎冠脉后5 min和20 min二个时间点、>160 bpm或<60 bpm二种心率、以及短阵室速等先兆事件。     

小型猪心肌梗死介入治疗后无复流动物模型的制备

目的制备猪急性心肌梗死冠状动脉介入治疗（AMI—PCI）后无复流（no—reflow）动物模型。方法五指山小型猪26头,行左、右冠状动脉造影和左心室造影,记录有创血流动力学参数,通过球囊闭塞、微血栓注入造成左前降支无复流,监测体表和冠脉内心电图变化。结果制模共有21头猪成活,19头达到AMI—PCI后无复流动物模型标准,即TIMI血流≤2级,校正的TIMI血流记帧法（CTFC）≥36．2帧,制模成功率73．1％。无复流模型建立成功后心率增快,血压下降,心肌耗氧量增加,左心室舒张期末压和肺毛细血管楔压升高,较闭塞前均具有统计学差异（P〈0．05）。实验过程中,体表心电图和冠状动脉内心电图均出现类似人AMI再灌注的心电图演变规律。结论选择性冠状动脉前降支急性闭塞、再灌注、微血栓注入制备的无复流小型猪动物模型是可行的。     

Exercise training improves endothelium-mediated vasorelaxation after chronic coronary occlusion.

The present study evaluated combined effects of chronic coronary occlusion and exercise training on endothelial function. Gradual occlusion was produced by placement of an ameroid constrictor around the proximal left circumflex (LCX) coronary artery of female swine. Two months after placement of the ameroid, animals were restricted to their pens or exercise trained for 16 wk. Epicardial arteries (>500 microm ID) were isolated from the collateral-dependent LCX coronary artery distal to the occlusion and the nonoccluded left anterior descending (LAD) coronary artery. Bradykinin- and ADP-mediated relaxation of LCX and LAD coronary arteries was enhanced after exercise training. Inhibition of nitric oxide synthase with N(G)-nitro-L-arginine methyl ester decreased bradykinin- and ADP-mediated relaxation in LCX and LAD myocardial regions. Importantly, combined inhibition of effects of endothelium-derived hyperpolarizing factor with increased extracellular K(+) (20-30 mM) and nitric oxide synthase completely abolished coronary LAD and LCX relaxation to bradykinin. Our data indicate that exercise training improves endothelium-mediated relaxation of arteries isolated after chronic coronary artery occlusion, likely as a result of enhanced production of nitric oxide and endothelium-derived hyperpolarizing factor.     

Intracoronary delivery of autologous bone marrow mononuclear cells radiolabeled by 18F-fluoro-deoxy-glucose: tissue distribution and impact on post-infarct swine hearts

Intracoronary injection of the bone marrow-derived mononuclear cells (MNCs) is emerging as a potentially novel therapy for ischemic heart failure. This study was aimed at assessing the efficacy of intracoronary MNC delivery in the myocardium. The in vivo distribution and myocardial homing of intracoronarily delivered MNCs in experimental Chinese swine with acute myocardial infarction (AMI) created by occlusion of left anterior descending (LAD) coronary artery for 90 min. MNCs radiolabeled with 18F-fluoro-deoxy-glucose (18F-FDG) were delivered using a coronary catheter into the infarct-related coronary artery 1 week after AMI. Dual-nuclide single photon emission computed tomography (SPECT) revealed that 1 h after cell infusion, 6.8 +/- 1.8% of 18F-FDG-labeled MNCs occurred in the infarcted myocardium with the remaining activity found primarily in the liver and spleen. In the heart, MNCs were detected predominantly in the under-perfused myocardium. The infused cells retained in the hearts at a rate highly correlated with the under-perfused lesional sizes. Pathological examination further demonstrated that 6 weeks after infusion, compared to controls, the hearts receiving MNCs exhibited less fibrosis and inflammatory infiltrate, more viable tissue, and higher vascular density. Cardiac function was significantly improved in the MNC-infused hearts. Thus, 18F-FDG labeling and dual-nuclide SPECT imaging is capable of monitoring in vivo distribution and homing of MNCs after intracoronary infusion. MNC coronary delivery may improve cardiac function and positive ventricular remodeling in the heart with AMI.     

Catheter-based antegrade intracoronary viral gene delivery with coronary venous blockade

The purpose of this study is to evaluate the feasibility of percutaneous antegrade myocardial gene transfer (PAMGT). A consistent and safe technique for in vivo gene transfer is required for clinical application of myocardial gene therapy. PAMGT with concomitant coronary venous blockade was performed in 12 swine. The myocardium was preconditioned with 1 min of occlusion of the left anterior descending and left circumflex arteries. The anterior interventricular vein was occluded during left anterior descending artery delivery, and the great cardiac vein at the entrance of the middle cardiac vein was occluded during left circumflex artery delivery. With arterial and venous balloons inflated (3 min) and after adenosine (25 mug) injection, PAMGT was performed by antegrade injection of an adenoviral solution (1 ml of 10(11) plaque-forming units in each coronary artery) carrying beta-galactosidase or saline through the center lumen of the angioplasty balloon. In one set of animals, PAMGT was performed with selective coronary vein blockade (n = 9); in another set of animals, PAMGT was performed without coronary vein blockade (n = 5). At 1 wk after gene delivery, the animals were killed. Quantitative beta-galactosidase analysis was performed in the left and right ventricular walls. PAMGT was successfully performed in all animals with and without concomitant occlusion of the coronary veins. Quantitative beta-galactosidase analysis showed that PAMGT with coronary blockade was superior to PAMGT without coronary blockade. beta-Galactosidase activity increased significantly in the beta-galactosidase group compared with the saline group: 1.34 +/- 0.18 vs. 0.81 +/- 0.1 ng (P 相似文献   

Effects of gradual coronary artery occlusion and exercise training on gene expression in swine heart

Gradual occlusion (O) of the swine left circumflex coronary artery (LCX) with an ameroid occluder results in complete O within 3 weeks, collateral vessel development, and compensatory hypertrophy. The purpose of this investigation was to determine the independent and combined effects of O and exercise training (E) on gene expression in the swine heart. Adult Yucatan miniature swine were assigned to one of the following groups (n = 6–9/group): sedentary control (S), exercise-trained (E), sedentary swine subjected to LCX occlusion (SO), and exercise-trained swine with LCX occlusion (EO). Exercise consisted of progressive treadmill running conducted 5 d/wk for 16 weeks. Gene expression was studied in myocardium isolated from the collateral-dependent left ventricle free wall (LV) and the collateral-independent septum (SEP) by RNA blotting. E and O each stimulated cardiac hypertrophy independently (p < 0.001) with no interaction. O but not E increased atrial natriuretic factor expression in the LV, but not in the SEP. E decreased the expression of β-myosin heavy chain in the LV, but not in the SEP. E retarded the expression of collagen III mRNA in SEP; but not in the LV. Exercise training and coronary artery occlusion each stimulate cardiac hypertrophy independently and induce different patterns of gene expression.     

Up-regulated synthesis of mature-type adrenomedullin in coronary circulation immediately after reperfusion in patients with anterior acute myocardial infarction

OBJECTIVE: Levels of adrenomedullin (AM), a potent vasodilatory peptide, have been shown to increase in the early stage of acute myocardial infarction (AMI). The purpose of this study was to determine whether coronary sinus-aortic step-up of mature forms of AM is accelerated in patients with AMI after reperfusion. METHODS: The subjects were 29 consecutive patients with a first episode of anterior AMI and 10 normal controls. All patients with AMI underwent balloon reperfusion therapy within 24 h after symptom onset. Plasma levels of two molecular forms of AM (an active, mature form [AM-m] and an intermediate, inactive glycine-extended form [AM-Gly]) in the aorta and coronary sinus (CS) were measured by specific immunoradiometric assay after reperfusion. RESULTS: Plasma levels of AM-m and AM-Gly in the aorta and CS were higher in AMI patients than in controls. CS-aortic step-up of AM-m, which is an index of myocardial production of AM-m, was significantly greater in AMI patients than in controls (1.7 +/- 1.4 vs. 0.4 +/- 0.3 pmol/L, P < 0.01). However, there was no significant difference in CS-aortic step-up of AM-Gly (P = 0.30). AMI patients with left ventricular dysfunction (n = 10) had a significantly higher CS-aortic AM-m step-up than AMI patients without left ventricular dysfunction (n = 19). AM-m in the aorta and CS negatively correlated with the left ventricular ejection fraction (r = -0.50, r = -0.48, P < 0.01). CONCLUSIONS: Myocardial synthesis of AM-m is accelerated in patients with reperfused AMI, especially in patients with critical left ventricular dysfunction. Increased myocardial synthesis of active AM may protect against cardiac dysfunction, myocardial remodeling, or both after the onset of AMI.     

Early results of endovascular treatment of chronic coronary occlusion in patients with ischemic heart disease

The early results of endovascular treatment of chronic coronary occlusion were studied. Immediate success rates were 67%. The factors that promote successful endovascular treatment in patients with this condition were as follows: less than 2-month disease duration, well-developed intersystemic collaterals, no "bridge" collaterals. Successful recanalization for chronic coronary occlusion improves the quality of life and bicycle ergometer test finding in patients, which reduces their needs of nitrates and beta-blockers. Coronary occlusion stenting yields better immediate angiographic results than does balloon angioplasty: residual stenosis and the minimum diameter of stenosis after stenting were 13.61 +/- 6.3% and 2.69 +/- 0.4 mm, respectively; those after balloon angioplasty were 23.1 +/- 8.1% and 2.31 +/- 0.37 mm, respectively.     

Protective effect of peptide semax the rat heart in acute myocardial infarction

Semax, a member of ACTH-derived peptides family, has been employed in the treatment of acute ischemic stroke in patients. It decreased neurological deficit and reduced NO hyperproduction in the rat brain, caused by acute cerebral hypoperfusion. We suggested that semax is also able to protect rat heart from ischemic damage in acute myocardial infaction (AMI). AMI was induced by left coronary artery occlusion, myocardial ischemic area averaged 30 % of left ventricle. In 2 hours after coronary occlusion, the AMI group developed 11 % reduced mean arterial blood pressure and 48 % increased diastolic blood pressure in left ventricle in comparison with sham-operated control group. However, infusion of either dobutamine, which directly stimulates myocardial contractility, or sodium nitroprusside and phenylephrine, that change vascular resistance and thus cardiac afterload, did not reveal distinctions in hemodynamic parameters between groups. These data indicate absense or only moderate cardiac dysfunction in rats with AMI and are consistent wih morphometrical and histochemical studies that did not detect any necrotic or apoptotic (TUNEL-test) changes in left ventricular cardiomyocytes in spite of development of distinct ischemic disturbances of mitochondria and nuclear in about 50 % of cardiomyocytes in 2 hours after AMI. Semax (150 microg/kg), given i. p. 15 min and 2 hours after coronary occlusion, caused no effect on cardiac function, but completely prevented ischemia-induced ultrastructural changes of cardiomyocytes. This protective effect was accompanied by the ability of peptide to blunt the increase in plasma concentrations of nitrates, observed in AMI group.     

Exercise training increases basal tone in arterioles distal to chronic coronary occlusion

Endurance exercise training increases basal active tone in coronary arteries and enhances myogenic tone in coronary arterioles of control animals. Paradoxically, exercise training has also been shown to augment nitric oxide production and nitric oxide-mediated relaxation in coronary arterioles. The purpose of the present study was to examine the effect of exercise training on basal active tone of arterioles (approximately 150 microm ID) isolated from the collateral-dependent region of hearts exposed to chronic coronary occlusion. Ameroid occluders were surgically placed around the proximal left circumflex coronary artery of miniature swine. Arterioles were isolated from both the collateral-dependent and nonoccluded myocardial regions of sedentary (pen confined) and exercise-trained (treadmill run; 14 wk) pigs. Coronary tone was studied in isolated arterioles using microvessel myographs and standard isometric techniques. Exposure to nominally Ca2+-free external solution reduced resting tension in all arterioles; decreases were most profound (P < 0.05) in arterioles from the collateral-dependent region of exercise-trained animals. Furthermore, nitric oxide synthase (NOS) inhibition (N(omega)-nitro-L-arginine methyl ester; 100 microM) unmasked markedly increased nitric oxide-sensitive tone in arterioles from the collateral-dependent region of exercise-trained swine. Blockade of K+ channels revealed significantly enhanced K+ channel contribution to basal tone in collateral-dependent arterioles of exercise-trained pigs. Protein content of endothelial NOS (eNOS) and phosphorylated eNOS (pS1179), determined by immunoblot, was elevated in arterioles from exercise-trained animals with the greatest effect in collateral-dependent vasculature. Taken together, we demonstrate the interaction of opposing exercise training-enhanced arteriolar basal active tone, nitric oxide production, and K+ channel activity in chronic coronary occlusion, potentially enhancing the capacity to regulate blood flow to collateral-dependent myocardium.