用左室辅助装置和药物治疗逆转心力衰竭

研究曾报告，少数严重心力衰竭（简称心衰）患者长期用一种左室辅助装置（LVAD）减轻心肌负荷，心肌可望恢复，时间长短不一。恢复越频，时间越长，可望减少或推迟日后心脏移植的需要。     

葡萄糖、1，6－二磷酸果糖对心肌保护作用的实验研究

本实验采用离体鼠心模型证实，用含葡萄糖的停跳液单次灌注心脏，心肌组织乳酸产生增加，引起心肌组织酸中毒，心肌结构破坏严重，心功能恢复差，心肌酶漏出较多。而用分别含有葡萄糖和１．６—二磷酸果糖的停跳液多次灌注心脏的两个组，能及时将乳酸冲洗掉。防止了心肌酸中毒，心肌结构损伤减轻，心功能恢复改善，心肌酶漏出较少。研究表明在停跳液中加入葡萄糖、１．６─二磷酸果糖并结合多次灌注方法，能改善心肌保护的效果。     

腺苷在急性心肌梗死再灌注损伤中的心肌保护作用

急性心肌梗死（AMI）是一种严重的心血管疾病，其发病率、致残率及病死率都很高，有效的治疗措施是通过溶栓或经皮冠状动脉介入治疗（PCI）尽早恢复病变心肌的有效血液供应，从而减少心肌坏死、防止心室重构、改善心功能、减少心律失常，有效降低病死率。然而，缺血心肌恢复再灌注后，因再灌注损伤产生心肌形态及功能异常变化，甚至可能使部分缺血存活的心肌坏死而失去活性。严重影响了缺血心肌再灌注治疗的效果。令人鼓舞的是大量的研究已经证实腺苷能够预防和逆转无复流现象，防治心肌缺血再灌注损伤。现就心肌再灌注损伤及腺苷在AMI再灌注损伤中的心肌保护作用做一综述。[第一段]     

无创性检查技术估测心肌活力

无创性检查技术估测心肌活力上海医科大学附属华山医院严萍萍综述．戴瑞鸿审校缺血可引起不伴心肌坏死的心肌功能障碍，这种状态下的心肌被认为是有活力的心肌。因这种心肌的代谢完整，当冠脉血运重建后心肌功能还有恢复的可能，心肌功能障碍但心肌仍有活力临床上有二种状...     

依那普利预处理对心肌内源性保护机制的影响

目的探讨依那普利预处理对心肌内源性保护机制的影响。方法用依那普利预处理大鼠心肌48h，心脏低温保存6h，Langendorff模型再灌注，观察心功能及磷酸肌酸激酶同工酶(CK-MB)变化。结果依那普利预处理组左心室收缩-舒张压差、+dp/dt、冠状动脉流量(CF)等保存6h后功能恢复百分率明显高于、心肌CK-MB漏出明显低于非依那普利预处理组。依那普利预处理同时加用蛋白激酶C(PKC)抑制剂多粘菌素B(PMB)，保存后功能恢复降低至非依那普利预处理组水平；单独用PMB预处理，对心功能恢复无影响。结论依那普利预处理大鼠心肌可以减轻心肌缺血损害，改善心脏保存后功能恢复。其心肌保护作用机制可能与PKC活性有关。     

急性心肌梗塞后应用多巴酚丁胺负荷超声心动图对心肌存活性的研究

本文目的应用多巴酚丁胺负荷超声心动图研究急性心肌梗塞后梗塞区域心肌存活性。选择36例急性心肌梗塞患者，用5μg／kg·min多巴酚丁胺静脉滴注，体表超声心动图于用药前后对比观察梗塞区域心肌室壁运动和收缩期增厚率（T％），识别心肌存活性。36例患者分为576段心肌，基础状态下94段心肌运动消失，T％为0。静注5μg/kg·min多巴酚丁胺后，94段心肌中30段心肌恢复或部分恢复运动，T％增加121～60．0％。结果提示94段运动消失的心肌中30段（31．9％）具有存活性。表明多巴酚丁胺负荷超声心动图对急性心肌梗塞后存活心肌的识别是安全、可靠的，具有十分重要的临床意义。     

葡萄糖,1,6—二磷酸果糖对心肌保护使用的实验研究

本实验采用离体鼠心模型证实，用含葡萄糖的停跳液单次灌注心脏，心肌组织乳酸产生增加，引起心肌组织酸中毒，心肌结构破坏严重，心功能恢复差，心肌酶漏出较多。而用分别含有葡萄糖和１．６－二磷酸果糖的停跳液多次灌注心脏的两个组，能及时乳时将乳酸冲洗掉。防止了心肌酸中毒，心肌结构损伤减轻，心功能恢复改善，心肌酶漏出较少。研究表明在停跳液中加入葡萄糖，１．６－二磷酸果糖并结合多次灌注方法，能改善心肌保护的效果。     

禁食大鼠可能经抑制mTOR减低心肌摄取葡萄糖

目的 确定禁食降低心肌摄取葡萄糖的动态变化过程，探寻禁食降低大鼠心肌摄取葡萄糖能力的可能机制，为阐明禁食提高缺氧耐力作用奠定基础。 方法 测量不同禁食时间和恢复饮食组雄性SD大鼠体质量、血糖和血酮水平；采用M型超声心动图测量SD大鼠禁食后及恢复饮食后心脏泵血功能；对各组SD大鼠行18F-FDG PET/CT显像，定量观测心肌FDG摄取；检测不同葡萄糖浓度培养心肌细胞的mTOR和AMPK表达与活性。 结果 SD大鼠体质量随禁食时间延长显著下降，并在恢复饮食24 h后恢复至接近禁食前水平；禁食24 h血糖显著降低， 48 h达稳定水平，相反，禁食24 h血酮显著升高，在48 h达稳定水平；在恢复饮食24h后，血糖与血酮均恢复至正常水平。禁食各时间点及恢复饮食后心脏泵血功能均无明显改变。PET/CT显示心肌18F-FDG摄取（SUV ratio）在禁食24 h后显著减低，并在正常饮食24h后恢复。降低培养心肌细胞的葡萄糖浓度，mTOR和AMPK的蛋白表达水平未见改变，但是，mTOR活性降低，AMPK活性增加。 结论 禁食引起低血糖可直接降低mTOR活性，另一方面，低血糖通过激活AMPK，间接抑制mTOR 活性，可能进而抑制心肌对18F -FDG摄取。     

腺苷受体对缺血/再灌注心脏保护作用的研究进展

恢复冠状动脉血流和心肌再灌注对于缺血缺氧的心肌复苏是十分必要的，然而缺血心肌在再灌注时也可导致心肌损伤。腺苷是组织缺血时所释放的一种内源性生理活性物质，越来越多的证据证明，腺苷在心血管疾病的治疗中发挥着重要作用，尤其是对心肌的保护作用倍受关注，本文就此方面的研究现状作一综述。     

实验性顿抑心肌微血管结构和功能改变

目的 探讨心肌顿抑时心肌微血管结构和功能改变。方法 制备冠状动脉左前降支（LAD）不同阻断时间（15min和60min)后再灌注犬心肌顿抑模型，在不同观察时间点静脉注射含全氟丙烷声振白蛋白微泡造影剂，采用二次谐波成像和间歇发射技术行心肌声学造影。由主动脉根部分别注射乙酰胆碱（ACH）和硝酸甘油（NG）后重复心肌声学造影，并计算用药后／前二维超声上所示心肌灰阶峰值比值（PVIR）和顿抑区与正常区心肌灰阶峰值比值的比值PVIRR。心肌标本行透射电镜检查。结果 （1）LAD阻断15min组再灌注早期NG－PVIR和ACH－PVIR明显减低，但分别在再灌注60min和120min时恢复至结扎前水平；（2）LAD阻断60min组再灌注早期NG－PVIR减低，至再灌注120min时才恢复到结扎前水平，而再灌注ACH-PVIR明显减低，随着再灌注时间的延长虽有逐渐回升趋势，但至再灌注120min仍未恢复至结扎前水平；（3）两组PVIRR的变化与PVIR一致，唯恢复稍慢；（4）LAD阻断15min组心肌毛细血管和内皮细胞结构未见明显改变，而LAD阻断60min组毛细血管内皮细胞肿胀，内皮细胞间连接间隙稍增宽。结论 顿抑心肌微血管舒张功能受损，缺血时间较长则还有微血管结构改变，其受损的细胞主要是内皮细胞。     

Staged reperfusion attenuates myocardial stunning in dogs. Role of transient acidosis during early reperfusion.

BACKGROUND. Acidosis during early reperfusion is reported to be beneficial for myocardial stunning. We tested in 31 dogs the hypothesis that staged reperfusion is beneficial to myocardial stunning. METHODS AND RESULTS. Contractile dysfunction was observed 3 hours after the onset of reperfusion after 15 minutes of occlusion of the coronary artery. In the staged reperfusion, pH of the coronary venous blood was lower for 20 minutes and fractional shortening was significantly improved compared with the control reperfusion group. When we increased pH of the reperfused myocardium by an intracoronary infusion of sodium bicarbonate, beneficial effects of the staged reperfusion were abolished. Furthermore, an intracoronary infusion of hydrogen chloride, which mimicked the changes in pH in coronary venous blood of the staged reperfusion, attenuated myocardial stunning. CONCLUSIONS. These results indicate that acidosis during staged reperfusion primarily attenuates myocardial stunning. This procedure is clinically applicable for attenuation of reperfusion injury.     

丙酮酸对顿抑心肌功能及能量代谢的作用

目的　了解丙酮酸对顿抑心肌功能及能量代谢的影响 ,并分析其可能机制。方法　结扎家兔左冠状动脉前降支 2 0min后 ,再灌注 6h造成短暂缺血 再灌注心肌顿抑模型 ,观察血流动力学、抗氧化酶、脂质过氧化物、血清游离脂肪酸 (FFA)、乳酸 (LD)以及心肌组织的ATP含量和超微结构变化。结果　与顿抑组比较 ,丙酮酸可明显缓解缺血及再灌后心肌功能的损害 ,抑制血清FFA、LD水平的升高 ,降低MDA含量 ,提高SOD活性 ,抑制心肌组织ATP含量降低 ;电镜所见心肌损伤明显比顿抑组轻。丙酮酸组与对照组比较 ,各指标均为显著性差异。结论　丙酮酸可以减少心肌细胞能量消耗 ,保护线粒体的结构和功能 ,对顿抑心肌具有一定保护作用     

Evidence for a role of platelet activating factor in the pathogenesis of irreversible but not reversible myocardial injury after reperfusion in dogs

The role of platelet activating factor (PAF) in myocardial injury after either brief (15 minutes, stunned myocardium) or prolonged (90 minutes, infarcted myocardium) coronary artery occlusion and 3 hours of reperfusion of the left anterior descending coronary artery was investigated in barbital-anesthetized dogs. Regional myocardial blood flow was measured by radioactive microspheres, regional segment shortening by sonomicrometry, and infarct size by the triphenyltetrazolium chloride stain. Infarct size expressed as a percentage of the area at risk was significantly reduced by the intravenous administration of two structurally unrelated PAF antagonists, BN 52021 (10 mg/kg and 1 mg/kg/hr) and CV-3988 (3 mg/kg and 0.3 mg/kg/hr). Infarct size was 38% +/- 5% in the saline (control) group, (n = 7), 22% +/- 5% in the BN 52021 group (n = 7), and 19% +/- 5% in the CV-3988 group (n = 8). However, the intravenous administration of BN 52021 (5 and 10 mg/kg) and CV-3988 (5 mg/kg) had no effect on functional recovery (regional segment shortening) in the stunned myocardium after brief occlusion and reperfusion. Regional myocardial blood flow, hemodynamic data, and the incidence of cardiac arrhythmias were not significantly affected by PAF antagonists in both series of experiments at any time. These data suggest that PAF may play an important role in the pathogenesis of an evolving myocardial infarction that follows a prolonged coronary artery occlusion and reperfusion. Furthermore, PAF antagonists may have a beneficial role in reduction of the injury produced during an acute infarction. Finally, these data indicate that PAF does not appear to be an important mediator of myocardial stunning.     

Decreased myofilament responsiveness in myocardial stunning follows transient calcium overload during ischemia and reperfusion.

The purpose of this study was to test the hypothesis that abnormal intracellular calcium handling characterizes myocardial stunning. Isolated, isovolumic, buffer-perfused ferret hearts were loaded with the bioluminescent calcium indicator aequorin for simultaneous measurement of individual calcium transients and left ventricular pressure. After 15 minutes of global ischemia and 20 minutes of reperfusion, left ventricular developed pressure was significantly reduced (75 +/- 7 versus 93 +/- 6 mm Hg, p < 0.05). During ischemia, [Ca2+]i levels were significantly elevated compared with preischemic levels, both during systole (1.38 +/- 0.31 versus 0.88 +/- 0.2 microM, p < 0.05) and end diastole (0.85 +/- 0.16 versus 0.38 +/- 0.13 microM, p < 0.05). Early during reperfusion, [Ca2+]i was also significantly elevated during systole (1.63 +/- 0.44 versus 0.88 +/- 0.20 microM, p < 0.05) and end diastole (0.75 +/- 0.15 versus 0.38 +/- 0.13 microM, p < 0.05). After 20 minutes of reperfusion, myocardial stunning occurred, but [Ca2+]i was not significantly different from preischemic levels. Thus, myocardial stunning does not result from decreased levels of activator calcium. The force-pCa relation generated by the stunned hearts was shifted downward compared with that generated by the control hearts, consistent with a decrease in maximum calcium-activated force (Fmax). At steady state during tetanus, the decrease in Fmax was confirmed, but there was no significant difference in the slope of the force-pCa relation of the stunned hearts versus controls. Thus, we conclude that stunned myocardium is characterized by decreased Fmax without desensitization of the myofilaments to [Ca2+]i.(ABSTRACT TRUNCATED AT 250 WORDS)     

Intravenous magnesium reduces infarct size after ischemia/reperfusion injury combined with a thrombogenic lesion in the left anterior descending artery

Experimental studies have demonstrated that intravenous magnesium (Mg) can protect the ischemic myocardium and has an antithrombotic effect. In patients with myocardial infarction, the reperfusion injury is complicated by the presence of a thrombogenic area in the affected coronary artery that may cause repetitive thrombus formation and embolization. We investigated the effect of Mg on infarct size in a randomized study in pigs. Myocardial infarction was induced by a 50-minute mechanical occlusion of the left anterior descending artery combined with an arterial injury, which stimulated a dynamic thrombus formation with emboli shedding on reperfusion. Magnesium sulfate (6 mmol/20 min plus 3 mmol/h) or saline was started at 30 minutes after coronary occlusion. Real-time ventricular pressure-volume loops were generated from the left ventricle by using a microtip pressure manometer and a conductance catheter. Platelet accumulation in the myocardium was evaluated by using 111In-labeled platelets. After 4 hours of reperfusion, the infarct size/area at risk ratio in the placebo group was 46+/-0.06% (n=8) compared with 22+/-0.07% (n=6) in the Mg-treated animals (P=0. 03). Ejection fraction decreased significantly in the control group but not in the Mg-treated animals (P=0.03). Platelet accumulation in the myocardium did not change significantly between the Mg- and placebo-treated animals (placebo group, 191+/-19%; Mg group, 177+/-29%; NS). The present study demonstrates that intravenous Mg infusion is able to reduce infarct size by >50% and preserve the ejection fraction in this model where ischemia/reperfusion injury was evaluated in the presence of a thrombogenic area in the nutrient artery.     

Ischemic preconditioning reduces infarct size in swine myocardium

We evaluated the hypothesis that stunning swine myocardium with brief ischemia reduces oxygen demand in the stunned region and increases tolerance of myocardium to longer periods of ischemia. Wall function was quantified with ultrasonic crystals aligned to measure wall thickening, and stunning was achieved with two cycles of left anterior descending coronary artery (LAD) occlusion (10 minutes) and reperfusion (30 minutes), after which the LAD was occluded for 60 minutes and reperfused for 90 minutes. Infarct size (as a percent of risk region) was then determined by incubating myocardium with para-nitro blue tetrazolium. Regional oxygen demand was measured as myocardial oxygen consumption before the 60-minute LAD occlusion in the stunned region; tracer microspheres were used to determine blood flow, and blood from the anterior interventricular vein and left atrium was used to calculate oxygen saturations. After the second reperfusion period, wall thickening in the stunned region was reduced to 1.4 +/- 2.4% compared with 36.7 +/- 2.5% (mean +/- SEM) before ischemia (p less than 0.001). Regional myocardial oxygen consumption after stunning (3.1 +/- 0.7 ml O2/min/100 g) was no different from regional myocardial oxygen consumption before stunning (3.7 +/- 0.6 ml O2/min/100 g). In the nine pigs "preconditioned" by stunning, infarct size was 10.4 +/- 6.3% of the risk region compared with 48.0 +/- 12.7% in the six control pigs subjected to 60 minutes of ischemia without prior stunning (p less than 0.005). The risk regions were similar (14.4 +/- 1.5% vs. 14.6 +/- 1.9% of the left ventricle, preconditioned vs. control pigs, respectively). We conclude that stunning swine myocardium with two cycles of a 10-minute LAD occlusion followed by reperfusion increases ischemic tolerance but that changes in regional demand in stunned myocardium do not predict the marked reduction in infarct size that follows a subsequent 60-minute period of ischemia.     

The role of post-ischaemic reperfusion in the development of microvascular incompetence and ultrastructural damage in the myocardium

Summary To determine the contribution of oxygenated reperfusion to the development of myocardial microvascular incompetence and ultrastructural damage following ischaemia, isolated buffer perfused rat hearts were subjected to either temporary (n = 15) or permanent (n =15) ischaemia for 15, 30 or 45 minutes. The temporarily ischaemic hearts were reperfused for 5 min with oxygenated Krebs Henseleit buffer. All hearts were then fixed by perfusion fixation with nitrogen-bubbled glutaraldehyde. The transmural development of microvascular incompetence was determined quantitatively by scanning electron microscopy using nuclear track photographic emulsion as an intravascular marker of competent capillaries, and ultrastructural damage was examined by transmission electron microscopy. Thirty or more minutes of ischaemia where required to significantly reduce the mean density of competent capillaries in the subendocardial third of the left-ventricular wall. Such ischaemic myocardium con tained relatively normal, open unobstructed vessels, indicating that the microvascular incompetence arising during ischaemia per se was not due to ultrastructural change in the capillaries. Subendocardial myocardium reperfused following 15 min ischaemia also showed little ultrastructural change, but did show a significant reduction in the density of competent capillaries. However, reperfusion of more severely ischaemic myocardium resulted in obvious ultrastructural damage as well as significant further reduction in capillary competence. These findings demonstrate that oxygenated reperfusion of ischaemic myocardium paradoxically results in the further development of microvascular incompetence and, in severely ischaemic myocardium, also to additional ultrastructural damage.This research was supported by grants from the Medical and Health Research Councils of New Zealand.     

Assessment of myocardial salvage after ischemia and reperfusion using magnetic resonance imaging and spectroscopy

To test the hypothesis that contrast-enhanced magnetic resonance imaging (MRI) and magnetic resonance spectroscopy (MRS) can differentiate reversible from irreversible myocardial injury, these modalities were used to study ischemia and reperfusion in a rat model. The presence of ischemia and reperfusion were confirmed with radiolabeled microspheres (n = 6). Groups of animals were subjected to either 16 (n = 17), 30 (n = 14), 60 (n = 11), or 90 (n = 14) minutes of left coronary artery (LCA) occlusion and 60 minutes reperfusion. After albumin-gadolinium (Gd)-DTPA injection, contrast-enhanced, T1-weighted, spin-echo proton images were acquired at baseline and every 16 minutes during LCA occlusion and reperfusion. In separate experiments, 31phosphorus (31P) spectra were acquired at similar time points during ischemia and reperfusion. After 16 minutes occlusion, normally perfused myocardium enhanced significantly compared with ischemic myocardium on MRI (104 +/- 7.9% vs. 61 +/- 11.0%, p less than 0.05, n = 5, mean +/- SEM, % of baseline value). MRS showed reduced phosphocreatine (PCr) and adenosine triphosphate (ATP) (58.8 +/- 2.4%, p less than or equal to 0.01; 81.4 +/- 2.4, p less than or equal to 0.01, n = 12). After 16 or 30 minutes ischemia, reflow resulted in uniform MRI signal intensity of the ischemic zone compared with normal myocardium (93.5 +/- 11.3 vs. 80.9 +/- 7.0, p = NS, n = 11, % of baseline value at 30 minutes reperfusion) and PCr recovery on MRS (94.3 +/- 4.0%, p = NS, n = 20, % baseline value at 30 minutes reflow). After 60 and 90 minutes ischemia, reflow resulted in marked enhancement of reperfused compared with normal myocardium on MRI (254.0 +/- 30.0 vs. 78.3 +/- 9.2, p less than or equal to 0.01, n = 10) and no recovery of PCr on MRS (64.1 +/- 3.0, p = NS, n = 14). Triphenyltetrazolium chloride (TTC) staining revealed transmural myocardial infarction (MI) in all hearts subjected to 60 or 90 minutes ischemia and reflow, and small nontransmural MIs in only 2/11 hearts subjected to 16 or 30 minutes ischemia and reperfusion. Thus, 1) MRI with albumin-Gd-DTPA is useful for identifying myocardial ischemia by enhancing the contrast between normally perfused and ischemic myocardia; 2) MRI with albumin-Gd-DTPA is useful for identifying reperfusion after myocardial ischemia; and 3) after reperfusion, reversible can be distinguished from irreversible myocardial injury by characteristic findings on MRI and MRS.     

Preconditioning does not attenuate myocardial stunning.

BACKGROUND. Despite numerous reports that one or more episodes of brief coronary artery occlusion preconditions the myocardium and dramatically reduces myocardial infarct size produced by a subsequent prolonged ischemia, we recently demonstrated that preconditioning does not attenuate contractile dysfunction in the peri-infarct tissue. However, the specific effects of preconditioning on myocardium in which wall motion has not been compromised by the preconditioning regimen per se and is further submitted to a short ischemic insult (that is, not confounded by necrosis) remain unknown. METHODS AND RESULTS. We addressed these issues in the canine model of myocardial stunning. Eighteen anesthetized dogs underwent 15 minutes of coronary occlusion followed by 3 hours of reperfusion. Before the 15-minute coronary occlusion, each dog received one of three treatments: no intervention (control group, n = 6), one episode of 5-minute coronary occlusion/5-minute reperfusion (PC5 group, n = 6), or one episode of 2.5-minute coronary occlusion/5-minute reperfusion (PC2.5 group, n = 6). Segment shortening (SS) in the ischemic/reperfused midmyocardium was monitored by sonomicrometry, and myocardial blood flow was assessed by injection of radiolabeled microspheres. All three groups were equally ischemic during the 15-minute coronary occlusion: Midmyocardial blood flow averaged 0.05 +/- 0.02, 0.07 +/- 0.04, and 0.08 +/- 0.03 ml/min/g in control, PC2.5, and PC5 groups, respectively. Before the 15-minute coronary occlusion, PC5 dogs exhibited significant stunning (SS = 55% baseline; p less than 0.01 versus control), whereas PC2.5 dogs did not (SS = 91% baseline; p = NS versus control). However, segment shortening during the subsequent 15-minute coronary occlusion was equally depressed at -25% to -42% of baseline values among the three groups. Furthermore, all three groups demonstrated a similar degree of stunning after reperfusion: SS at 3 hours after reflow averaged 24 +/- 12%, 34 +/- 16%, and 48 +/- 12% of baseline in control, PC2.5, and PC5 groups, respectively (p = NS). The degree of recovery of function after reperfusion correlated with the amount of midmyocardial blood flow during coronary artery occlusion. However, this relation was not different among the three groups: Specifically, for any given collateral flow during ischemia, preconditioning did not reduce the degree of stunning. CONCLUSIONS. Preconditioning neither preserves contractile function during a reversible ischemic insult nor prevents myocardial stunning during the initial hours of reflow.     

Endothelium dependent vasodilatation following brief ischaemia and reperfusion in anaesthetised swine

STUDY OBJECTIVE--The aim as to compare the responses of intracoronary infusions of ATP, an endothelium dependent vasodilator, with adenosine following brief ischaemia (10 min) and reperfusion in a model of myocardial stunning. DESIGN--In group 1 (n = 6), coronary blood flow and endocardial (endo) and epicardial (epi) percent segment length shortening were measured in the distribution of the left anterior descending coronary artery before and during maximal intracoronary infusions of either adenosine or ATP (20 micrograms.kg-1.min-1). Measurements were obtained before and after myocardial stunning both at control heart rate and during atrial pacing (150 beats.min-1). In group 2 (n = 6), myocardial blood flows by microspheres and arterial-venous lactate and oxygen differences were determined following the same ischaemia-reperfusion protocol to characterise transmural changes in blood flow and metabolism in this model of stunning. EXPERIMENTAL MATERIAL--The experiments were done on 12 anaesthetised swine, weight 25-39 kg. MEASUREMENTS AND MAIN RESULTS--In group 1, baseline endo and epi segment length shortening were 16(SD 3)% and 14(6)% and following reperfusion were reduced to 10(4)% and 8(6)% respectively (p less than 0.05). Prior to stunning, minimal coronary resistances during adenosine and ATP were 0.81(0.40) and 0.76(0.25) mm Hg.min.ml-1 respectively and following reperfusion were 0.86(0.31) (NS) and 0.85(0.23) (NS) mm Hg.min.ml-1 respectively. Infusion of either vasodilator enhanced function by 30% following reperfusion whereas no such effect was observed prior to ischaemia. In group 2, no maldistribution of blood flow was observed following the same ischaemia-reperfusion protocol to account for this vasodilator enhancement in function. Percent lactate extraction values were 29(11)% and 25(14)% at preischaemic control and paced heart rates respectively, and following reperfusion were lowered to 0(12)% without pacing (p less than 0.05) and -1(34)% during pacing (p less than 0.05). CONCLUSIONS--Brief ischaemia and reperfusion in swine induces myocardial stunning without altering the vasodilator responses of either ATP, an endothelium dependent vasodilator, or adenosine. Recruitment in postischaemic segment length shortening was observed during infusions of both vasodilators at a time when maldistribution of flow was not observed. Possible mechanisms include either enhanced washout of lactate from the reperfused myocardium or greater utilisation of substrates during higher blood flows.