远端器官预缺血改善冠状动脉缺血再灌注时心肌血供及减少心律失常发生率

远端器官缺血性预处理 (RPC)可减少缺血再灌注后心肌坏死范围。本研究旨在观察RPC对缺血再灌注心脏不同部位血流及心律失常发生率的影响。方法 :19头成年绵羊随机分为对照组 (n =9)及RPC组 (n =10 )。RPC组动物接受 3次左侧股动脉阻断 (5min)及再灌注 (5min) ,随后两组动物均分别依次阻断左冠状动脉前降支 (LAD) 10min ,再灌注 10min ;左冠状动脉第一分支 (D1)阻断及再灌注 10min后阻断左旋支 (LCX) 10min ,再灌注后观察 12 0min。结果 :LCX再灌注 10min时RPC组左室心内膜前壁、间隔及心外膜间隔心肌血流量 (分别为 0 .86± 0 .2 7,1.10±0 .34及 1.2 0± 0 .5 1ml·min-1·g-1)显著高于对照组 (分别为 0 .6 4± 0 .2 8,0 .6 9± 0 .2 3及 0 .5 8± 0 .2 6ml·min-1·g-1) ,P <0 .0 5。RPC显著减少再灌注后心室纤颤的发生率 (对照组 8/ 9,RPC组 2 / 10 ,P <0 .0 1)。冠状动脉阻断及再灌注后对照组主动脉平均压低于RPC组 ,但差异无显著性 (P >0 .0 5 )。结论 :RPC显著减少心肌缺血及再灌注期心室纤颤的发生 ,其机制可能与RPC显著改善心内膜血液供应有关。     

在静息血流无限制的慢性冠状动脉狭窄中静息心肌收缩功能与血流储备的关系

目的 :评价静息心肌收缩功能与血流储备的关系。　　方法 :以安放“水膨胀”式缩窄器的方法建立 11只慢性多支冠状动脉 (冠脉 )狭窄闭胸犬。术后 7～ 10天在静息状态下以二维超声心动图测定室壁增厚百分率 (% WT) ,同时以放射性微球测定心肌血流量 (MBF)和 MBF储备。　　结果 :在 40个心室壁运动异常的心肌节段与 42个心室壁收缩功能正常的心肌节段之间 ,静息心室壁和心内膜下血流均无明显差异 ,但后者的心室壁和心内膜下血流储备均明显低于前者。静息状态 % WT与 MBF储备密切相关 (P<0 .0 0 1)。　　结论 :在静息状态血流无限制的慢性冠脉狭窄犬 ,% WT异常心肌节段的 MBF储备明显降低 ,静息状态 % WT与MBF储备密切相关 ,表明局部收缩功能异常可能是由于反复“需氧增多”性心肌缺血所致。     

静息血压达标的高血压病患者运动血压与血管内皮功能相关性研究

目的 探讨静息血压达标的高血压病患者运动血压与血管内皮功能之间的关系. 方法 60例静息血压达标的高血压病患者行6min步行试验,按运动后的血压是否增高分为运动血压增高组（增高组,n=30）和非增高组（n=30）.同时选取30例血压正常者为对照组.检测运动前血流介导的血管舒张功能（FMD）、运动前后血浆NO和内皮素-1浓度,记录运动前和运动后即刻、10min、20min、30min收缩压、舒张压及心率. 结果 FMD增高组（0.084±0.01）%显著低于非增高组（0.13±0.01）%和对照组（0.15±0.02）%（P〈0.05）.运动前增高组NO浓度低于、内皮素-1浓度高于非增高组和对照组;3组运动后即刻NO浓度较运动前明显升高（P〈0.05）,但增高组明显低于非增高组和对照组（P〈0.05）.FMD与舒张压差值呈负相关（P〈0.05）;运动前后NO差值与运动后收缩压差值呈负相关（P〈0.05）.与舒张压差值呈正相关（P〈0.05）. 结论血压控制良好的高血压患者运动后血压增高可能与内皮功能受损有关.     

Exaggerated Vasopressor Response to Exercise and Cerebral Blood Flow Velocity

We studied 10 young adults, normotensive at rest, comprising a control group (n = 5) with normal blood pressure responsiveness to exercise and an experimental group exhibiting greater percentage of body fat and body mass index (BMI) than the controls, with exaggerated blood pressure (vasopressor) responsiveness to exercise (EEBPR) (n = 5). Lower absolute and varying oxygen consumption/body weight normalized units of middle cerebral arterial blood flow velocity (MCAV) were found during exercise in the experimental group (P < .01). These findings support the hypothesis that the combination of EEBPR and high BMI is associated with low MCAV that may put such individuals at risk for cerebral hypoperfusion and cognitive deficits.     

Transcatheter Endocardial Ablation: Acute Effects of Direct Current Countershock on Regional Myocardial Blood Flow

Effect of DC Shock Ablation on Myocardial Blood Flow. Introduction: High energy direct current ablative shocks delivered through endocardial electrode catheters have been used as a treatment for various cardiac arrhythmias including ventricular tachycardia. Frequently, these shocks result in depression of myocardial function, at least transiently. Methods and Results: This study assessed the effect of a 200-joule direct current shock delivered endocardially to the apex of the heart in ten adult mongrel dogs. Arterial blood pressures were monitored continuously. Myocardial contraction was monitored via two-dimensional echocardiography. Regional myocardial blood flows were measured using radionuclide labeled microspheres before delivery of the shock, 30 seconds after delivery of the shock, and at 5 and 10 minutes after the shock. The results of the study demonstrated that there was a marked drop in arterial blood pressure immediately after the shock that gradually recovered over a 20-minute period. Regional myocardial blood flow at the site of catheter ablation was severely depressed immediately after the shock. The degree of myocardial blood flow depression was inversely related to the distance from the site of ablation. At 5–10 minutes after ablation there was a marked hyperemic response in areas that suffered from depressed flow immediately after the shock. Two- dimensional echocardiography demonstrated depressed contractile function immediately after the shock with gradual recovery over a 10- to 20-minute period. The catheter shock also generated prominent echo densities within the myocardium surrounding the ablative site. In contrast to the intracavitary echo densities that cleared quickly, the intramyocardial densities cleared much more slowly. Conclusion: The results of the study confirm the clinical observation that human left ventricular function is depressed acutely following a high-energy ablative shock delivered to the left ventricular endocardium. Our results also demonstrated for the flrst time the effect of such ablative shocks on regional myocardial blood flow. Such depressions of blood flow may help explain the sudden drop in contractile function of the heart. The persistent intramyocardial echoes seen after the shock probably represented generation of intramyocardial bubbles that could obstruct arterial flow as well as disrupt cellular function. (J Cardiovasc Electrophysiol, Vol. 3, pp. 40–47, February 1992)     

偏头痛急性发作期SPECT脑血流灌注显像的研究

目的观察偏头痛急性发作期局部脑血流灌注（rCBF）分布的特点及氟桂利嗪（西比灵）治疗后脑血流灌注的改变情况，进一步探讨偏头痛的发病机制及单电子发射计算机断层扫描（SPECT）在其临床诊疗中的应用价值。方法利用99m^Tc-ECD标记的放射性药物对22例偏头痛病人于急性发作期行SPECT脑灌注显像，对图像进行目测及半定量分析。比较头痛部位与脑灌注异常部位的相关性；自身头痛侧与非头痛侧脑血流灌注的不对称性；以及脑灌注异常程度与偏头痛的严重程度、发作频率之间的关系。结果82％病人在偏头痛急性发作期，SPECT表现为相关部位局部脑血流量减低；脑灌注改变的部位与头痛部位相关；对于一侧头痛病人，头痛侧与非头痛侧的脑血流量有明显差异，尤其在额叶、顶叶、颞叶明显（P〈0．05或P〈0．01）；局部脑灌注减低的程度在一定条件下与头痛的严重程度和发作频率成正比，但不成线性关系：10例病人在西比灵治疗前后rCBF比较，4例恢复正常，3例低灌注仍然存在，但rCBF评分增加，3例无明显变化。结论偏头痛病人在急性期普遍存在脑血流灌注异常。与CT、磁共振成像（MRI）、颅多普勒超声（332D）等辅助检查工具相比，SPECT可以反映脑细胞功能及脑血流的变化，在偏头痛的临床诊疗中有一定的参考价值。     

Nitric Oxide Inhibition Impairs Blood Flow During Exercise in Hearts With a Collateral-Dependent Myocardial Region

Objectives. We sought to determine the importance of nitric oxide (NO) production in maintaining coronary blood flow during exercise in hearts with collateral-dependent myocardium.Background. Coronary collateral vessels demonstrate endothelium-mediated NO-dependent vasodilation in response to agonists such as acetylcholine. However, the contribution of endogenous NO production to maintaining vasodilation of coronary collateral vessels during exercise has not been previously studied.Methods. Collateral vessel growth was induced in 13 chronically instrumented dogs by intermittent 2-min occlusions, followed by permanent occlusion of the left anterior descending coronary artery (LAD). One week after permanent LAD occlusion, myocardial blood flow was measured with microspheres during rest and treadmill exercise at 6.4 km/h at a 15% grade. Measurements were then repeated after blockade of NO production with N-nitro-l-arginine (LNNA) (20 mg/kg body weight intravenously).Results. LNNA caused a 62 ± 4% (mean ± SEM) inhibition of the coronary vasodilation produced by acetylcholine. During rest conditions, LNNA caused a slight decrease in blood flow to the collateral region (p = NS), with no change in normal zone blood flow. During exercise, LNNA caused a decrease in mean blood flow to the collateral region (from 2.24 ± 0.19 to 1.78 ± 0.26 ml/min per g after LNNA, p < 0.05). This decrease resulted from a near doubling of the collateral vascular resistance (p < 0.05), with a trend toward an increase in small vessel resistance in the collateral zone. LNNA also reduced myocardial blood flow to the normal region during exercise (from 2.99 ± 0.24 to 2.45 ± 0.28 ml/min per g, p < 0.05) as the result of a 44 ± 13% increase in coronary vascular resistance (p < 0.05).Conclusions. NO contributes to the maintenance of coronary collateral blood flow during exercise. In contrast to the normal heart, endogenous NO production also maintains blood flow in remote myocardial regions during exercise. These results suggest that control of blood flow during exercise in normal myocardium is altered by the presence of an occluded coronary artery.     

Heart Failure Impairs Muscle Blood Flow and Endurance Exercise Tolerance in COPD

Heart failure, a prevalent and disabling co-morbidity of COPD, may impair cardiac output and muscle blood flow thereby contributing to exercise intolerance. To investigate the role of impaired central and peripheral hemodynamics in limiting exercise tolerance in COPD-heart failure overlap, cycle ergometer exercise tests at 20% and 80% peak work rate were performed by overlap (FEV₁ = 56.9 ± 15.9% predicted, ejection fraction = 32.5 ± 6.9%; N = 16), FEV₁-matched COPD (N = 16), ejection fraction-matched heart failure patients (N = 15) and controls (N = 12). Differences (Δ) in cardiac output (impedance cardiography) and vastus lateralis blood flow (indocyanine green) and deoxygenation (near-infrared spectroscopy) between work rates were expressed relative to concurrent changes in muscle metabolic demands (ΔO₂ uptake). Overlap patients had approximately 30% lower endurance exercise tolerance than COPD and heart failure (p < 0.05). ΔBlood flow was closely proportional to Δcardiac output in all groups (r = 0.89–0.98; p < 0.01). Overlap showed the largest impairments in Δcardiac output/ΔO₂ uptake and Δblood flow/ΔO₂ uptake (p < 0.05). Systemic arterial oxygenation, however, was preserved in overlap compared to COPD. Blunted limb perfusion was related to greater muscle deoxygenation and lactate concentration in overlap (r = 0.78 and r = 0.73, respectively; p < 0.05). ΔBlood flow/ΔO₂ uptake was related to time to exercise intolerance only in overlap and heart failure (p < 0.01). In conclusion, COPD and heart failure add to decrease exercising cardiac output and skeletal muscle perfusion to a greater extent than that expected by heart failure alone. Treatment strategies that increase muscle O₂ delivery and/or decrease O₂ demand may be particularly helpful to improve exercise tolerance in COPD patients presenting heart failure as co-morbidity.     

高血压患者心肌微循环损伤与运动试验中血压和心率变化的相关性研究

目的 探讨高血压患者心肌微循环损伤与运动试验中血压、心率变化的关系.方法 选取住院的高血压患者74例,根据心肌声学造影实时评估心肌微循环灌注,分为微循环显像正常组和异常组.搜集研究对象一般临床资料、生化指标和平板运动参数等指标.比较两组患者各指标间的差异,分析高血压患者心肌微循环与运动后血压、心率的关系.结果(1)高血...     

Intracoronary Ketanserin Augments Coronary Collateral Blood Flow and Decreases Myocardial Ischemia During Balloon Angioplasty

Aims: To test the hypothesis that ketanserin augments coronary collateral blood flow and decreases myocardial ischemia during balloon angioplasty. Methods and Results: Forty-four patients with single vessel disease and stable angina were studied. Collateral flow was determined during balloon inflations, based on the distal velocity time integral (13 patients) or on coronary wedge/mean arterial pressure measurements (10 patients). The 2nd and 3rd inflations lasted the same time and between them 1.5 mg intracoronary ketanserin in 10 ml normal saline was administered over 3 min. In 21 control subjects normal saline alone was given. In the flow velocity group the velocity time integral was 78.5 ± 53.1 mm during the 2nd inflation and 106.0 ± 43.2 mm during the 3rd (p < .05), while the ST deviation was 1.1 ± .7 and .7 ± .7 mm, respectively (p. < .05). In the intracoronary pressure group the CWP/MBP was .40 ± .10 during the 2nd inflation and .45 ± .11 during the 3rd (p. < .05), while the ST deviation was 1.2 ± .8 and .8 ± .8 mm respectively (p. < .05). In the controls no variables changed during the tested inflations. Conclusion: Intracoronary administration of ketanserin augments coronary collateral flow and decreases myocardial ischemia during balloon angioplasty. This could be of clinical significance in the management of acute ischemic syndromes.     

急性高血糖犬心表冠状动脉和心肌微血管储备功能的实验研究

目的　探讨急性高血糖对犬心表大冠状动脉和心肌微血管血流量和血流储备的影响。方法　静注双嘧达莫前后 ,应用血流仪和心肌对比超声心动图 (MCE)测量犬基础状态和高血糖状态时冠状动脉前降支和心肌微血管的血流量。结果　应用双嘧达莫前 ,基础状态和高血糖状态的前降支和心肌微血管的血流量 ( 13 .94± 2 .92比 15 .0 5± 8.61ml/min和 45 .49± 14 .2 8比 48.62± 2 9.5 9,P >0 .0 5 )以及微血管密度 ( 5 7.0 5± 7.87比 68.65± 10 .0 0 ,P >0 .0 5 )均无差异 ;应用双嘧达莫后 ,前降支血流量和血流储备无明显变化 ,而心肌微血管的血流量 ( 91.71± 42 .67比 41.16± 2 3 .15 ,P <0 .0 1)、血流储备 ( 2 .15± 1.3 0比 0 .84± 0 .44 ,P <0 .0 5 )和血管密度 ( 86.78± 2 1.84比65 .18± 2 8.5 8,P <0 .0 5 )明显下降。结论　急性高血糖减少双嘧达莫负荷后的心肌微血管的血流量、血流储备和血管密度     

Modeling Cerebral Blood Flow Control During Posture Change from Sitting to Standing

Hypertension, decreased cerebral blood flow, and diminished cerebral blood flow velocity regulation, are among the first signs indicating the presence of cerebral vascular disease. In this paper, we will present a mathematical model that can predict blood flow and pressure during posture change from sitting to standing. The mathematical model uses a compartmental approach to describe pulsatile blood flow velocity and pressure in a number of compartments representing the systemic circulation. Our model includes compartments representing the trunk and upper extremities, the lower extremities, the brain, and the heart. We use physiologically based control mechanisms to describe the regulation of cerebral blood flow velocity and arterial pressure in response to orthostatic hypotension resulting from postural change. To justify the fidelity of our mathematical model and control mechanisms development, we will show validation results of our model against experimental data from a young subject.     

Impact of Resting and Ischemic Blood Flow on Infarct Probability in Ischemic Preconditioning-a New Approach to Infarct Size-Blood Flow Data by Logistic Regression

The linear regression analysis of infarct size (IS)vischemic myocardial blood flow (MBF) does not account for the heterogeneity of MBF and infarcted tissue; moreover, it cannot assess a blood flow threshold for infarction (MBFT) accurately, as with ischemic preconditioning (IP) the close relationship between ischemic MBF and IS otherwise observed is lost. Finally, the impact of resting blood flow on myocardial infarction cannot be considered in such analysis. Therefore, in a retrospective data analysis of 32 enflurane-anaesthetized swine undergoing 90 min severe ischemia and 120 min reperfusion without (CON,n=12) or with IP induced by either 3 (IP3,n=8) or 10 min ischemia (IP10,n=12) and 15 min reperfusion, a MBFT was assessed by logistic regression (LR) in individual tissue pieces. MBFT was arbitrarily defined as that ischemic MBF (microspheres) at which infarct probability was 0.2, derived from the ratio of infarcted (n=141, TTC) to all tissue samples (n=684). The duration of the preconditioning ischemia and MBF both at rest and during the sustained ischemia were significant predictors of infarct probability. Ischemic MBFT at an infarct probability of 0.2, was 0.089±0.023 ml/min/g in CON. MBFT was decreased to 0.051±0.03 ml/min/g with IP3 (P<0.05vCON) and further to 0.004±0.037 ml/min/g with IP10 (P<0.05vCON, IP3). Corresponding to the leftward shift of MBFT, the relationships between infarct probability and MBF were shifted in parallel by IP with no change in their slopes.