体外反搏下不同反搏压对动脉内血流动力学环境影响的研究

为了研究体外反搏下不同反搏压对动脉内血流动力学环境的影响，以寻求较佳的体外反搏作用机制，选用了3周龄雄性断乳乳猪四头，进行了慢性体外反搏实验。详细记录了各实验体在基础状态及不同反搏压的体外反搏状态下心动周期里颈动脉内的动态血流动力学数据，包括压力、心电及血流量，进而计算了各种状态下的实验体颈动脉内壁面切应力（WSS）的动态分布。实验及计算结果表明，体外反搏能明显提高心动周期内实验体颈动脉的血流灌注、WSS水平及舒张期压力水平；从提高心动周期的切应力水平出发，反搏压设定为0．03mPa～0．035mPa为佳。另外，体外反搏改变了心动周期里的血流脉动模式，认为血流模式的改变可能对心动周期内的WSS水平有一定的影响作用。     

体外反搏对脑动脉血流量影响的建模和仿真研究

目的　研究体外反搏对脑动脉血流量的影响。方法　将实际测量的正常的颈动脉血压和进行体外反搏时的颈动脉血压作用于正常情况下和缺血情况下脑血流动力学数学模型，模拟上述情况下脑动脉血流的变化。结果　缺血和体外反搏都引起脑动脉血流的变化。结论　体外反搏可以明显增加大脑的血流灌注和改变脑动脉血流变化的时相模式。     

灌注压变化对左冠脉血流影响的建模和仿真研究

目的　通过对左冠状动脉的建模与仿真 ,对体外反搏提高缺血心肌灌注血流的机理进行研究。方法　根据牛顿定律和连续性方程 ,用电路分析模型来表示冠状动脉的每一小部分。通过每个部分的模拟电路模型对整个左冠状动脉进行建模。以主动脉血压的实测数据作为输入数据 ,利用Pspice软件进行仿真。 结果　仿真结果表明在体外反搏的情况下 ,左冠状动脉分支在舒张期的灌注血流得到了明显提高。结论　使用体外反搏的方法改变灌注压可以提高左冠脉血流灌注     

体外反搏对失血性休克犬大脑和皮肤微血管血流灌注的作用

应用激光多普勒测定微血管血流灌注技术，观察体外反搏提高灌注压力对失血性休克犬大脑皮层及皮肤微血管血流灌注的作用。结果显示，体外反搏可明显提高休克犬主动脉平均压力，增加休克犬大脑皮层及皮肤微血管血流灌注。在回输失血复苏后，对照组和反搏组主动脉平均压力恢复接近失血前水平，但反搏组微血管灌注的回升却明显高于对照组。结果提示体外反搏在犬失血性休克期预处理能改善其微循环障碍，有利于复苏期微血管的灌注     

对急性缺血犬动脉剪切应力影响的实验研究

为研究体外反搏对心肌缺血的治疗机理,分别测量在正常情况下、缺血1小时、缺血2小时、缺血1小时后反搏1小时、反搏2小时犬头臂干、颈动脉、胸主动脉、腹主动脉处的实时血流量,而后通过数学计算得出各处的实时剪切应力.结论是急性心肌缺血使各处动脉血管剪切应力的脉动性下降;体外反搏的作用可增加各处动脉剪切应力的脉动性.     

主动脉球囊反搏术（IABP）后的观察与护理

主动脉球囊反搏是一种以左心室功能辅助为主的循环辅助方式，是目前临床应用较广泛、有效的循环辅助装置。它是通过穿刺股动脉将一定容积的球囊放置在胸主动脉，球囊导管与体外压力泵相连，球囊在心脏舒张期快速充气，以增加冠状动脉的灌注压，增加冠状动脉血流。球囊在心脏收缩期快速放气，即减少了左心室射血阻力，又减少了心室做功和氧耗，     

体外反搏对急性缺血犬动脉剪切应力影响的实验研究

为研究体外反搏对心肌缺血的治疗机理。分别测量在正常情况下,缺血１小时,缺血２小时、缺血１小时反反搏１小时、反搏２小时犬头臂干、颈动脉、胸主动脉、腹主动脉处的实时血流量,而后通过数学计算得出各处的实时剪切应力,结论是急性心肌缺血使各处动脉血管剪切应力的脉动性下降;体外反搏的作用可增加各处动脉剪切应力的脉动性。     

体外反搏对缺血心肌穿壁血流影响的建模与仿真研究

在前期研究工作的基础上,为了深入研究体外反搏治疗心肌缺血的机理,用建模与仿真的方法研究体外反搏对缺血心肌跨壁血流的影响,以6条雄性犬的左心室压和主动脉压的实测数据作为输入对缺血心肌中的穿壁血流进行仿真。结果表明,用体外反搏的方法提高灌注压使缺血心肌穿壁血流进行仿真。结果表明,用体外反搏的方法提高灌注压使缺血心肌穿壁血流有明显增加。     

体外反搏搏动性血流在动,静脉系统中的传递

体外反搏通过对下肢及臀部施加外压，将下肤及臀部的动、静脉血分别驱回主动脉和下腔静脉，产生上行性搏动血流。由于动、静脉的生理特性不同，体外反搏的搏动性血流在动、静系统中传导有所不同。本文观察体外反搏驱动的搏动性血流在狗的主动脉及下腔静脉中的传导。结果：反搏搏动性血流在主动脉中传导良好；而在下腔静脉中的传导衰减明显。结果表明：体外反搏驱动的搏动性血流在主动脉中的良好传导是反搏治疗的基础；而其在下腔静脉的衰减传导又是降低反搏治疗负效应的有利条件     

IABP在临床的应用和护理

主动脉内球囊反搏(IABP)：(Intra-aortic bal oon pump)是机械性辅助循环方法之一,是由固定在导管的圆柱形气囊构成,将其安放在胸主动脉部位,通过物理作用,提高主动脉内舒张压,增加冠状动脉供血和改善心肌功能。主动脉内球囊反搏的工作原理：导管近端位于左锁骨下动脉末梢,远端位于肾动脉。主动脉内球囊反搏泵工作时驱动气体往返进出气囊。在心脏搏动的舒张期,球囊从排气状态突然膨胀充气,在胸降主动脉内占有了一定的体积,将原来占据该体积的血液顺、逆着动脉走行向终末端器官灌注。在收缩期,球囊从充气状态突然收缩排气,其所占据的体积被周围血液迅速回流填充。其产生双重血流动力学变化：主动脉收缩压降低,主动脉舒张压升高,平均动脉压升高,左心室舒张末期压力降低,左心室后负荷降低,射血分数增加,心输出量增加,心内膜下心肌存活率增加,体循环血管阻力下降。     

Segment stroke work and metabolism depend on coronary blood flow in the pig

We determined the mechanical and metabolic effects of graded myocardial ischemia in 23 open-chest, anesthetized pigs. By connecting the midportion of the left anterior descending artery (LAD) to the carotid artery via a constant volume, calibrated pump, we reduced the flow in the LAD to 0, 25, 50, and 75% of control rates for periods of 1 h. Flows of 100% and 150% were also examined. Using pairs of ultrasonic crystals to measure segment dimensions, we calculated segment shortening and thickening, and total and systolic stroke work in the ischemic and normally perfused segments. Blood gases, pH, and lactate and inosine balances were determined from the regional coronary venous blood. At coronary blood flows of 0, 25, 50, and 75% of normal resting flow, total segment work was 8 +/- 8, 25 +/- 4, 51 +/- 5, and 80 +/- 6% of control, respectively, while systolic segment work was -2 +/- 5, -10 +/- 5, 40 +/- 5, and 86 +/- 7% of control, respectively (means +/- SE). Thus, the decrease in total segment stroke work is proportional to the decrease in flow over the range 0-100%. However, no useful work (i.e., systolic work) is done until flow exceeds 25%. Segment shortening and thickening are significantly depressed with flows diminished by only 25%. Segmental inosine production correlates with lactate production and parallels decreased mechanical performance.     

Effects of alpha-adrenergic receptor blockade on coronary circulation in conscious dogs

The effects of three alpha-adrenergic-receptor blocking agents (phentolamine, prazosin, and trimazosin) were compared on the coronary circulation and left ventricular (LV) function in chronically instrumented conscious dogs. The three alpha-adrenergic-receptor blocking agents were administered in equidepressor doses (mean arterial pressure fell by approximately 20%) and in the presence of beta-adrenergic-receptor blockade and constant heart rate. LV systolic pressure, LV end-diastolic pressure, and LV end-diastolic diameter also fell similarly with the three drugs. Phentolamine decreased the time rate of change of LV pressure (LV dP/dt) by 21 +/- 3%, whereas trimazosin and prazosin decreased LV dP/dt only by 14 +/- 2 and 11 +/- 2%, respectively. LV velocity was not changed with trimazosin and prazosin but decreased with phentolamine by 12 +/- 4%. The three drugs exerted differential effects on the coronary circulation. Only trimazosin increased coronary blood flow (18 +/- 5%). Trimazosin decreased late diastolic coronary resistance (LDCR) by 35 +/- 2%, which was significantly more than reductions in LDCR induced by prazosin (22 +/- 2%) and by phentolamine (11 +/- 3%). A test dose of phenylephrine (5.0 micrograms/kg) increased mean arterial pressure by 53 +/- 3.5 mmHg. After trimazosin, prazosin, and phentolamine, the same dose of phenylephrine increased mean arterial pressure by 24 +/- 2.1, 14 +/- 1.6, and 1.9 +/- 0.6 mmHg, respectively. The response after phentolamine was significantly less than with trimazosin (P less than 0.01) and prazosin (P less than 0.02). Thus the capacity of these three alpha-adrenergic-receptor blocking drugs to dilate coronary vessels is inversely proportional to their capability to block exogenous alpha-adrenergic-receptor agonists.     

Resistance training in men is associated with increased arterial stiffness and blood pressure but does not adversely affect endothelial function as measured by arterial reactivity to the cold pressor test

Resistance training is a popular mode of exercise, but may result in stiffening of the central arteries. Changes in carotid artery diameter were determined using the cold pressor test (CPT), which results in production of nitric oxide via sympathetic activation and is one of the novel methods available for assessing endothelial function in the carotid artery. To investigate the effect of resistance training on endothelial function, we designed a cross-sectional study of carotid arterial vasoreactivity to CPT in men participating in regular resistance training with increased carotid arterial stiffness compared with age-matched control subjects. Twelve resistance-trained middle-aged men (age 38.7 +/- 1.7 years) and 17 age-matched control subjects (age 36.8 +/- 1.2 years) were studied. The direction and magnitude of changes in carotid artery diameter were measured by B-mode ultrasonography during sympathetic stress induced by submersion of the foot in ice slush for 90 s. Carotid arterial beta-stiffness index, and systolic and mean arterial blood pressure were higher (7.7 +/- 0.7 versus 6.0 +/- 0.4 arbitrary units, 116 +/- 2 versus 131 +/- 4 mmHg and 86 +/- 2 versus 95 +/- 2 mmHg, respectively, all P < 0.05) in the resistance training group compared with control subjects. There were, however, no significant differences in the amount or percentage change in carotid artery diameter in CPT between the two groups (resistance training group, 0.33 +/- 0.07 mm and 5.2 +/- 1.1%; control group, 0.37 +/- 0.06 mm and 5.8 +/- 0.9%, respectively). These findings suggest that while carotid arterial stiffening and higher blood pressure are observed in regular resistance-trained men, these are not associated with abnormalities in carotid arterial vasoreactivity to sympathetic stimulus, which implies intact endothelial function.     

Blood flows in the maxillocarotid anastomoses and internal carotid artery of conscious dogs

Although the external carotid artery is known to contribute to the cerebral blood flow in anesthetized dogs, quantitative information on the anastomoses and their role in conscious dogs is lacking. This study was carried out to determine blood flows in these anastomoses and the internal carotid artery, and also to examine the functional significance of the anastomoses in conscious dogs. Fifteen-micron radioactive microspheres were injected into common and external carotid arteries of four conscious dogs through chronically implanted catheters. Blood flows were determined by the reference sample method and by comparing microsphere distributions in the brain and the masseter muscle. Blood flows were estimated to be 140 +/- 32, 7.7 +/- 1.4, and 3.3 +/- 1.1 ml/minute (mean +/- SD) in the common carotid artery, internal carotid artery, and anastomoses on each side, respectively. Additional evidence indicated that the anastomotic flow so determined was primarily the flow in the anastomotic artery. Humoral responses to angiotensin II infusions were also studied in conscious dogs. External carotid angiotensin increased plasma 11-hydroxycorticosteroid concentration (used as an index of ACTH secretion) but did not increase plasma vasopressin concentration to the same extent as common carotid infusion. Therefore, the external carotid artery is functionally important in perfusing the brain in conscious dogs.     

The relationship between carotid and coronary atherosclerotic damage in dialysis patients

BACKGROUND: Data relating carotid ultrasound (CU) to atherosclerotic damage evaluated by coronary angiography in hemodialysis patients are scarce. METHODS: We carried out a cross-sectional study in 33 uremic subjects (age 55 +/- 12 years, 22 male, 7 diabetic), who have been on dialysis for 41 +/- 48 months (range 2-192). Twenty-two underwent a coronary angiography in order to complete clinical evaluation for inclusion on the kidney transplantation waiting list, and 11 because of coronary artery disease (CAD); Gensini's score was calculated. Intima-media thickness (IMT) and presence of plaques were related to the degree of coronary stenosis and to cardiovascular risk factors. Patients were divided into two groups depending on mean IMT (group 1 IM 0.9 mm, n=15). RESULTS: Group 2 was older (60 +/- 8 vs 50 +/- 12 year, p=0.01), had higher frequency of CAD (53 vs 16%, p=0.02) and had higher prevalence of coronary artery stenosis >or= 75% in the right (60 vs 22%, p=0.02), left anterior descending (46 vs 16%, p=0.06) and left circumflex coronary arteriers (60 vs 11%, p=0.05) than group 1. IMT was not related to the degree of CAD evaluated by Gensini's score. IMT sensibility and specificity in detecting the presence of hemodynamically significant coronary stenosis were 64% and 68%, respectively. Coronary narrowing was correlated with the degree of stenosis of common, internal and external carotid arteries (Spearman's rank correlation coefficient). During two years of follow-up, six major cardiac events were recorded and they were related to Gensini's score. CONCLUSIONS: In uremic patients, ultrasonographic evaluation of carotid arteries is a simple, noninvasive examination that could be a helpful tool in detecting coronary atherosclerotic damage, but IMT does not appear to add more information regarding risk stratification of CAD.     

Monocyte adhesion and changes in endothelial cell number, morphology, and F-actin distribution elicited by low shear stress in vivo.

Left common carotid arteries of New Zealand white rabbits were ligated rostral to origin of the thyroid artery to reduce flow in the carotid upstream of this branch, and the vessels were examined 5 days later. Estimates of mean shear stress in the upstream carotid artery indicated a decrease of 73% (from 12.1 +/- 1.6 dynes/cm2 to 3.26 +/- 0.58 dynes/cm2). The contralateral common carotid artery carried collateral flow and experienced a 170% increase in shear stress (from 11.3 +/- 1.6 dynes/cm2 to 30.5 +/- 4.6 dynes/cm2). There was an adaptive reduction in the diameter in the left common carotid artery (low shear) from 2.07 +/- 0.06 mm to 1.75 +/- 0.12 mm, but the diameter of the right carotid was unchanged. Fluorescence microscopy and scanning electron microscopy of endothelium exposed to low shear revealed attachment of leukocytes (5.02 +/- 1.59 cells/mm2, mean +/- SE) that were identified as monocytes using the monoclonal antibody HAM 56. Laser confocal microscopy demonstrated that they were migrating across the endothelial cell monolayer. Fluorescence microscopy and scanning electron microscopy of left common carotid artery (low shear) also revealed cell morphology suggestive of endothelial cell desquamation. Endothelial cell loss was confirmed by morphometric determination of cell number (1.29 +/- 0.13 x 10(4) cells/mm length in experimental animals versus 1.71 +/- 0.08 x 10(4) cells/mm length in sham-operated animals). This endothelial cell loss may be an adaptation to a narrowing of carotid arteries exposed to low shear, which reduces luminal surface area of the vessel. Staining of F-actin with rhodamine phalloidin showed that endothelial cells exposed to low shear were less elongated and had fewer stress fibers than normal cells. By contrast, increasing shear stress by two- to threefold caused an increase in the number of stress fibers and a reduction in peripheral actin staining. Distal carotid ligation provided a consistent and well-defined in vivo technique for manipulating shear stresses imposed on a large population of endothelial cells.     

Hemodynamic effects of sildenafil in men with severe coronary artery disease

BACKGROUND: The cardiovascular effects of sildenafil are important because of the frequent presence of underlying cardiac disease in men with erectile dysfunction and reports indicating serious cardiac events temporally associated with the use of this drug. METHODS: We assessed the systemic, pulmonary, and coronary hemodynamic effects of oral sildenafil (100 mg) in 14 men (mean [+/-SD] age, 61+/-11 years) with severe stenosis of at least one coronary artery (stenosis of >70 percent of the vessel diameter) who were scheduled to undergo percutaneous coronary revascularization. Blood-flow velocity and flow reserve were assessed with a Doppler guidewire in 25 coronary arteries, including 13 severely diseased arteries (mean stenosis, 78+/-7 percent) and 12 arteries without stenosis, used as a reference; maximal hyperemia was induced (to assess flow reserve) with the intracoronary administration of adenosine both before and after sildenafil. RESULTS: Oral sildenafil produced only small decreases (<10 percent) in systemic arterial and pulmonary arterial pressures, and it had no effect on pulmonary-capillary wedge pressure, right atrial pressure, heart rate, or cardiac output. There were no significant changes in average peak coronary flow velocity, coronary-artery diameter, volumetric coronary blood flow, or coronary vascular resistance. Coronary flow reserve at base line was lower in the stenosed arteries (1.26+/-0.26) than in the reference arteries (2.19+/-0.44) and increased about 13 percent in both groups of arteries combined after the administration of sildenafil (from 1.70+/-0.59 to 1.92+/-0.72, P=0.003). The ratio of coronary flow reserve in coronary arteries with stenosis to that in the reference arteries (0.57+/-0.14) was not affected by sildenafil. CONCLUSIONS: No adverse cardiovascular effects of oral sildenafil were detected in men with severe coronary artery disease.     

Impaired flow-mediated vasodilation of epicardial coronary artery in vasospastic angina.

To evaluate whether the flow-mediated vasodilation and coronary flow reserve are impaired or not in patients with vasospastic angina (VA), we measured the changes of epicardial coronary artery diameter and flow reserve in spasm related-left anterior descending coronary artery (LAD). The flow mediated-response of epicardial coronary arteries in 15 VA were compared with 15 controls. Using quantitative coronary angiography, we measured the diameter of proximal (pLAD) and middle segment (mid-LAD) of LAD under baseline conditions, during increased blood flow after distal adenosine injection and after proximal administration of nitroglycerin. An increased fraction of average peak velocity after injection of adenosine was similar in both groups [control 340 (mean)+/-24 (SEM)%; VA 330+/-19%]. Flow-mediated vasodilation was preserved in all controls (pLAD 13.1+/-1.4%; mid-LAD 15.8+/-2.5%) but it was significantly impaired in patients with VA (pLAD -1.0+/-1.8%; mid-LAD 0.1+/-3.5%). The vasodilator response to nitroglycerin was comparable in controls (pLAD 25.8+/-2.8%; mid-LAD 27.2+/-2.8%) and VA (pLAD 26.2+/-5.2%; mid-LAD 26.7+/-3.5%). Coronary flow reserve is preserved in patients with VA. However, the flow-mediated response of spasm related-epicardial coronary artery is impaired. This may play an important role in the pathogenesis of coronary artery spasm.     

Use of vascular Doppler ultrasound to detect acute estradiol vascular effect in postmenopausal women

OBJECTIVES: To report on a simple practical test for assessing acute estradiol vascular effects on healthy and unhealthy postmenopausal women. INTRODUCTION: Estradiol acts in the endothelium to promote vasodilatation through genomic and non-genomic mechanisms, but its vascular action may be impaired in diabetes mellitus, hypertension, smoking and obesity. METHODS: Nineteen postmenopausal women (nine healthy and 10 with two or more of the above factors) of similar age and time since menopause were examined with vascular Doppler ultrasound. Resistance indexes and systolic and diastolic flow velocities were determined for the brachial and internal carotid arteries at baseline and 20 minutes after administration of a nasal estradiol formulation, available on the market, which reaches 1,200-1,500 pg/ml in the serum in 10-30 minutes. Estradiol blood levels were measured at 30 minutes. RESULTS: The carotid resistance index increased 14.2% (vasoconstriction) in the unhealthy group after estradiol, from a mean +/- S.E. of 0.56 +/- 0.016 at baseline to 0.64 +/- 0.05 (p=0.033), and remained unchanged in healthy women. Brachial diastolic flow velocity increased 19.7% (vasodilatation) in healthy women, from 16.2 +/- 1.93 to 19.4 +/- 0.64 cm/s (p=0.046), and did not change in the unhealthy subjects. Estradiol levels were similar in both groups. DISCUSSION: Healthy postmenopausal women showed brachial vasodilatation while unhealthy postmenopausal women displayed vasoconstriction at the carotid artery. Vascular responses to estradiol were divergent between the groups. CONCLUSIONS: The acute estradiol test, coupled with Doppler ultrasound, seemed to be able to differentiate women with normal and abnormal endothelial function in a simple, non-invasive manner.     

Role of total arterial compliance and peripheral resistance in the determination of systolic and diastolic aortic pressure.

The goal of the study was to define the major arterial parameters that determine aortic systolic (Ps) and diastolic (Pd) pressure in the dog. Measured aortic flows were used as input to the two-element windkessel model of the arterial system, with peripheral resistance calculated as mean pressure over mean flow and total arterial compliance calculated from the decay time in diastole. The windkessel model yielded an aortic pressure wave from which we obtained the predicted systolic (Ps, wk) and diastolic (Pd, wk) pressure. These predicted pressures were compared with the measured systolic and diastolic pressures. The measurements and calculations were carried out in 7 dogs in control conditions, during aortic occlusion at four locations (the trifurcation, between trifurcation and diaphragm, the diaphragm and the proximal descending thoracic aorta) and during occlusion of both carotid arteries. Under all conditions studied the predicted systolic and diastolic pressure matched the experimental ones very well: Ps, wk = (1.000 +/- 0.0055) Ps with r = 0.958 and Pd, wk = (1.024 +/- 0.0035) Pd with r = 0.995. Linear regression for pulse pressure gave PPwk = (0.99 +/- 0.016) PP (r = 0.911). We found the accuracy of prediction equally good under control conditions and in presence of aortic or carotid artery occlusions. Multiple regression between pulse pressure and arterial resistance and total arterial compliance yielded a poor regression constant (r2 = 0.19) suggesting that the two arterial parameters alone cannot explain pulse pressure and that flow is an important determinant as well. We conclude that, for a given ejection pattern (aortic flow), two arterial parameters, total arterial resistance and total arterial compliance are sufficient to accurately describe systolic and diastolic aortic pressure.