大鼠蛛网膜下腔出血后急性脑血管痉挛血及脑组织一氧化氮和内皮素含量的动态观察

目的 探讨一氧化氮（ＮＯ）、内皮素（ＥＴ）在蛛网膜下腔出血（ＳＡＨ）后急性脑出血痉挛（ＣＶＳ）中的作用。方法 对ＳＡＨ模型组和假手术组大脑检测术后２４ｈ内局部脑血流量（ｒＢＣＦ）、血浆及脑组织ＮＯ、ＥＴ含量的动态改变,并测量基底动脉（ＢＡ）管径,３ｄ后行海马组织病理检查。结果 ＳＡＨ后２４ｈ内ｒＣＢＦ迅速而持续降低,ＢＡ痉挛;３ｄ后海马ＣＡ１区神经元明显受损,血清ＮＯ明显减少,脑组织ＮＯ显著增多,     

电刺激小脑顶核改善缺血性脑损害的研究进展

电刺激小脑顶核（ＦＮ）可以增加局部脑血流量（ｒＣＢＦ），缩小梗塞体积，而不伴随脑代谢率的改变。提示对脑缺血可能有益。对是电刺激ＦＮ可以改善实验性脑缺血的研究现状、发展趋势和对缺性脑损害的脑保护作用及其作用机理作一综述。     

卡托普利对犬缺血再灌注损伤心脏保护作用实验研究

目的观察含４．６μｍｏｌ／Ｌ卡托普利的停搏液及再灌注血液对低温体外循环下犬在体心脏的心肌保护作用。方法１６只杂种犬随机分为Ａ组：对照组及Ｂ组：卡托普利组。Ａ组仅用Ｓｔ．Ｔｈｏｍａｓ改型停搏液，Ｂ组采用含有４．６μｍｏｌ／ＬＣｐｌ的Ｓｔ．Ｔｈｏｍａｓ改型停搏液及再灌注血液。测定血流动力学参数、冠状静脉窦血清肌酸激酶（ＣＫ）及肌酸激酶同工酶（ＣＫＭＢ）浓度、心肌组织丙二醛（ＭＤＡ）、Ｋ＋、Ｎａ＋、Ｃａ２＋及水含量。结果心脏复跳后，Ｂ组主动脉血流量、冠状动脉血流量、±ｄｐ／ｄｔｍａｘ恢复百分率高于对照组（Ｐ＜０．０５），而冠状静脉窦血ＣＫ及ＣＫＭＢ，心肌组织ＭＤＡ、Ｎａ＋、Ｃａ２＋及水含量则低于对照组（Ｐ＜０．０１）。结论卡托普利可通过改善冠脉循环、清除氧自由基及减轻钙超载等作用保护心肌。     

急性期降血压治疗对脑梗塞脑血流量,脑功能的影响

目的研究急性期降血压治疗对脑梗塞患者脑血流量（ＣＢＦ）和脑功能的影响。方法１４４例高血压脑梗塞患者随机分为降血压组和非降血压组，疗程１４天，治疗前后１３３Ｘｅ吸入法测定ＣＢＦ和进行脑电图（ＥＥＧ）脑干听觉诱发电位（ＢＡＥＰ）检查。结果两组治疗前ＣＢＦ、ＥＥＧ和ＢＡＥＰ异常率均相似，治疗后虽均有所改善，但降血压组ＣＢＦ、ＥＥＧ和ＢＡＥＰ改善率明显低于非降血压组（Ｐ＜０．０５～０．０１）。结论脑梗塞患者急性期血压升高有利于维持脑血流量和脑功能。     

兔脑缺血后局部脑血流量和皮质脑电图变化及与氧化型低密度脂蛋白的关系

目的研究高胆固醇和高糖饮食对脑缺血后局部脑血流量（ｒＣＢＦ）和皮质脑电图（ＥＥＧ）的影响及与氧化型低密度脂蛋白（ｏｘＬＤＬ）的关系。方法对４９只兔分别给予１％胆固醇、１０％糖水和标准食３种饮食共５周，行颈总动脉结扎或颈内动脉栓塞，同时同点连续记录皮质ＥＥＧ和每３０分钟测１次ｒＣＢＦ，并提取血浆低密度脂蛋白（ＬＤＬ）进行薄层层析（ＴＬＣ）和测定脂质过氧化物（ＬＰＯ）及血脂。结果（１）标准食兔较栓塞组ｒＣＢＦ及皮质ＥＥＧ总能量和平均频率显著降低（Ｐ值＜０．０１），糖水组与标准食组相似；（２）各组皮质ｒＣＢＦ与ＥＥＧ总能量呈显著正相关；（３）胆固醇食兔栓塞组和结扎组缺血侧ｒＣＢＦ及ＥＥＧ均显著降低，血浆和ＬＤＬ中ＬＰＯ含量显著增高，ＬＤＬ的ＴＬＣ分析示有较多Ｘ带形成。结论长期高胆固醇食导致血浆和ＬＤＬ中ＬＰＯ及Ｘ带增多，ｏｘＬＤＬ形成，加速动脉粥样硬化，加重脑缺血时ｒＣＢＦ和ＥＥＧ能量和频率的降低。     

一个新的实验性冠状动脉痉挛动物模型

本研究探索一个实验性冠状动脉痉挛（ＣＡＳ）动物模型。健康犬１２只，分三组，静脉麻醉开胸分离左冠脉前降支。Ⅰ组（５只）:冠脉滴敷脑垂体后叶注射（ＩＰＰ）诱发ＣＡＳ；Ⅱ组（５只）:先形成冠脉部分狭窄再加上诱发ＣＡＳ；对照组（２只）:冠脉滴敷生理盐水。ＣＡＳ的判断及结果:Ⅰ、Ⅱ组施药后冠脉血流量（ＣＢＦ）明显减少（阳性例数５／５），心电图呈缺血性改变（阳性例数４／５）及严重室性心律紊乱，第Ⅱ组改变更显著。对照组的ＣＢＦ及心电图无改变。本实验诱发ＣＡＳ方法易行，成功率高，重复性好。其优点是诱发ＣＡＳ的部位可以选择，作用时间相对可控；血管收缩剂不直接进入血液循环，对冠脉以外其它血管动力学无影响，也控制了血液内各种因子检测的准确性。本实验模型可以用于进行ＣＡＳ的病理生理、生化、病理形态和治疗学的研究。     

断层脑血流显像在脑血管病中的应用现状

断层脑血流量显像技术不仅为临床医务工作者提供患者脑血流量（ＣＢＦ）、脑氧代谢率（ＣＭＲＯ２）和脑葡萄糖代谢率（ＣＭＲＧｌｕ）、脑血容量（ＣＢＶ）等重要信息，而且能测定中枢神经系统（ＣＮＳ）中某些受体分布特征及在疾病发生和发展过程中ＣＮＳ内某些受体数量及神经递质的变化，对脑血管病诊断、疗效观察、预后评价均有重要作用     

激光多普勒血流测定法在局部脑血流量监测中的应用

激光多普勒血流测定法（ＬＤＦ）是一种连续、实时、微创和敏感的脑组织微循环血液动力学监测新技术。文章介绍了ＬＤＦ的工作原理、测量值的相关因素,以及在局部脑血流量（ｒＣＢＦ）监测中的应用等,并与其他脑血流监测方法作了比较,归纳了其优缺点和应用领域。     

蛛网膜下腔出血后的急性脑血管痉挛

蛛网膜下腔出血（ＳＡＨ）后发生的脑血流量（ＣＢＦ）减少和脑缺血可能由急性脑血管痉挛引起,但是ＣＢＦ也受颅内压（ＩＣＰ）和脑灌注压（ＣＰＰ）的影响。本研究的目的是评价ＳＡＨ后急性脑血管痉挛与ＣＢＦ、ＩＣＰ、ＣＰＰ和细胞外谷氨酸浓度变化的关系。本研究由３...     

糖尿病合并脑梗死脑血流量和脑功能的研究

糖尿病对老年脑梗死患者脑干听觉诱发电位（ＢＡＥＰ）、脑电图（ＥＥＧ）和脑血流量（ＣＢＦ）的影响，国内外少见报道，我科１９４年６月～１９９８年１２月随机选择６５例无糖尿病和４５例合并糖尿病的动脉粥样硬化血栓性脑梗死患者，对ＢＡＥＰ、ＥＥＧ、ＣＢＦ进行了...     

Selective vulnerability of the brain: new insights into the pathophysiology of stroke

Stroke is a major cause of morbidity and mortality in the United States with 250,000 cases per year. Cerebral ischemia is the largest category of stroke with cardiac arrest, profound hypotension, and vascular occlusion the principal causes. Traditional approaches to the treatment of ischemic stroke focus on maintaining cardiac output, blood pressure, cerebral blood flow, and on preventing thrombosis. Recently, attention has been focused on developing new therapies that are directed toward abnormal biochemical events at excitatory synapses. Ischemia causes impairment of brain energy metabolism and the release of excessive amounts of glutamate into the extracellular space. This process secondarily excites neurons and further depletes energy stores. The excitotoxic hypothesis of brain injury proposes that glutamate is a principal cause of damage in ischemia. Three components of this hypothesis have been tested and largely proved in experimental studies in tissue culture and in animal models of stroke. First, elevated concentrations of glutamate cause excessive excitation at a subset of glutamate receptors, the N-methyl-D-aspartate (NMDA) receptor. Second, excitation at this receptor leads to excessive influx of sodium chloride and water which causes acute neuronal damage, and calcium which causes delayed and more permanent damage. Third, pharmacologic blockade at the NMDA receptor-ion channel complex prevents ischemic neuronal damage. Studies using specific pharmacologic compounds that block glutamate's action hold particular promise for treating stroke in humans, including competitive antagonists at the NMDA glutamate binding site (for example, 2-amino-5-phosphonovalerate, AP5), noncompetitive antagonists at the calcium channel (for example, MK-801, dextromethorphan, ketamine), and agents that might be directed at the glycine, zinc, and magnesium sites.     

Methylprednisolone treatment in acute myocardial infarction. Effect on regional and global myocardial function.

The effects of methylprednisolong treatment on acute myocardial ischemia were studied in nine closed chest dogs. After 1 hour of proximal occlusion of the left anterior descending coronary artery, an intravenous bolus injection (50 mg/kg body weight) of methylprednisolone was administered and its effects studied during an additional 2 hours of occlusion. After 2 hours of treatment the following significant mean alterations from levels after 1 hour of occlusion were noted: an increase of 16.7% in heart rate and decreases of 23% in left ventricular end-diastolic pressure, 32% in stroke volume, 14% in cardiac output and 37% in stroke work. Peak systolic pressure, maximal rate of rise of left ventricular pressure (dP/dt), left ventricular end-diastolic volume, systemic vascular resistance and coronary sinus blood flow changed less than 10%. Ejection fraction and regional cardiac wall motion were not improved. Metabolic dysfunction of the coronary-occluded myocardium, revealed by regional lactate as well as potassium derangements, persisted throughout the 2 hour treatment period. Comparison of these results with equivalent data from an untreated series of nine dogs with 3 hours of occlusion demonstrated no improvement in the treated series. Methylprednistone failed to restore regional cardiac metabolic and mechanical function, and treatment was associated with a further rise in S-T segment elevations. Administration of methylprednisolone after 1 hour of proximal left anterior descending coronary occlusion apparently does not reverse cardiac dysfunction in the first 2 hours of treatment.     

Left ventricular performance in canine endotoxin shock

Left ventricular performance was studied in 6 control and 7 experimental open-chest, heart-paced dogs before and after a single 1 mg/kg dose of E. coli endotoxin under pentobarbital anesthesia. Positive maximal dp/dt, time to peak ventricular pressure (PVP time), cardiac output, stroke work, tension-time index (TTI), coronary flow, and cardiac oxygen consumption were derived from left ventricular pressure, aortic flow, left atrial pressure, coronary sinus flow and A-V oxygen difference. During a control period and for 2 h post-endotoxin, while mean arterial pressure (afterload) and heart rate were held constant, +dp/dt max, PVP time, cardiac output, and cardiac work were related to left ventricular end diastolic pressure to obtain ventricular function curves. Positive maximal dp/dt was found depressed early (60 min) during the 2 h period of endotoxicosis studied (P less than .05). PVP time values increased after endotoxin administration but not significantly. Coronary sinus flow was found to be significantly elevated at 2 h post-endotoxin. The findings indicate the presence of early (60 min) and sustained depression of ventricular performance at elevated coronary blood flows during endotoxicosis.     

The effects of atrial fibrillation on regional blood flow in the awake dog

To determine the acute effects of atrial fibrillation on regional blood flow, measurements were made in awake dogs with this arrhythmia induced and sustained by rapid atrial stimulation. Atrial fibrillation reduced cardiac output (from 3.7 +/- 0.3 to 3.0 +/- 0.2 L/min, P less than 0.05), but mean aortic and left atrial pressures were not changed. Although average ventricular myocardial blood flow remained the same, dogs with an average basal myocardial blood flow less than 106 mL/min/100g showed an immediate increase (from 85 +/- 5 to 120 +/- 9 mL/min/100g, P less than 0.05), whereas those with a higher basal value showed a decrease (from 144 +/- 14 to 110 +/- 18 mL/min/100g, P less than 0.05). Moreover, change in myocardial blood flow with atrial pacing, at a rate equal to the average ventricular rate of atrial fibrillation, was directionally similar to that found during atrial fibrillation. However, left atrial myocardial blood flow increased significantly both during atrial fibrillation and pacing. Sustained atrial fibrillation resulted in a fall in splanchnic and renal cortical flow. Brain blood flow also decreased during atrial fibrillation. While the fall in cerebral blood flow was immediately evident, in the cerebellum and brain stem, this decrease was not statistically significant until the 15 min measurement. Also, presence of a ligated common carotid artery did not influence cerebral regional blood flow either under basal conditions or with atrial fibrillation. Thus, in awake dogs the fall in cardiac output that occurs with atrial fibrillation may be accompanied by diverse effects on regional circulations.     

Consequences of reperfusion after coronary occlusion. Effects on hemodynamic and regional myocardial metabolic function

Hemodynamic and regional metabolic measurements were obtained in seven closed chest dogs during a control period, 3 hours of coronary occlusion and 5 hours of reperfusion. Reperfusion resulted in intermittent ectopic arrhythmias in five dogs and severe shock in two. It usually caused increases in heart rate, coronary sinus flow and maximal isovolumetric rate of rise in left ventricular pressure (dP/dt), which were associated with a decrease in systemic pressure, left ventricular end-diastolic pressure, systemic vascular resistance and stroke work. A transitory increase in cardiac output occurred. Global myocardial oxygen consumption, which was reduced during occlusion, increased with reperfusion. Reperfusion induced abnormal lactate metabolism and myocardial potassium loss in the previously occluded area and often in the nonoccluded segment as well. Histopathologic changes of accelerated necrosis, reactive hyperemia and hemorrhage were often noted after reperfusion.These studies indicate that reperfusion after 3 hours of occlusion caused serious abnormalities in hemodynamic states, metabolic function and morphologic features of the heart.     

The effects of nisoldipine alone and in combination with beta-adrenoceptor blockade on systemic haemodynamics and myocardial performance in conscious pigs

The peak effects of 10 mg nisoldipine p.o. with or without 80mg propranolol p.o. on systemic and regional haemodynamics inconscious pigs were investigated. Nisoldipine increased heartrate (70%), cardiac output (67%) and maxLVdP/dt (75%), but decreasedmean arterial pressure (21%) as systemic vascular conductanceincreased by 120%. Left ventricular systolic and end-diastolicpressures were not affected. Vasodilatation occurred in mostorgans. The increase in left ventricular blood flow (150%) favouredthe epicardial (195%) over the endocardial (110%) layers. Asa result the endo–epi blood flow ratio decreased by 30% When nisoldipine was administered simultaneously with propranolol,heart rate (29%), cardiac output (35%) and systemic vascularconductance (65%) increased, but maxL VdP/dt did not change.Mean arterial (18%) and left ventricular systolic (10%) pressuredecreased; left ventricular end-diastolic pressure was againunaffected. In most organs vasodilatation was attenuated, butstill present, compared to the changes after nisoldipine alone.The increase in epicardial blood flow (70%) again exceeded thatin endocardial blood flow (35%), however, the endo–epiratio decreased by only 15%. In the presence of propranolol,nisoldipine did not exert a negative inotropic action whilethe reflex-tachycardia was attenuated. In addition, no detrimentaleffects on perfusion of regional vascular beds were observed.     

The effects of nisoldipine alone and in combination with beta-adrenoceptor blockade on systemic haemodynamics and myocardial performance in conscious pigs

The peak effects of 10 mg nisoldipine p.o. with or without 80mg propranolol p.o. on systemic and regional haemodynamics inconscious pigs were investigated. Nisoldipine increased heartrate (70%), cardiac output (67%) and maxLVdP/dt (75%), but decreasedmean arterial pressure (21%) as systemic vascular conductanceincreased by 120%. Left ventricular systolic and end-diastolicpressures were not affected. Vasodilatation occurred in mostorgans. The increase in left ventricular blood flow (150%) favouredthe epicardial (195%) over the endocardial (110%) layers. Asa result the endo–epi blood flow ratio decreased by 30% When nisoldipine was administered simultaneously with propranolol,heart rate (29%), cardiac output (35%) and systemic vascularconductance (65%) increased, but maxL VdP/dt did not change.Mean arterial (18%) and left ventricular systolic (10%) pressuredecreased; left ventricular end-diastolic pressure was againunaffected. In most organs vasodilatation was attenuated, butstill present, compared to the changes after nisoldipine alone.The increase in epicardial blood flow (70%) again exceeded thatin endocardial blood flow (35%), however, the endo–epiratio decreased by only 15%. In the presence of propranolol,nisoldipine did not exert a negative inotropic action whilethe reflex-tachycardia was attenuated. In addition, no detrimentaleffects on perfusion of regional vascular beds were observed.     

Hemodynamic and myocardial metabolic consequences of PEEP

The cardiac effects of positive end expiratory pressure (PEEP) were examined in 50 patients six hours after elective coronary bypass surgery. Increasing the level of PEEP from 5 to 10 to 15 cm H2O decreased cardiac index (evaluated by thermodilution), stroke index and left ventricular end diastolic volume index without a change in left ventricular ejection fraction (evaluated by nuclear ventriculography). Right ventricular end diastolic volume index remained unchanged. Coronary sinus blood flow (measured by the continuous thermodilution technique) and myocardial oxygen and lactate consumption were unchanged with the application of 15 cm H2O PEEP. In 21 patients, volume loading (250 ml [mL] of plasma) was performed at 5 cm, and again at 15 cm H2O PEEP. Volume loading produced a similar increase in cardiac volumes and cardiac index at 5 and 15 cm H2O PEEP. Right and left ventricular performance and left ventricular systolic function were not altered by PEEP (by analyses of covariance). Coronary sinus blood flow and myocardial oxygen consumption increased with volume loading at 5 and 15 cm H2O of PEEP, but myocardial lactate utilization tended to increase at 5 cm, and decrease at 15 cm H2O PEEP (p = 0.08). Of the 33 patients who underwent complete hemodynamic and metabolic measurements, 16 increased cardiac lactate utilization at 15 cm H2O PEEP and 17 decreased cardiac lactate utilization at 15 cm H2O PEEP. PEEP decreased cardiac index, perhaps by reducing left but not right ventricular volumes. Volume loading during PEEP restored cardiac index and revealed no depression in myocardial performance or systolic function. With the application of PEEP, myocardial metabolism was maintained in half the patients, but ischemic metabolism was observed in the other half.     

Influence of hypertonic mannitol on regional myocardial blood flow and ventricular performance in awake, intact dogs with prolonged coronary artery occlusion.

The influence of hypertonic mannitol on regional myocardial blood flow and ventricular performance in awake, intact, unsedated dogs with myocardial infarction resulting from chronic occlusion of the proximal left anterior descending coronary artery was studied. tmannitol given to increase serum osmolality 20 mOsm increased regional myocardial blood flow to that portion of the left ventricle supplied by the occluded left anterior descending coronary artery by 22 +/- 2.8% (1.06 +/- 0.19 to 1.36 +/- 0.23 ml/min with g-1) without changing the inner:outer wall flow ratio. Mannitol also significantly increased regional myocardial blood flow to other areas of the left ventricle and the ventricular septum. Mean aortic pressure, maximal LV dP/dt, LV dP/dt/P, and cardiac output also increased significantly after mannitol. Thus hypertonic mannitol increases regional myocardial blood flow and ventricular performance in the awake, unsedated dog with prolonged occlusion of the proximal left anterior descending coronary artery. The increase in regional myocardial blood flow after mannitol under these circumstances probably is at least in part secondary to the increase in blood pressure and contractility. The increases in regional myocardial blood flow after mannitol in this study are less impressive than those that have been previously reported in the setting of either no myocardial ischaemia or acute myocardial ischaemia; this is probably due to the vasodilatation that chronic myocardial ischaemia itself produces in the canine heart.     

Capillary supply and cardiac performance in the rabbit after chronic dobutamine treatment.

STUDY OBJECTIVE--Growth of capillaries in the adult heart can occur after long term vasodilator treatment. This study investigated the effects of increased stroke volume and/or force of contraction in addition to coronary blood flow on myocardial capillary growth. DESIGN--Coronary blood flow, cardiac function, and capillary supply were evaluated after chronic treatment with the inotrope dobutamine, at a dose shown to increase contraction force (dP/dt) acutely by 20% (p less than 0.05) and coronary blood flow by 60% (NS). EXPERIMENTAL MATERIAL--New Zealand Red rabbits received dobutamine (20 micrograms.kg-1.min-1 by intravenous infusion) for 2 weeks prior to measurements, under pentobarbitone anaesthesia, of coronary blood flow by radiolabelled microspheres, left ventricular dP/dtmax and maximum noradrenaline induced cardiac work, computed from cardiac output (thermodilution) and blood pressure. Capillary density.mm-2 was estimated in frozen 12 microns sections of left ventricular myocardium stained for alkaline phosphatase. MEASUREMENTS AND MAIN RESULTS--Capillary density was 29% greater after 2 weeks dobutamine infusion than in saline infused controls, which exceeds increases observed after longer infusions of vasodilators alone. Cardiac function was improved; maximum stroke work was significantly higher, stroke volume capacity larger, and dP/dt increased more during noradrenaline challenge. Coronary blood flow was unchanged in dobutamine treated hearts, hence efficiency of utilisation of coronary flow in terms of work was enhanced. Heart to body weight ratio was also greater after dobutamine, at 0.238(SEM 0.008) v 0.206(0.120), p less than 0.05. CONCLUSIONS--Greater capillary growth can be elicited in the heart by increased stretch and/or force of contraction of myocytes in addition to moderate changes in blood flow than by increased blood flow alone. Chronic dobutamine treatment induced adaptive enhancement of maximal cardiac work capacity.