参附青注射液对休克大鼠血压、心脏血液动力学和肠系膜微循环的影响

采用内毒素休克和心源性休克大鼠模型，观察参附青注射液对血压、心肌收缩力、肠系膜微循环的影响。结果表明，该方对内毒素休克大鼠上述指标有明显改善，而仅改变心源性休克大鼠的微循环     

参附青注射液对休克大鼠血压、心脏血液动力学和肠系膜微循环的影响

采用内毒素休克和心源性休克大鼠模型，观察参附青注射液对血压、心肌收缩力、肠系膜微循环的影响。结果表明，该方对内毒素休克大鼠上述指标有明显改善而仅改变心源性休克大鼠的微循环。     

心元对狗心肌缺血的改善作用研究

心元对心肌缺血引起的心肌收缩力下降和心输出量减少等有改善作用，并抑制缺血所致的血清磷酸酸激酶的升高，减少缺血区组织的范围。     

鹿角方对实验性心力衰竭兔血流动力学的影响

采用腹主动脉半结扎术复制家兔慢性心衰模型，发现术后１２ｄ其心脏重量指数增加，心脏舒张、收缩功能降低，与假手术组和正常对照组相比，差异显著。给心衰兔喂服鹿角方，可显著改善其心脏收缩功能，但对舒张功能无明显作用     

三七总皂苷对心肌缺血大鼠血流动力学影响实验研究

[目的]探讨三七总皂苷(PanaxNotoginsenySaponins,PNS)对大鼠急性心肌缺血(acutemyocardialischemia,AMI)模型血流动力学的影响。[方法]Wistar大鼠建立急性心肌缺血模型,随机分为假手术组、模型组、PNS小剂量组、PNS大剂量组。治疗7d后,分别测定左室血流动力学指标,包括左室收缩压(LVSP),左室舒张末期压(LVEDP),左室内压最大上升及下降速率(±dp/dtmax)。[结果]PNS可以降低LVEDP,升高±dp/dtmax。[结论]PNS治疗AMI可以改善心脏功能,大剂量应用对左室收缩和舒张功能均有显著提高作用。     

艾司洛尔对气管插管期间脑电双频指数的影响

目的　探讨艾司洛尔对气管插管期间血流动力学和脑电双频指数(BIS)的影响。方法　30例行腹腔镜胆囊切除术的患者,随机分为2组:艾司洛尔组(试验组)和生理盐水组(对照组)。全麻诱导: 2组均靶控输注异丙酚,血浆浓度为4μg·mL-1, 维库溴铵0. 1mg·kg-1。试验组在异丙酚输注5min后,予艾司洛尔1mg·kg-1, 并以150μg·(kg·min)-1维持;对照组予生理盐水。异丙酚输注10min后,行气管插管。观察诱导前、插管前及插管后1, 3, 5min平均动脉压(MAP)、心率(HR)及BIS的变化。结果　插管后1, 3min,对照组MAP、HR显著高于诱导前,试验组与诱导前比较差异无显著性。插管后1, 3min,对照组BIS较插管前显著升高,试验组BIS与插管前比较差异无显著性。结论　气管插管时,艾司洛尔即可减轻病人的心血管反应,又可抑制插管刺激引起的大脑皮层兴奋性的增加。     

红景天注射液对麻醉犬心脏血流动力学及心肌耗氧量的影响

目的:研究红景天注射液治疗冠心病的药理作用及作用机制。方法:将实验犬20只,随机分为空白对照组、阳性药对照组和红景天注射液小、大剂量组。经戊巴比妥钠30mg·kg^-1静脉麻醉后开胸,分别测定冠脉血流量、心输出量、左室内压、左室内压上升最大速率(dp/dt_max)、冠状静脉窦血氧含量、动脉血氧含量、心肌耗氧量、心搏出量、耗氧指数、心脏指数、冠脉阻力、总外周阻力及氧利用率等。结果:动物静脉注射红景天注射液后,冠脉阻力、动脉血压、总外周阻力、耗氧指数、心肌耗氧量、心率明显降低,心输出量、心搏出量及冠状静脉窦血氧含量明显上升,与药前及空白对照组比较均有显著性差异(P<0.05-0.01);左室内压和心肌收缩力则无明显改变。结论:结果表明,用红景天注射液可扩张冠脉血管、降低心脏后负荷,在不明显增加心肌收缩力和左心室压力的情况下,心输出量和每博出量明显增加,心脏有效作功得到加强;还能使冠状静脉窦血氧含量显著增加,心肌耗氧指数降低,心肌耗氧量下降,从而改善心肌的供血供氧,调整心脏血管的顺应性,对心血管系统起到调整和改善作用。这可能是红景天注射液治疗冠心病的药理机理。     

Nitric oxide does not play a major role in the regulation of systemic hemodynamic responses to acute normovolemic hemodilution

Background: The mechanisms of cardiovascular changes following acute normovolemic hemodilution (ANH) have not been fully elucidated. We tested the hypothesis that inhibition of nitric oxide synthesis attenuates ANH-induced cardiovascular responses.
Methods: We observed the effects of N^ω-nitro-L-arginine methyl ester (L-NAME) pretreatment on ANH-induced cardiovascular responses and compared these effects with those elicited by phenylephrine (PHE). Twenty dogs anesthetized with isoflurane were divided into two groups: one group was pretreated with L-NAME and the other with PHE. Both groups were normovolemically hemodiluted using 6% hydroxyethyl starch to reduce the hemoglobin concentration to approximately 50% of the pretreatment value.
Results: Pretreatment with either L-NAME or PHE caused a significant increase in mean aortic blood pressure (MAP) and systemic vascular resistance (SVR) with a significant decrease in cardiac output (CO) and stroke volume (SV). However, no remarkable differences in these variables were seen between groups. In both groups ANH produced increases in heart rate, CO, SV, and maximal left ventricular dP/dt with a significant decrease in SVR. No significant differences in these variables were apparent after ANH except that MAP was decreased in the PHE group but not in the L-NAME group.
Conclusion: Our results suggest that nitric oxide does not play a major role in mediation or modulation of the systemic vascular responses to ANH.     

Coronary and systemic hemodynamic effects of clevidipine, an ultra-short-acting calcium antagonist, for treatment of hypertension after coronary artery surgery

BACKGROUND: The aim was to evaluate the use of clevidipine, a new vascular selective, ultra-short-acting calcium antagonist for blood pressure control after coronary artery bypass grafting (CABG). METHODS: The effects of clevidipine on central hemodynamics, myocardial blood flow and metabolism were studied at two different phases after CABG. In phase 1 (n=13), the hypertensive phase, the effects of clevidipine were compared to those of sodium nitroprusside (SNP) when used to control postoperative hypertension. In phase 2 (n=9), the normotensive phase, a clevidipine dose-response relationship was established. RESULTS: At a target mean arterial pressure (MAP) of 75 mmHg, systemic vascular resistance (SVR) and heart rate (HR) were lower, preload, stroke volume (SV) and pulmonary vascular resistance (PVR) were higher, while there were no differences in myocardial lactate metabolism or oxygen extraction with clevidipine compared to SNP. In the normotensive phase, clevidipine induced a dose-dependent decrease in MAP (-19%), SVR (-27%) and PVR (-15%), accompanied by an increase in SV (10%), but no reflex increase in HR or changes in cardiac preload. Clevidipine caused a direct coronary vasodilation, as indicated by a decrease in myocardial oxygen extraction from 54% to 45%. Myocardial lactate metabolism was unaffected by clevidipine. The blood clearance of clevidipine was 0.05 l x min(-1) x kg(-1), the volume of distribution at steady state was 0.08 l x kg(-1) and the initial and terminal half-lives were <1 min and 4 min, respectively. CONCLUSIONS: Clevidipine rapidly reduced MAP and induced a systemic, pulmonary and coronary vasodilation with no effect on venous capacitance vessels or HR. Clevidipine caused no adverse effects on myocardial lactate metabolism. Clevidipine thus appears suitable to control blood pressure after CABG.     

超声检测血透患者颈动脉粥样硬化斑块及血流动力学分析

目的超声检测维持性血透（MHD）患者颈动脉动脉粥样硬化情况并分析其血流动力学参数与影响因素。方法75例MHD患者。采用高频B超检测其颈动脉粥样硬化斑块情况及血流动力学参数，并记录临床及生化数据，按斑块有无分为阳性组和阴性组。对两组各数据进行比较，并对斑块产生的各危险因素进行Logistic回归分析。结果MHD患者颈动脉斑块发生率为49．33％。好发于颈总动脉窦部及主干。与斑块阴性组患者相比，阳性组患者颈总动脉内径增大（P=0．013）、颈动脉内膜中层厚度（IMT）明显增厚（P〈0．001）。血流动力学参数分析提示舒张末期血流速度（Ved）明显降低（P=0．001），阻力指数（RI）明显升高（P=0．004），搏动指数（PI）升高（P=0．037），剪切率（SR）降低（P=0．023）。两组年龄、收缩压、血浆前白蛋白、血磷水平均有显著差异（P均〈0．01）。斑块阳性组的KT／V值低于阴性组（P=0.021）。Logistic多元回归分析结果提示高收缩压（β=0．097，P=0．037）和高血磷水平（β=2．800，P=0．049）是颈动脉斑块发生的主要危险因素。结论MHD患者颈动脉粥样硬化斑块产生与高收缩压和高血磷密切相关，其血流动力学基础特征在于血流阻力增加导致血流流速减慢，剪切应力降低。