牡荆素对麻醉犬血流动力学及心肌耗氧量的影响

目的研究牡荆素对麻醉犬血流动力学及心肌耗氧量的影响。方法杂种犬30只,人工呼吸下开胸,给药后观察其心率（HR）、血压（MAP）、心输出量（CO）、冠脉血流量（CBF）、左室压（LVP）及血氧含量。计算冠脉阻力（CVR）和体循环总外周阻力（TPR）等血流动力学指标。采用多普勒超声血流仪测定麻醉犬冠脉流量和心输出量,用血气分析仪测定血氧含量。结果牡荆素可减慢心率和左心室内压,并显著增加麻醉犬冠脉血流量和心输出量,降低总外周血管阻力和冠脉阻力,提高心搏出量、心搏指数及心脏指数。结论牡荆素可显著改善麻醉犬血流动力学参数。     

栀蛭注射液对犬心脑血管作用的影响

目的了解栀蛭注射液在动物体内对心脑血管的药理学作用基础。方法采用电磁流量计直接测定犬脑血管流量,并测定犬Ⅰ、Ⅱ血流动力学参数。结果给犬静脉注射栀蛭注射液,对犬颈内动脉血管有一定的扩张作用,能增加每百克脑组织血流量,降低脑血管阻力;能增加犬冠状动脉和主动脉的血流量、增加每分钟百克心肌血流量、增加心搏出量、降低总外周血管阻力和冠脉阻力作用。结论栀蛭注射液有直接扩张心脑血管的作用。     

白藜芦醇对麻醉犬心脏血流动力学的影响

目的:探讨白藜芦醇对麻醉犬心脏血流动力学的活性,为其进一步开发及应用于临床提供基础。方法:13～17kg健康Beagle犬,3%戊巴比妥钠静脉注射麻醉,手术后连续测血压、左室内压;分离升主动脉根部,测心输出量;分离冠状动脉左旋支根部,测冠脉流量;四肢皮下插入针状电极,测心电图;十二指肠给药后连续观察120min,观察血流动力学的变化。结果:白藜芦醇可显著增加冠脉血流量,降低冠脉阻力;明显增加心输出量,降低总外周阻力;明显增加心搏出量、心搏指数、心脏指数;提高左室作功指数;减慢心率、心肌张力时间指数;但对麻醉犬收缩压、舒张压、平均压、左室内压等未见明显影响。结论:白藜芦醇对犬血流动力学具有一定活性。     

芍药苷对正常麻醉开胸犬血流动力学及心肌耗氧量的影响

目的:观察芍药苷对正常麻醉开胸犬血流动力学及心肌耗氧量的影响。方法:经十二指肠给药,以血压、左室内压、左室作功、冠脉阻力、心肌耗氧量等为观测指标,研究芍药苷对犬血流动力学及心肌耗氧量的影响。结果:芍药苷具有降低左室内压,降低左室作功指数、降低血压、降低总外周阻力、降低冠脉阻力;降低心肌耗氧量的作用。结论:芍药苷可通过增加冠脉流量,增加氧的供应,降低心肌耗氧量,改善心脏血流动力学。     

益气通脉口服液对麻醉犬心脏血流动力学的影响

研究了益气通脉口服液对麻醉犬心脏血流动力学的影响。结果表明,益气通脉口服液可显著增加冠脉血流量、降低冠流阻力、明显增加心输出量、心搏出量、降低外周阻力、增加左室作功     

蝙蝠葛酚性碱对犬血流动力学及冠脉循环的影响蝙蝠葛酚性碱对犬血流动力学及冠脉循环的影响

目的研究蝙蝠葛酚性碱（PAMD）对正常麻醉犬血流动力学、冠脉循环及心肌氧代谢的影响。方法设立生理盐水阴性对照组及PAMD 3.5和7.0 mg·kg^-1两剂量组，在不同时间点观察各组犬血流动力学、冠脉循环及心肌氧代谢的相关指标的改变。结果与药前相比，PAMD两剂量组均可降低左心室收缩压（LVSP）和±dP/dt_max，减慢心率，增加心肌氧含量、降低心肌氧利用率，且具有增加冠状动脉血流量，降低冠状动脉阻力和外周阻力的作用。对血压、心输出量和左室舒张末压（LVEDP）无显著影响。结论PAMD能改善血流动力学、冠脉循环及心肌氧代谢。     

麝香保心分散片对冠脉结扎犬血流动力学的影响

目的研究麝香保心分散片对冠脉结扎犬血流动力学的影响。方法采用麻醉犬开胸结扎左冠状动脉前降支 (LAD)产生急性心肌梗死 (AMI)模型 ,测定AMI 3h犬的心脏血流动力学参数。结果十二指肠给予麝香保心分散片 ,能明显增加心输出量 (CO)和搏出量 ,增加心肌血流量 ,降低冠脉阻力 ,增加左室收缩内压 (LVSP)及室内压最大上升和下降速率 (±dp/dtmax) ,轻度减慢心率 ,明显降低左室舒张末期压 (LVEDP) ,增加冠脉结扎犬心脏指数 (CI)及搏功 ,降低总外周阻力 ,对平均动脉压有下降趋势。结论麝香保心分散片主要以改善心肌收缩和舒张功能 ,增加缺血心肌供血等环节 ,发挥抗心肌缺血作用     

荭草苷对麻醉犬心功能与血流动力学的影响

目的 研究荭草苷对麻醉犬心功能与血流动力学的影响.方法 麻醉犬开胸,测定心脏血流动力学参数,并分离冠状动脉左旋支,放置探头测量冠脉血流量,同步测量心输出量.结果 0.5、1.0、2.0 mg·kg-1荭草苷可降低麻醉犬的血压,减少心肌耗氧量以及减慢心率,降低左室舒张末期压,左心室内压最大上升和下降速率,同时增加冠脉血流量.结论 荭草苷通过减少心肌耗氧量,降低左室舒张末期压及左心室内压最大上升和下降速率,使冠脉流量增加等环节发挥改善麻醉犬心功能与血流动力学的作用.     

白川降压胶囊对麻醉犬血流动力学的影响

目的研究白川降压胶囊对麻醉犬血流动力学的影响。方法采用有创血流动力学实验方法,观察不同剂量白川降压胶囊对麻醉犬血流动力学的影响。结果白川降压胶囊大剂量(每公斤体质量0.18g)可明显降低麻醉犬收缩压、舒张压和平均动脉压,并有降低外周血管阻力及冠状动脉阻力、增加冠脉血流量的作用。结论白川降压胶囊有明显降低麻醉犬血压和改善心脏功能的作用。     

当归对犬血流动力和心肌氧代谢的影响

本文研究了当归注射液对麻醉犬血流动力和清醒高血压犬血压和心率的作用。麻醉犬于静脉注射当归2 g/kg后,血压降低、冠脉、脑和外周血流量增加,血管阻力降低,心排出量稍增加,总外周阻力降低,心肌氧消耗量减少。清醒高血压犬静脉注射当归2 g/kg后,血压和心率均先有增加,随后减少。     

Hemodynamic and myocardial metabolic effects of the beta-agonist prenalterol in ischemic left ventricular dysfunction

Hemodynamic and myocardial metabolic parameters in ischemic left ventricular (LV) dysfunction were evaluated in response to the beta-agonist prenalterol. Twenty micrograms/kg intravenous prenalterol increased resting heart rate and cardiac output and decreased LV filling pressure, systemic vascular resistance, and pulmonary artery pressure. Resting coronary blood flow and myocardial oxygen consumption increased but net myocardial lactate and oxygen extraction did not change significantly. During pacing induced tachycardia (121 +/- 4 beats/min), prenalterol improved cardiac index and stroke work index; whereas, LV filling pressure, systemic vascular resistance, and pulmonary artery pressure decreased. Coronary blood flow and myocardial oxygen extraction did not change significantly. Net myocardial lactate extraction during pacing decreased insignificantly; one patient developed overt lactate production. Thus, prenalterol improves cardiovascular function at rest and during pacing-induced tachycardia in ischemic LV failure, but at the cost of higher resting myocardial oxygen consumption. The majority of subjects had no adverse metabolic response.     

地奥心血康对犬心肌缺血及血流动力学的影响

本文研究地奥心血康对结扎冠状动脉所造成的犬急性心肌缺血及心脏血流动力学的影响。地奥心血康１００ｍｇ／ｋｇ，ｉｖ，能明显减少心肌缺血范围，减轻缺血损伤程度；可使心率明显减慢，血压、心输出量、左室内压、左室作功、心肌耗氧量、冠状动脉阻力和总外周阻力下降，冠状动脉血流量增加。提示该药有抗心肌缺血作用，并能改善心脏血流动力学。     

甲基黄酮醇胺对麻醉犬的心血管作用

甲基黄酮醇胺（ＭＦＡ）２和５ｍｇ·ｋｇ－１ｉｖ减慢麻醉犬心率,降低血压,但对左心室收缩压,左心室舒张末压和左心室内压最大上升及下降速率（±ｄｐ／ｄｔｍａｘ）没有显著影响．ＭＦＡ５ｍｇ·ｋｇ－１ｉｖ后３０ｍｉｎ麻醉犬心输出量增加２％,总外周阻力下降１６％;冠脉血流量增加３８％,冠脉阻力下降３９％．ＭＦＡ２和５ｍｇ·ｋｇ－１ｉｖ分别使心肌耗氧指数下降１８％和２３％．研究表明,ＭＦＡ具有增加麻醉犬冠脉血流量,降低心肌耗氧量,降低外周血管阻力的作用．     

Cardiac and systemic hemodynamic actions of the slow channel calcium blocking agent, KB-944

The effects of KB-944 (10-400 micrograms/kg/min, i.v.), a new slow channel calcium blocking agent, on myocardial oxygen utilization, regional myocardial perfusion and hemodynamics were measured in anesthetized dogs. KB-944 produced significant dose-related increases in coronary blood flow and decreases in heart rate, left ventricular systolic pressure, aortic blood pressure and peripheral vascular resistance. At high doses, peak positive and negative dP/dt were both reduced and left ventricular end diastolic pressure increased. KB-944 reduced arterial-venous oxygen content difference across the heart while significantly increasing coronary blood flow. The pressure rate product, an index of myocardial oxygen consumption, was also reduced. KB-944 produced a uniform and dose-related increase in transmural tissue flow within the left ventricular free wall. These results indicate that KB-944, a new slow channel calcium blocking agent, is a potent peripheral and coronary vasodilator with negative inotropic and chronotropic properties and may be potentially useful in coronary artery disease or hypertension.     

Hemodynamic activity of L6150

Summary The systemic and coronary hemodynamic effects of the new antihypertensive agent L 6150 (3-hydrazino-6-[N,N-bis(2-hydroxyethyl) amino]pyridazine) have been investigated in anesthetized and unanesthetized dogs, in comparison with hydralazine.The depressor effect induced by L 6150 is due to a fall of peripheral resistance and, in conscious animals, is accompanied by an increase of cardiac output and heart rate, suggesting that the main activity of the drug is related to a vasodilator effect.The compound was shown to markedly increase coronary blood flow. This effect, which in conscious dogs can be explained, at least in part, on the basis of an increased myocardial metabolism, was observed to occur in anesthetized animals even in conditions of reduced cardiac output and myocardial oxygen consumption.In anesthetized dogs the same systemic, hemodynamic modifications were induced by L 6150 and by higher doses of hydralazine. Furthermore the percent increase of coronary blood flow induced by L 6150 was significantly higher than that induced by hydralazine, for the same degree of modifications of myocardial oxygen uptake. In conscious dogs, L 6150 induced the same systemic hemodynamic modifications as hydralazine with the exception of heart rate, which was increased more by the former drug. The coronary blood flow increase was more marked following L 6150 than following hydralazine, even when the two drugs induced the same increase of cardiac output.This work was presented, in part, at the Joint Meeting of German Pharmacological Society and Italian Pharmacological Society, Heidelberg, September 1970.     

Nifedipine reduces arrhythmias but does not alter prostanoid release during coronary artery occlusion and reperfusion in anaesthetised greyhounds

We examined the effects of nifedipine, a calcium slow-channel blocking drug, on haemodynamics, blood gases, cardiac arrhythmias, and prostanoid release in anaesthetised greyhounds before, during, and after a 40-min occlusion of the left anterior descending coronary artery. Fifteen minutes after commencing treatment with nifedipine (5 micrograms/kg + 0.67 micrograms kg-1 min-1), there were significant reductions in arterial blood pressure, left ventricular end-diastolic pressure, and vascular resistance, with increases in cardiac output and stroke volume. Although coronary artery blood flow was unchanged, oxygen extraction was decreased, indicating that nifedipine reduced oxygen consumption. Nifedipine prevented the haemodynamic changes that occur in control dogs during acute myocardial ischaemia and markedly reduced the number of arrhythmias during coronary artery occlusion. The incidence of ventricular fibrillation induced by release of the occlusion was significantly reduced from 88% in the control group to 22% in the group receiving nifedipine. The release of thromboxane B2 and 6-keto PGF1 alpha (stable breakdown products of thromboxane A2 and prostacyclin, respectively) from the acutely ischaemic myocardium was not altered by nifedipine. It is concluded that this low dose of nifedipine had marked antiarrhythmic activity during both coronary artery occlusion and reperfusion. The relationship to dosage and possible mechanisms for this effect are discussed.