川芎嗪对家兔心肌缺血再灌注损伤的保护作用

实验观察了川芎嗪对家兔心肌缺血再灌注损伤时心脏血流动力学、血清中和心肌组织中氧自由基和脂质过氧化物的影响。川芎嗪保护组与非保护组比较显示，①左室内压峰值（ＬＶＳＰ）明显升高（Ｐ＜０．０５）、左室内压上升最大速率（ＬＶ＋ｄｐ／ｄｔｍａｘ）和左室内压下降最大速率（ＬＶ－ｄｐ／ｄｔｍａｘ）均升高非常显著（Ｐ＜０．０１）；②血清中丙二醛（ＭＤＡ）明显降低（Ｐ＜０．０５），而谷胱甘肽过氧化物酶／脂质过氧化物（ＧＳＨ－ＰＸ／ＬＰＯ）升高非常明显（Ｐ＜０．０１）；③缺血再灌注损伤区心肌组织中ＭＤＡ显著降低，并伴随超氧化物歧化酶（ＳＯＤ）和ＧＳＨ－ＰＸ／ＬＰＯ显著升高（均Ｐ＜０．０５）。表明川芎嗪可通过提高对氧自由基的清除及拮抗脂质过氧化反应而保护缺血再灌注损伤的心肌。     

心肌顿抑时红细胞变形性变化机理及其意义初探

目的和方法：本文通过一次性阻断兔冠脉左室支１５ｍｉｎ后再灌注复制在体心肌顿抑（ＭＳ）模型，动态观察心肌缺血前后红细胞变形指数（ｄｅｆｏｒｍａｂｉｌｉｔｙｉｎｄｅｘ，ＤＩ）、红细胞超氧化物歧化酶（ｓｕｐｅｒｏｘｉｄｅｄｉｓｍｕｔａｓｅ，ＳＯＤ）活力、红细胞ＡＴＰ、红细胞丙二醛（ＭＤＡ）含量和心功能参数（左室舒张末压、左室收缩压±ｄｐ／ｄｔｍａｘ）变化。结果：缺血末心功能下降最显著（Ｐ＜００１）；再灌注０５ｈ时ＭＤＡ明显升高，而ＤＩ、ＳＯＤ明显下降（Ｐ＜００１）。随继续再灌注上述指标逐渐恢复。各时点ＡＴＰ无明显变化。再灌注０５ｈ时红细胞ＭＤＡ与ＤＩ、ＳＯＤ均呈显著负相关（Ｐ＜００１），ＤＩ与＋ｄｐ／ｄｔｍａｘ正相关（Ｐ＜００５）。结论：ＭＳ早期红细胞变形性降低与暂时性氧化－抗氧化失衡有关；再灌注早期红细胞变形性降低可能参与ＭＳ早期发生机制     

大豆磷脂脂质体对心肌缺血－再灌注家兔左心室功能和梗塞范围的影响

膜磷脂降解、丢失是心肌缺血－再灌注损伤的重要发病环节。本实验观察了静脉滴注大豆磷脂脂质体（１１０ｍｇ磷脂／ｋｇ／次×２次）对心肌缺血（４５ｍｉｎ）－再灌注（２３ｈ１５ｍｉｎ）家兔左心室的舒缩功能和梗塞范围的影响。结果发现经处理的动物的左室±ｄｐ／ｄｔｍａｘ均明显大于对照组，梗塞范围明显小于对照组（Ｐ＜０．０５，Ｐ＜０．０１）。提示大豆磷脂脂质体能明显改善在体缺血－再灌注心肌的舒缩功能，缩小梗塞范围。     

维拉帕米对失血性休克犬心脏的保护作用及机制

杂种犬１１只，由股动脉放血使平均动脉压（ＭＡＰ）维持在６．０ｋＰａ９０ｍｉｎ后回输全部血液，继续观察１５０ｍｉｎ。在休克３０ｍｉｎ后，对照组和维拉帕米处理组（Ｖｅｒ组）分别静脉滴注生理盐水和Ｖｅｒ溶液［（１０μｇ／ｋｇ·ｍｉｎ）１５ｍｉｎ］，液体总量为３ｍｌ／ｋｇ。对照组犬在失血后心率（ＨＲ）加快，左室ｄｐ／ｄｔｍａｘ显著降低，回输血液后ＭＡＰ虽有回升，但仍低于基础值，左室ｄｐ／ｄｔｍａｘ无明显改善；Ｖｅｒ使休克犬ＨＲ减慢，血液回输后ＭＡＰ缓慢恢复至基础值，左室ｄｐ／ｄｔｍａｘ显著高于对照组；电镜观察可见对照组心肌肌原纤维和线粒体等有明显的损伤，而Ｖｅｒ组心肌超微结构基本正常。结果还显示：Ｖｅｒ组犬心肌中丙二醛含量、黄嘌呤氧化酶活性低于对照组，而超氧化物歧化酶活性高于对照组。结果表明：Ｖｅｒ对失血性休克犬的心脏具有保护作用，其机制可能与其阻滞膜Ｃａ２＋内流、抑制脂质过氧化有关。     

7.5%NaCl/6%右旋糖酐抗高原创伤失血性休克大鼠的作用

目的：７５％ＮａＣｌ／６％右旋糖酐（ＨＳＤ）对平原创伤休克和低压舱模拟高原创伤休克均有很好的治疗作用，本实验目的是探讨ＨＳＤ对高原（西藏拉萨高原现场）创伤失血性休克急救作用及其量效关系。方法：初进高原大鼠２４只，分为生理盐水对照组（６只），ＨＳＤ４ｍＬ／ｋｇ，６ｍＬ／ｋｇ和８ｍＬ／ｋｇ治疗组（各６只），动物戊巴比妥钠（ｉｐ）麻醉，右侧股骨粉碎性骨折加放血（６０ｋＰａ维持７０ｍｉｎ）复制创伤失血休克模型，观察静脉一次输注上述几个剂量ＨＳＤ对创伤失血性休克大鼠血流动力学指标和动物存活时间的影响，以生理盐水作对照。结果：一次性静脉输注ＨＳＤ４ｍＬ／ｋｇ、６ｍＬ／ｋｇ、８ｍＬ／ｋｇ均能显著提升休克大鼠血压，改善包括左室内压（ＬＶＳＰ），左室内压最大变化速率（±ｄｐ／ｄｔｍａｘ），心肌最大收缩速度（Ｖｐｍ），心肌收缩向量环面积（Ｌｏ）在内的血流动力学指标，维持时间超过２ｈ，同时可明显延长休克动物的存活时间，其中４ｍＬ／ｋｇ效果不太明显，６ｍＬ／ｋｇ，８ｍＬ／ｋｇ效果较好，但这两剂量效果相当，无显著差异。结论：ＨＳＤ４～８ｍＬ／ｋｇ对高原创伤失血休克大鼠有较好的早期急救作用，剂量以６～８ｍＬ／ｋｇ较为合适。     

δ,κ亚型阿片受体在促甲状腺素释放激素抗兔失血性休克中的作用

目的和方法：用兔侧脑室给药观察了δ亚型阿片受体拮抗剂ＩＣＩ１７４，８６４和κ亚型阿片受体特异性拮抗剂ｎｏｒ－ｂｉｎａｌｔｏｒｐｈｉｍｉｎｅ（Ｎｏｒ－ＢＮＴ）预处理对促甲状腺素释放激素（ＴＲＨ）抗休克作用的影响。结果：ＴＲＨ（５０μｇ，ｉｃｖ）可明显升高失血性休克兔平均动脉压（ＭＡＰ），左室收缩压（ＬＶＳＰ），改善失血性休克心肌收缩力指标如心室内压最大上升和下降速率（±ｄｐ／ｄｔｍａｘ），心肌纤维收缩速度（Ｖｃｅ４０，Ｖｐｍ）和心肌收缩向量环面积（Ｌｏ）。δ－亚型阿片受体特异拮抗剂ＩＣＩ１７４，８６４预处理可取消ＴＲＨ的上述作用，κ－亚型阿片受体特异拮抗Ｎｏｒ－ＢＮＴ预处理不能取消ＴＲＨ的作用。结论：ＴＲＨ的抗休克作用与δ－亚型阿片受体有关，与κ－亚型阿片受体关系不大     

TRH抗高原创伤失血性休克大鼠的作用

目的：大量文献及本实验室以前的研究表明，促甲状腺素释放激素（ＴＲＨ）对平原创伤失血性休克有很好的治疗作用，对低压舱模拟高原创伤失血性休克大鼠、山羊也有较好的治疗作用。为了进一步验证其抗高原创伤失血性休克作用，本实验在西藏拉萨现场观察了ＴＲＨ对高原创伤失血性休克大鼠的治疗作用。方法：初进高原大鼠１５只，分生理盐水对照组（７只），ＴＲＨ治疗组（８组），右侧股骨粉碎性骨折加放血（６０ｋＰａ，维持１ｈ）复制创伤失血休克模型，观察静脉一次性输注ＴＲＨ（５ｍｇ／ｋｇ）和等容量生理盐水对创伤失血休克大鼠血流动力学指标和动物存活时间的影响。结果：ＴＲＨ（５ｍｇ／ｋｇ）一次性静脉输注能显著提升休克大鼠血压，改善包括左室内压（ＬＶＳＰ），左室内压最大变化速率（±ｄｐ／ｄｔｍａｘ），心肌最大收缩速度（Ｖｐｍ），心肌收缩向量环面积（Ｌｏ）在内的血流动力学指标，维持时间超过２ｈ，同时可明显延长休克动物的存活时间。结论：ＴＲＨ一次静脉输注有较好抗高原创伤失血休克作用，值得进一步临床验证。     

心肌缺血／再灌注对球结膜微循环的影响以及一氧化氮的调节作用

对照观察兔急性心肌缺血／再灌注时球结膜微循环的变化，测定动物血浆中内皮舒张因子／一氧化氮（ＥＤＲＦ／ＮＯ）、血栓素Ｂ２（ＴＸＢ２）、６－酮－前列腺素Ｆ１α（６－Ｋｅｔｏ－ＰＧＦ１α）、超氧化物歧化酶（ＳＯＤ）、丙二醛（ＭＤＡ）的浓度变化，并用光镜和电镜对缺血／再灌注心肌组织作形态学观察。结果发现：（１）兔心肌缺血／再灌注后球结膜微循环异常；表现为Ａ３、Ａ４微动脉血管管径缩小，毛细血管交换距离增大。（２）血浆中ＥＤＲＦ／ＮＯ水平降低；（３）血浆ＴＸＢ２、ＭＤＡ水平升高，ＳＯＤ、６－Ｋｅｔｏ－ＰＧＦ１α下降；（４）光镜下：缺血区心肌组织细胞肿胀变性。电镜下：内皮细胞肿胀，部分毛细血管腔内有红细胞、白细胞附壁阻塞，线粒体肿胀，糖原颗粒减少。结果提示：心肌在较短时间缺血后再灌注（缺血３０ｍｉｎ再灌注３０ｍｉｎ）后就可产生组织损伤，这可能与血管内皮受损，ＥＤＲＦ／ＮＯ合成释放减少，缩血管物质ＴＸＡ２升高，血小板、白细胞粘附、聚集在血管内皮上，氧自由基产生过多等有关。上述因素共同作用导致缺血／再灌注心肌微循环功能障碍进而引起组织形态改变。     

一氧化氮对离体心脏功能的影响

目的：初步探讨一氧化氮对心脏功能的作用及其可能机制。方法：本实验利用Ｌａｎｇｅｎｄｏｒｆ离体工作心脏灌流装置及技术,观察了ＮＯ供体ＳＩＮ－１、硝普钠灌流心脏后心功能及心肌某些生化指标的改变情况。结果：心脏功能多项指标明显下降,以ＬＶＳＰ,±ｄｐ／ｄｔｍａｘ为甚。伴之心肌ｃＧＭＰ含量的升高及心肌细胞膜Ｎａ＋－Ｋ＋－ＡＴＰ酶活性的下降。结论：一氧化氮通过调控心肌ｃＧＭＰ的合成及肌膜Ｎａ＋－Ｋ＋－ＡＴＰ酶活性而影响心肌功能。     

失血性休克条件下心肌细胞动作电位和心肌力学的改变的…

家兔失血性休克低血压５．３ＫＰａ观察３ｈ，测定平均动脉压（ＭＢＰ），左心室收缩压（ＬＶＳＰ）、左心了大收缩速度以及心肌细胞电生理和组织内外钾钠。结果说明（１）失血性休克后ＬＶＳＰ下降，且和ＭＢＰ平行；（２）ｄｐ／ｄｔｍａｘ在失血性休克后即刻急剧下降，１５ｍｉｎ后上升４８％，以后逐渐下降，３ｈ降至对照值的２０％；（３）休克时细胞外钾钠显著升高；（４）心肌细胞静息电位（ＲＰ）、动作曜闰振幅（ＡＰＨ）下     

Increased cardiac contractility in rats exposed to 5 bar

The left ventricular pressure, arterial blood pressure and heart rate were studied in three series of pentobarbital-anaesthetized rats exposed to 5-bar normoxic (PO2 = 0.2 bar) environments: nitrogen-oxygen (15 and 60 min) and helium-oxygen (15 min). The maximal left ventricular pressure (LVP max) and the maximal velocities of LVP rise (+ dP/dt max) and fall (- dP/dt) were significantly (P less than 0.01) increased immediately after reaching normoxic 5 bar (He, 13-28%; N2, 13-23%) and during the exposure at 5 bar (He, 22-44%; N2, 13-18%). The pulse pressure increased significantly (He, 50-62%; N2, 30-34%; P less than 0.01) during the hyperbaric exposure. No changes in heart rate or end-diastolic and mean arterial pressure were detected. The present findings indicate an enhanced cardiac contractility (+ dP/dt max) at 5 bar, with the greatest increase found when He was used as inert gas. The increased contractility was of significant duration (at least 60 min), and was not completely reversed until 5-10 min after decompression.     

小鼠病毒性心肌炎的心肌结构及左室功能变化的初步研究

目的:探讨病毒性心肌炎时的心肌结构与收缩力变化的关系。方法:建立病毒性心肌炎的动物模型,观测病毒损伤阶段和免疫损伤阶段心肌的超微结构和心肌收缩力改变。结果:病毒性心肌炎早期的心肌细胞的线粒体超微结构发生了变化,心肌细胞收缩力下降,左室压(LVP)为(14.2±0.8)kPa,dp/dt为(273.1±10.0)kPa/s,正常对照LVP为(17.1±0.7)kPa,dp/dt为(359.8±9.3)kPa/s,P＜0.01;后期心肌组织严重损害,不仅有线粒体溶解破坏,而且肌原纤维变细、减少等,并且心肌收缩力指标明显下降,LVP为(11.8±0.2)kPa,dp/dt为(209.5±6.9)kPa/s,与早期相比差异有显著,P＜0.01。结论:病毒性心肌炎早期,即病毒损伤期,造成心脏功能下降的原因主要是病毒引起心肌细胞的超微结构改变,特别是对线粒体的损伤,使心肌细胞供能障碍,心肌收缩力减小;病毒性心肌炎后期,免疫反应造成心肌组织损害较病毒直接损害更严重,造成心肌收缩力明显减小。     

大鼠实验性左室心肌梗塞对右室收缩性能的影响

对左室心肌梗塞(MI)是否会直接影响右室功能,至今尚有争议。本实验观察大鼠左室MI时右室dp/dt max的改变及其与左室dp/dt max和梗塞范围(IS)间的关系。结果发现冠脉结扎后1天,在左室dp/dt max显著降低的同时,右室dp/dt max也显著降低,且与左室dp/dt max呈显著的直线正相关,而与IS呈显著的直线负相关。在冠脉结扎后3天时,左室dp/dt max有显著恢复,但仍低于对照水平,而右室dp/dt max已恢复正常,且与左室的dp/dt max和IS间不再具有显著的直线相关关系。由此证明;在大鼠左室MI早期,右室收缩性能可受到直接影响,影响的程度与IS及左室收缩性能降低的程度相关;但当左室收缩性能恢复到一定程度时,这种影响消失。     

Erythropoietin changes contractility, cAMP, and nitrite levels of isolated rat hearts

There is enough evidence that erythropoietin (EPO) may be involved in cardiovascular function. Therefore we have investigated the possible effects of EPO on left ventricular developed pressure, +dP/dt(max), heart rate, tissue cAMP, and nitrite levels. Isolated rat hearts were perfused under constant flow (10 ml/min) conditions with modified Krebs-Henseleit solution and recombinant human erythropoietin at doses of 100, 200, 500, and 1,000 IU/kg was administered as bolus injections. EPO at 100 IU/kg decreased, but higher doses (500 and 1,000 IU/kg) raised the developed pressure and +dP/dt(max). However, it did not affect heart rate or coronary perfusion pressure when all the respective doses were applied. EPO at 100 IU/kg increased nitrite, and at 1,000 IU/kg it raised cAMP. Our results suggest that EPO may produce dose-dependently negative and positive inotropic effects on myocardial contractility in isolated rat hearts. NO and cAMP may be involved in negative and positive inotropic effects of EPO, respectively.     

Temporal relationship of contractility and myocardial potassium balance following beta-adrenergic stimulation of the in situ pig heart

Lower intracellular Na+ during beta-adrenergic stimulation provides an increased driving force for Na-Ca exchange, which might attenuate the inotropic response. Since (1) Na+ reduction is coupled to K+ uptake, and (2) K+ uptake lags behind the positive inotropic response to isoproterenol, we could examine the effect of Na-Ca exchange by comparing cardiac contractility and K+ balance following intracoronary isoproterenol infusion (0.6-0.8 microgram min-1). In 8 open-chest pigs, potassium concentrations were continuously measured by PVC-valinomycin mini-electrodes in arterial blood (a), and in myocardial venous blood in a shunt from the coronary sinus (cs) to the right atrium. Shunt flow, aortic flow, a left ventricular segment length and left ventricular pressure (LVP) were also continuously recorded. 64 (41-85)% (median and 95% confidence interval) of the LV dP/dt increase occurred within 1 min; thereafter contractility rose slowly. During the first minute of isoproterenol infusion, there was a small net myocardial K+ release, which then reversed to K+ accumulation. A maximum a-cs K+ concentration difference of 0.20 (0.09-0.39) mM occurred at 3.0 (2.0-4.25) min, falling to 0.05 (0.01-0.10) mM after 6.5 (3.75-8.75) min, at which point accumulated myocardial K+ uptake was 135 (27-219) mumol 100 g-1. Heart rate remained unchanged and intramural ECG indicated no sign of ischemia during the first 1.5 min of isoproterenol infusion. At 6.25 (5.0-8.0) min after stop of isoproterenol, LV dP/dt was 12 (9-24)% lower than before infusion (P less than 0.02) whereas myocardial K+ content remained higher than control. Thus, the monovalent cation shift succeeding the positive inotropic response was not associated with reduced contractility, but could explain the undershoot of LV dP/dt after stopping isoproterenol.     

Validation of a novel method to determine non-invasively the rate of central aortic pressure changes

Introduction: One of the most sensitive indices of myocardial contractility is represented by the rate of increase of intraventricular pressure during isovolumetric contraction (dP/dt) and (dP/dt_ejc), which represents the rate of change of pressure during ejection. Today these parameters can be obtained only by invasive catheterization methods. We developed a novel technique that leads to the non-invasive reconstruction of the central aortic pressure. The technique is based on the concept of applying multiple successive occlusive pressures on the brachial artery from peak systole to diastole using an inflatable cuff and plotting the values against time intervals. The hypothesis is that the time intervals required for the aortic pressure wave to overcome a given occlusive brachial pressure applied by a sphyngomanometer on the arm are equal to time needed to reach the same pressure in the central aorta plus the propagation time to the brachial point, which is constant in the same patient throughout the measurements.

Methods and results: We tested the hypothesis using an animal experiment. The new non-invasive device was mounted on the left forelimb of the animal. A Millar pressure transducer catheter was inserted to the aorta and the aorta pressure was recorded at time intervals of 1 ms. A second catheter was inserted into the coronary arteries and used to create controlled occlusion of the arteries using a balloon inflated to 10 atm. Measurements were obtained before the intervention was started, and throughout the sequence of repeated occlusions and deflations. At the end of the sequence, IV dobutamine was administered and results were monitored for 10 min while the heart rate and blood pressure were rising. Non-invasive dP/dt_ejc was reduced typically by 20% in response to balloon inflation. In long occlusion periods, stabilization and sometimes recovery of dP/dt_ejc is observed. By plotting dP/dt_ejc measured by the new non-invasive device versus catheter measurements a correlation factor of 0.843 was found.

Conclusion: A newly developed method of non-invasive measurement of central dP/dt has been found to correlate to invasive measurements in an animal model.     

非诺贝特和吡格列酮对压力过负荷大鼠心室重塑的影响及作用机制

目的： 探讨过氧化物酶体增殖物激活型受体（PPARs）的配体非诺贝特和吡格列酮对压力过负荷大鼠心功能、心室重塑的影响及其作用机制。方法： 取雄性Wistar大鼠腹主动脉缩窄致压力过负荷模型，术后48 h存活的40只随机分成：手术组（CAA组）、非诺贝特干预组（F组）、吡格列酮干预组（P组）及非诺贝特和吡格列酮联合干预组（F＋P组）。另以10只雄性Wistar大鼠为假手术对照。在给药处理12周后检测血流动力学参数、心室重塑指标、血浆和心肌肾素活性、血管紧张素Ⅱ、醛固酮及心肌的1型血管紧张素Ⅱ受体（AT1）mRNA表达变化。最终36 只大鼠获完整资料，上述各组分别为7、8、7、6和8只。 结果： F组、P组及F＋P组的左室湿重/体重、平均动脉压、左室收缩压、左室舒张末期压及心率低于CAA组，而左室压力上升、下降最大速率（±dp/dtmax）高于CAA组；F组、P组、F＋P组及CAA组间血浆和心肌肾素、血管紧张素Ⅱ、醛固酮活性无显著差异。P组和F+P组大鼠心肌AT1 mRNA 的表达水平低于F组。 结论： 尽管PPARα配体（非诺贝特）和PPARγ配体（吡格列酮）对血浆和心肌肾素活性、血管紧张素Ⅱ和醛固酮无明显影响，但PPARs信号通路激活能抑制压力过负荷大鼠心室重塑，降低前后负荷，并提高±dp/dtmax。PPARγ途径激活可抑制心肌AT1 mRNA的表达。     

Preload maintenance and the left ventricular response to prolonged exercise in men

This study examined whether left ventricular function was reduced during 3 h of semi-recumbent ergometer cycling at 70% of maximal oxygen uptake while preload to the heart was maintained via saline infusion. Indices of left ventricular systolic function (end-systolic blood pressure-volume relationship, SBP/ESV) and diastolic filling (ratio of early to late peak filling velocities into the left ventricle, E:A) were calculated during recovery and compared with baseline resting data. During exercise in seven healthy, trained male subjects, an arterial catheter allowed continuous assessment of arterial pressure, stroke volume (SV), cardiac output ( ) and an index of contractility (dP/dt(max)). A venous catheter assessed that central venous pressure (CVP) was maintained throughout rest, exercise and 10 min into recovery. Both systolic blood pressure and heart rate (HR) increased with the onset of exercise (from 132 +/- 5 to 185 +/- 19 mmHg and from 66 +/- 9 to 135 +/- 23 beats min(-1); increases from rest to the end of the first 5 min of exercise in SBP and HR, respectively) but systolic blood pressure did not change from 30 to 180 min of exercise ( approximately 150 mmHg), while heart rate only increased by 8 +/- 9 beats min(-1) (means +/- s.d.; P > 0.05). The attenuated increase in HR compared with other studies suggests that the maintained CVP ( approximately 5 mmHg) helped to prevent cardiovascular drift in this protocol. Stroke volume, and dP/dt(max) were all increased with the onset of exercise (from 85 +/- 8 to 120 +/- 18 ml, from 5.4 +/- 1.3 to 16.5 +/- 3.3 l min(-1) and from 14.4 +/- 4 to 28 +/- 8 mmHg s(-1); values from rest to the end of the first 5 min of exercise for SV, and dP/dt(max), respectively) and were maintained during exercise. There was no difference in the SBP/ESV ratio from pre- to postexercise. Conversely, E:A was reduced from 2.0 +/- 0.4 to 1.6 +/- 0.5 postexercise (P < 0.05), returning to normal values at 24 h postexercise. This change in diastolic filling could not be fully explained (r(2) = 0.39) by an increased heart rate and, with CVP unchanged, it is likely to represent some depression of intrinsic relaxation properties of left ventricular myocytes. Three hours of semi-supine cycling resulted in no evidence of a depression in left ventricular systolic function, while left ventricular diastolic function declined postexercise.     

The effect of endotoxin on the cardiovascular system

The dynamics of changes in myocardial contractility and pressure in the left ventricle of the heart and the femoral artery were studied in rabbits before and after intravenous infusion of 2 mg/kg endotoxin. The left ventricle was catheterized. The signal from the left-ventricular pressure transducer was fed into a microcomputer after analog-digital conversion for calculating the maximal rate of increase in intraventricular pressure. All the parameters studied began decreasing as early as the 5th minute after endotoxin administration. A statistically significant decrease (p less than 0.05) of the heart rate was recorded first on the 30th minute, than the left-ventricular pressure and maximal rate of intraventricular pressure increase took place on the 45th minute, and systolic and diastolic pressure in the femoral artery decreased on the 60th minute. The detected disorders of myocardial contractility provoke the appearance of hypotension the main role in the development of which is played by damage to the peripheral vascular network.     

The maximum derivatives of left ventricular pressure and transverse internal diameter as indices of the inotropic state of the left ventricle in conscious dogs

1. In normal, conscious dogs, I.V. infusion of isoprenaline caused inases in heart rate and the maximal derivatives of left ventricular pressure (dP/dt max) and left ventricular internal diameter (dD/dt max). The changes in both derivatives were linearly related to the increase in heart rate.2. Increments in heart rate produced by right atrial pacing caused only minimally significant increases in both dP/dt max and dD/dt max at heart rates of 180 beats/min. Increases in heart rate, with end diastolic diameter maintained constant, resulted in small but significant increases in dP/dt max and no significant increase in dD/dt max.3. Increasing preload by volume infusion had little effect on either derivative, while increasing afterload by phenylephrine administration produced a small but significant increase in dP/dt max and no change in dD/dt max.4. Both dP/dt max and dD/dt max are equally reliable as indices of the inotropic state of the myocardium and are minimally influenced by changes in preload, afterload or heart rate.