间硝苯吡啶与硝苯吡啶对左室功能及心肌氧耗的比较研究

间硝苯吡啶(M-Nif)为新合成的钙拮抗剂。实验表明,M-Nif可增加麻醉狗的CI、SI,降低麻醉猫的舒张压、TTI较Nif强而持久。Nif增加心率,M-Nif却无影响或略减少。M-Nif增加冠状窦氧含量,缩小动静脉氧差的强度弱于Nif,但降低心肌氧摄取率。二氧化碳产生率则较Nif强。提示M-Nif治疗充血性心力衰竭优于Nif。     

羟苯氨酮对麻醉狗心脏血流动力学与心肌氧消耗的影响*

目的:研究强心扩血管新药羟苯氨酮对心肌氧消耗的影响。方法:用多导生理记录仪和电磁流量计测定麻醉开胸狗心脏血流动力学参数,用血气分析仪测定动脉与冠状窦血氧含量,计算心肌氧代谢参数。结果:羟苯氨酮iv 0．5～4mg·kg~(-1)轻度减慢心率,中度降低血压、左室作功、冠脉阻力与总外周血管阻力,短暂增加心输出量与冠脉流量,明显降低心肌氧摄取率与氧消耗量。结论:羟苯氨酮降低心肌氧消耗与心脏负荷,增加心肌供血,有利于对心肌缺血的治疗。     

体外循环心脏手术中心肌保护方法的改进

采用充氧温血停跳液经主动脉根部间断灌注，或经冠状静脉窦持续逆行灌注，应用26例。其中单瓣置换8例，双瓣置换4例，主动脉窦瘤破裂修补2例，左房粘液瘤切除5例，心功能Ⅲ～Ⅳ级者22例。对照观察发现，充氧温血灌注法术中心脏自动复跳率高，术后循环功能稳定，严重心律失常及低心排综合征发生率低，对缺血心肌的保护优于冷晶体灌注法。     

四季青、丹参、毛冬青等对猫冠状窦流量、心肌氧耗量作用的初步分析

既往,作者曾报导四季青叶中所含之原儿茶醛具有明显增加猫冠状窦流量的作用,心肌氧耗量虽亦增加,但低于流量之增加,如以小剂量储血池内投药,可降低狗冠脉左旋支及下肢血管的阻力,静脉注射可明显降低     

免冠脉结扎后血管紧张素Ⅱ水平的变化

本文用兔模型研究了冠脉结扎后第24小时及28天周围静脉血、冠状窦血及不同状态的心肌组织(梗塞心肌、缺血损伤心肌及正常心肌)的血管紧张素Ⅱ水平(AgⅡ)。结果发现,在冠脉结扎后两个时间点,周围静脉及冠状窦血AgⅡ均有显著升高,但以冠状窦血为显著,冠脉结扎后24小时梗塞心肌及缺血损伤心肌均有显著的AgⅡ水平升高,28天则以梗塞周边区心肌AgⅡ升高为主。     

经股静脉途径改良方法放置冠状窦电极的可行性分析

目的：探讨电极在右房内成袢后置入冠状窦行电激动标测的可行性和安全性。方法：选择12例拟行射频消融术,但锁骨下静脉穿刺失败或股静脉途径常规方法放置冠状窦电极失败的患者。采用使电极在右房内成袢后置入冠状窦的方法。结果：电极成袢后置入冠状窦的成功率为91%,尚无并发症发生。结论：改良式股静脉途径放置冠状窦电极的操作较简单,电极在冠状窦内位置稳定,利于电激动顺序标测,建议作为放置冠状窦电极的可选操作方式。     

温氧合血停搏心肌对甲状腺激素的影响

目的了解常温体外循环（CPB）持续温血灌注心肌保护对甲状腺激素（TH）变化的影响并探讨其临床意义。方法选择22例常温CPB持续温血灌注停搏患者，分别于术前、术中、术后6、24、48、72h测定其血浆T3、T4、rT3的浓度，将其与22例冷停搏CPB患者的测定值进行对比分析。结果（1）温血组T4改变差异无显著意义（P〉0．05），冷停搏组术中Td降低（P〈0．01），术后6h恢复正常；（2）温血组术后T3降低，24hT3值较术前下降51．2％，48h达最低点，较术前下降56．8％，rT3增高，24h为术前的1．72倍，48h为术前的1．74倍。冷停搏组术后T3降低，24h达最低点，较术前下降64．5％，rT3增高为术前的2．64倍（P〈0．01）；（3）温血CPB主动脉阻断时间≥60min与〈60min比较，T3降低差异有显著意义（P〈0．01），时间越长，T3降的越低，rT3改变差异无显著意义（P〉0．05）；（4）当有严重低心排、急性肾功能衰竭等并发症时，T3呈进行性降低，rT3显著增高（P〈0．01）。结论（1）无论冷停搏CPB或持续温血灌注CPB均可导致术后低T3综合征；（2）与冷停搏组比较，温血组对T3、rT3影响较轻，T3、rT3改变的程度亦较小；（3）CPB主动脉阻断时间超过60min或有严重并发症时更易发生低T3综合征。     

主动脉窦瘤18例临床分析

18例主动脉窦瘤病人均经超声心动图检查,13例手术证实。18例中,右冠状窦瘤15例(破入右室12例,破入右室流出道3例),无冠状窦瘤2例(均破入右房),左冠状窦瘤1例(未破)。对手术病人进行了长期随访观察,并与未手术病人作了比较。在分析18例临床资料的基础上,对本病的病因、发病率、并发畸形、临床表现、诊断、鉴别诊断及治疗结合文献作了探讨。     

丹参素钠对麻醉犬心肌耗氧量的影响

目的观察丹参素钠静注对麻醉犬心肌耗氧量的影响。方法采用心导管法检测冠状静脉窦血样及动脉血氧等指标,研究丹参素钠对缺血心肌的作用。结果给药后5 min到120 min的各时间点,丹参素钠可明显增加麻醉犬心输出量、冠脉流量;降低冠脉阻力;降低总外周阻力;明显降低心肌氧摄取率,与生理盐水组比较有显著差异,作用强度与剂量有一定的量效关系。结论丹参素钠对心肌缺血损伤具有一定预防治疗作用。     

儿童窦口鼻道复合体的解剖变异与鼻窦炎

目的:研究儿童窦口鼻道复合体解剖结构变异与鼻窦炎的关系。方法:选取15岁以下患鼻窦炎的儿童153例(鼻窦炎组),与正常同龄儿童72例(对照组),分别进行鼻窦冠状CT扫描及鼻内窥镜检查。结果:正常对照组与鼻窦炎组解剖变异的比较及各年龄组的解剖变异的比较差异均有统计学意义(P<0.01)。结论:(1)儿童窦口鼻道复合体已经发育,可以通过CT扫描予以观察。(2)儿童窦口鼻道复合体通气和引流障碍是导致鼻窦炎迁延不愈和反复发作的关键。(3)儿童窦口鼻道复合体解剖变异随着年龄的增长其变异率有上升趋势。     

葛根素对急性心肌缺血狗区域性心肌血流与心脏血流动力学的作用

麻醉开胸狗ⅳ葛根素(puerarin)可减慢心率(HR)、降低主动脉压(MAP),用同位素标记微球法测得的缺血区侧枝冠脉血流量并不减少。从狗的右室旁路制备的心脏血流动力学实验发现葛根素明显减低张力一时间指数(TTI)与左室压力升高速度(LV dp/dt)。当MAP调整到给药前的水平时,TTI与LV dp/dt恢复,进入缺血区的侧技血流增加,非缺血区的冠脉血流量(CBF)亦增加。葛根素减低冠脉血管阻力(CVR)的作用比减低全身血管阻力(SVR)的作用更显著。葛根素不影响心肌收缩力,但增加局部心肌缺血时的侧枝血流并减少与心肌氧消耗有关的血流动力学参数。这些结果提示葛根素有益于治疗心肌缺血。     

间硝苯啶对猫冠脉流量,心肌耗氧量的量效关系

不同剂量m-Nif 10,20,40μg·kg~(-1)iv显著增加猫冠脉血流量(CBF),并呈明显量效反应关系,按作用峰值计算,分别增加原水平30,68,94％,Nif-20μg·kg~(-1)增加原水平49％,同时显著降低心肌耗氧量(MOC),按作用峰值计算,分别降低原水平29,46,55％,Nif降低原水平45％,心肌氧摄取减少,m-Nif分别减少原水平31,44,54％,Nif43％,血压分别降低原水平39,42,50％,Nif45％,m—Nif明显减慢心率,Nif则不减慢心率.m—Nif在40μg·kg~(-1)iv增加冠脉流量远较其他剂量强而持久,Nif较同量m-Nif作用弱而短。     

Measurement of oxygen tension in the ischemic myocardium using encased polargraphic oxygen electrodes

The ability to continuously monitor the delicate balance between blood flow and oxygen consumption would be a great asset in the study of myocardial ischemia. The present study was performed, in anesthetized dogs, to validate the use of encased polargraphic oxygen electrodes in the study of myocardial ischemia. Polargraphic oxygen electrodes were placed in the area to be rendered ischemic at fixed tissue depths of 3 mm (epicardium) and 9 mm (endocardium). Endocardial and epicardial oxygen tensions as well as the ratio of endocardial to epicardial oxygen tension and left circumflex coronary flow were monitored. Ischemia was induced by decreasing left circumflex coronary flow by 50%. Upon completion of a 20-min poststenotic period, endocardial pO₂, endocardial/epicardial ratio, and coronary flow were significantly decreased (59 ± 7, 52 ± 7, and 55 ± 4%, respectively) whereas epicardial pO₂ was slightly decreased. Nitroglycerin (10 μg/kg, i.v.) markedly increased endocardial pO₂ and endocardial/epicardial ratio above poststenotic control (13 ± 5 mmHg and 64 ± 10%, respectively) whereas epicardial pO₂ was not significantly decreased. The increases in endocardial pO₂ occurred at a point where coronary flow and mean arterial pressure were not significantly changed. Conversely, dipyridamole (125 μg/kg, i.v.) significantly increased coronary flow (26 ± 2 ml/min/100 g) although it did not appreciably alter endocardial or epicardial pO₂. It is concluded that encased polargraphic oxygen electrodes provide a quantitative method for determination of oxygen tension in the ischemic myocardium.     

Effects of nitrendipine on cardiovascular systems

Cardiovascular effects of nitrendipine were examined in anesthetized dogs, blood-perfused canine papillary muscles and isolated arteries. In anesthetized dogs, nitrendipine by intravenous (0.3-10 micrograms/kg) or intraduodenal (0.1 mg/kg) administration lowered blood pressure and increased coronary and vertebral blood flow. Nitrendipine also decreased the difference in oxygen concentrations between arterial and coronary sinus blood, which indicates that nitrendipine increased the oxygen supply to the heart. Myocardial oxygen consumption was slightly increased at a low dose (3 micrograms/kg, i.v.) accompanied with a small increase in max dP/dt, but was decreased at high doses (30-100 micrograms/kg, i.v.). A negative inotropic effect was observed in blood-perfused canine papillary muscles. However, nitrendipine is thought to be highly vasoselective because much higher doses were required to decrease the myocardial contraction than to increase the coronary blood flow. Furthermore, nitrendipine suppressed the contraction induced by KCl, acetylcholine, histamine, norepinephrine, 5-hydroxytryptamine and prostaglandin F2 alpha of porcine coronary arteries, and the rhythmic contraction induced by 3,4-diaminopyridine of canine coronary arteries. In isolated rabbit aortic preparations, nitrendipine strongly inhibited the KCl-induced contraction, but not the phenylephrine-induced contraction. These effects of nitrendipine were almost similar to those of nifedipine. It is suggested that nitrendipine decreases afterload (blood pressure), increases the blood flow and oxygen supply to the heart, and inhibits coronary spasm, which is due to the calcium antagonistic effect. Nitrendipine may be useful for the treatment of ischemic heart diseases.     

Lack of protection of ischemic myocardium by verapamil in conscious dogs

To determine whether coronary dilation and decreased myocardial oxygen requirements resulting from administration of verapamil, a calcium and slow current antagonist, protect ischemic myocardium in conscious dogs, we studied 15 treated and 15 control animals after coronary occlusion. Verapamil (0.2–0.7 mg/kg/h) was given by continoous infusion for 17 h beginning 5 h after the initial plasma creatine kinase (CK) elevation after coronary occlusion. Observed infarct size and infarct size predicted before verapamil were estimated from hourly plasma CK values and infarct size was estimated also from myocardial CK depletion measured directly, 24 h after occlusion. Changes in heart rate, blood pressure, and frequency of premature ventricular complexes (recorded every 30 min) after occlusion were similar in treated and control dogs. Coronary flow after verapamil, measured with radioactively labeled microspheres, did not increase in ischemic zones but increased by 90% in normal myocardium (p < 0.05). The differences between observed and predicted infarct size estimated from plasma CK changes in treated and controls were similar (3.0±2.2 (S.E.) and 2.0±1.4 CK-g-eq), and myocardial CK depletion was also comparable in the two groups (25 ± 2% and 23 ±2%). Thus although verapamil, administered five hours after the initial plasma CK elevation, increased coronary flow in normal myocardium, it did not augment flow in ischemic tissue or limit the extent of infarction.     

ACUTE ISCHEMIC PRECONDITIONING AND HIGH SUBCHRONIC CO EXPOSURE INDEPENDENTLY INCREASE MYOCARDIAL TOLERANCE TO ISCHEMIA

This study was designed to investigate whether exposure to carbon monoxide (CO) could alter or raise the ischemic tolerance induced by preconditioning. To this end, isolated rat hearts were aerobically perfused for 20 min. Hearts were then randomized to two groups: (1) a further 20-min aerobic perfusion, and (2) ischemic preconditioning (2 cycles of 5 min of ischemia followed by 5 min of reperfusion). Hearts were then subjected to 25 min of low-flow (0.3 ml/min.) global ischemia (37°C) and 30 min of reperfusion. In parallel studies, the same protocols were performed in hearts from rats previously exposed to subchronic CO (600 ppm for 2 wk). Ischemic preconditioning accelerated the development of ischemic contracture (onset = 6.0 ± 0.3 vs. 8.6 ± 0.9 min), increased the preischemic coronary flow (19.0 ± 1.0 vs. 11.6 ± 0.6 ml/min/ g), improved contractile recovery (73.7 ± 8.9 vs. 30.8 ± 7.5%), but was without effect on reactive hyperemia (151.2 ± 4.7 vs. 149.2 ± 5.1%) and incidence of ventricular arrhythmia during reperfusion (55.6 vs. 60.0%) compared to a control group. CO exposure alone increased the baseline coronary flow (20.1 ± 1.5 vs. 12.8 ± 0.6 ml/min/g) and the contracture magnitude (54.8 ± 6.8 vs. 37.1 ± 4.8%), improved both contractile recovery (66.1 ± 6.3 vs. 30.8 ± 7.5%) and ventricular arrhythmia incidence (22.2 vs. 60.0%), and increased the hyperemic coronary flow (26.7 ± 1.5 vs. 19.1 ± 0.7%). Preconditioning after CO exposure exacerbated ischemic contracture (shorter onset and higher magnitude), and increased the reactive hyperemia (29.8 ± 1.4%), but raised the beneficial effects on contractile recovery (85.4 ± 8.4%) without alteration of ventricular tachycardia prevention (22.2%). Thus, CO-exposed hearts could be preconditioned in the same way as normal myocardium.     

冠心苏合丸的药理研究及其简化制剂—苏冰滴丸的理论基础

用小鼠耐缺氧试验和麻醉狗冠状窦血流量(CSF)及心脏动-静脉血氧差(MA-VO₂)的实验研究冠心苏合丸及其成分的作用,发现:(1)冠心苏合丸能延长小鼠耐缺氧的时间;(2)冠心苏合丸能使心肌梗塞狗的CSF回升,减少心率和MA-VO₂,对非心肌梗塞狗不能提高CSF但亦能减少心率和MA-VO₂;(3)在本实验条件下,苏合香脂和冰片似为冠心苏合丸中起作用的两个成分,其余成分如檀香、青木香、乳香或其油均未能证实其效果。根据此理论,已制成一种新型制剂苏冰滴丸,治心绞痛有效。     

CLORICROMENE REDUCES INFARCT SIZE AND ALTERS POSTISCHAEMIC BLOOD FLOW DEFECTS IN DOG MYOCARDIUM

1. The aim of the present investigation was to evaluate the effect of cloricromene on myocardial infarct size, regional myocardial blood flow and neutrophil accumulation in a canine model of ischaemia-reperfusion. 2. Dogs were instrumented to measure blood pressure, left anterior descending (LAD) coronary flow (flow probe) and regional myocardial blood flow (coloured microspheres). Two groups were studied: (i) CLO (n= 8) received an infusion of cloricromene (15 μg/kg per min); and (ii) VEH (n= 8) received saline. Infusions began at the onset of ischaemia (60 min) and continued through reperfusion (180 min). 3. Haemodynamic responses were not different between groups. Cloricromene reduced the area of necrosis expressed as a percentage of the area at risk from 35 ± 3% in the VEH group to 23 ± 4% in the CLO group (P<0.05). Regional myocardial blood flow in the ischaemic region was different between groups; VEH dogs showed an early reperfusion hyperaemia followed by a progressive reduction in flow, while CLO dogs exhibited a gradual increase in reflow in the absence of an early hyperaemie response (P<0.05). Left anterior descending flow was enhanced during the reperfusion period in the CLO group compared with VEH (P<0.05). Cloricromene reduced polymorphonuclear neutrophil (PMN) infiltration (myeloperoxidase activity) in all myocardial regions when compared with VEH (non-ischaemic zone, 0.34 ± 0.54 vs 0.05 ± 0.01 IU/l00 mg; ischaemic zone, 2.03 ± 0.80 vs 0.24 ± 0.08 IU/100 mg; and necrotic zone, 0.56 ± 0.04 vs 3.59 ± 1.09 IU/100 mg for VEH vs CLO groups, respectively; P<0.01). In a separate in vitro preparation, cloricromene reduced adherence of platelet-activating factor (PAF)-stimulated PMN to canine coronary endothelium. Stimulation of PMN by 100 nmol/L PAF resulted in adherence of 176 ± 36 compared with 48 ± 12 cells/mm² in PAF-stimulated PMN treated with 100 p. mol cloricromene (P<0.001). 4. These data indicate that cloricromene reduces myocardial infarct size in a canine model of ischaemia-reperfusion injury. Postischaemic blood flow patterns are significantly different in cloricromene-treated dogs. Cloricromene-mediated reductions in infarct size, neutrophil accumulation and adherence may play a role in this effect.     

Effects of arotinolol on regional cerebral blood flow in hypertensive patients with a history of stroke

Although optimal blood pressure control is important for managing stroke patients, the use of antihypertensives in stroke patients often causes cerebral blood flow reduction leading sometimes to deterioration of symptoms. Effects of arotinolol, a β-blocker with a moderate α-blocking action, on the regional cerebral blood flow (rCBF) were investigated in 10 hypertensive patients with a history of stroke by using a noninvasive ¹³³Xe inhalation method. The rCBF was measured before and after administration of 15 mg/day arotinolol (three times a day) for 2–3 weeks. After the administration, the blood pressure was reduced in all the patients showing a change in average values of from 176/105 mmHg to 152/90 mmHg. The rCBF in the infarcted and healthy hemispheres was 44.3 ± 4.4 and 44.6 ± 5.0 ml/100 g/min before arotinolol and 44.9 ± 6.4 and 45.3 ± 6.5 ml/100 g/min after arotinolol, respectively. No significant rCBF change was observed after arotinolol in both hemispheres. During the administration, none of the patients suffered from dizziness or other ischemic symptoms. The above results suggest that arotinolol exerts little influence on the cerebral circulation and may be useful for the management of hypertension in stroke patients.     

RENAL AUTOTRANSPLANTS IN SHEEP: INVESTIGATION OF RENAL FUNCTION AND RENOVASCULAR HYPERTENSION

1. A novel surgical preparation of sheep with a cervical renal autotransplant has been developed. 2. Glomerular filtration rate and effective renal plasma flow were 25.1 ± 1.0 ml/min and 208 ± 10 ml/min respectively (n= 26). 3. The responses to water load and deprivation, to AVP injection, to Na depletion and intravenous hypertonic saline load show the kidneys responded in an appropriate physiological manner. 4. Constriction of the carotid-renal artery to reduce mean renal arterial pressure to 23 ± 4 mmHg (n= 4) resulted in an increase in systemic mean arterial pressure from 70 ± 4 mmHg to 75 ± 4 mmHg within 5 min. Systemic blood pressure further increased to 110 ± 7 mmHg with 2 h of constriction, when renal arterial pressure had increased to 45 ± 2 mmHg.