安静时Ⅰ度或Ⅱ度Ⅰ型房室阻滞二例

本文报道二例患者安静(非睡眠状态)时出现Ⅰ度或Ⅱ度Ⅰ型房室阻滞,说明清醒时,迷走神经和交感神经可以出现互相竞争的临界状态.只要稍微安静,迷走神经就占优势;稍活动时,交感神经就占优势.提示交感神经兴奋性减低.     

成人莫氏Ⅰ型房室传导阻滞是良性的吗?

传统观点认为,文氏型Ⅱ度房室传导阻滞(AVB),即莫氏Ⅰ型或MobitzⅠ型AVB是良性的。本文旨在分析MobitzⅠ型AVB患者的存活率,并评价年龄、症状、心脏病、迷走神经张力等危险因素对MobitzⅠ型AVB的影响以及安装心脏起搏器的益处。     

028成人莫氏I型房室传导阻滞是良性的吗?

传统观点认为，文氏型Ⅱ度房室传导阻滞（AVB），即莫氏Ⅰ型或MobitzⅠ型AVB是良性的。本文旨在分析MobitzⅠ型AVB患者的存活率，并评价年龄、症状、心脏病、迷走神经张力等危险因素对MobitzⅠ型AVB的影响以及安装心脏起搏器的益处。     

期前收缩揭示快频率依赖性Ⅰ度房室传导阻滞3例

快频率依赖性Ⅰ度房室传导阻滞(即3相Ⅰ度房室传导阻滞)是当心率增速到一定频率时出现单独或连续的Ⅰ度房室传导阻滞(Ⅰ°AVB)。心率减慢后恢复正常房室传导的一种少见的心律失常。临床上单纯窦性心率增快时出现Ⅰ°AVB,窦性心率减慢后Ⅰ°AVB消失时有发现,本文报道3个由于期前收缩(PS)之代偿间歇使其后第1个心动的窦性心律恢复正常房室传导的实例。     

室间隔缺损封堵术前后的心电图分析

目的:探讨42例室间隔缺损(VSD)封堵术前、后心电图的改变.方法:42例VSD患者在x线透视、经胸超声的监测下建立股动静脉轨道,经右心系统释放封堵器.对所有患者封堵术术前、术后即刻、3、7 d、直至出院后1,2个月的12导联心电图作连续观察和分析.结果:42例患者术后即刻出现Ⅰ度房室传导阻滞(AVB)4例、Ⅱ度AVB 1例、不完全性右束支传导阻滞(IRBBB)3例.3 d出现IRBBB 3例、完全性右束支传导阻滞(CRBBB)2例、Ⅰ度AVB 4例、Ⅱ度AVB 1例;术后7 d出现IRBBB 4例、CRBBB 3例、出现左束支传导阻滞2例、Ⅲ度AVB 2例.所有AVB经治疗后均痊愈.结论:VSD封堵术过程中可能会对房室传导产生一定影响.     

潘生丁试验的心电图特殊表现

潘生丁试验时出现窦性静止、Ⅱ°Ⅰ型房室传导阻滞(AVB)、Ⅲ°AVB、短暂性房速、双峰型T波、房早后第一个窦性T波倒置。     

房室结改良术中Ⅲ度房室传导阻滞的发生与预防

34例房室结改良术中3例发生Ⅲ度房室传导阻滞(AVB)。2例永久性Ⅲ度AVB发生在消融快通道时,1例—过性Ⅲ度AVB发生在下位法消融慢通道时。3例均发生在放电出现频率较快的非阵发性交界性心动过速时。针对这3例情况,本文讨论了发生Ⅲ度AVB的原因及预防措施。     

卧位性Ⅱ度Ⅰ型传导阻滞3例分析

1981～1991年我们遇到的部分房室Ⅱ度Ⅰ型传导阻滞3例,在平卧时出现,而在坐、立位或运动后则Ⅱ°Ⅰ型房室传导阻滞消失。本文并对其病因进行讨论。房室传导阻滞的真正原因。我们遇到的3例多为青年人,平素身体健康。其中二例近期有上呼吸感染的病史,伴有心悸,胸闷而就诊。一例平     

卧位性Ⅱ度Ⅰ型房室传导阻滞4例报告

Ⅱ度Ⅰ型房室传导阻滞是临床上常见的一种传导障碍,其发病机理可为心脏器质性病变(炎症、缺血、纤维化等)或药物(如洋地黄或奎尼丁过量)直接作用于心脏传导系统的结果,也可能由迷走神经兴     

射频消融术后发生迟发性房室阻滞的治疗体会

报道射频消融术(RFCA)后发生迟发性房室阻滞(AVB)发生的时间、心电图特征及用大剂量激素治疗的体会。9例迟发性AVB者中7例于放电过程中出现一过性Ⅲ度AVB。每日氢化考的松用量平均为500(300～800)mg,用药时间最短5天、最长15天。9例中8例完全恢复,平均恢复时间为8.3(5～15)天;1例遗留Ⅰ度AVB。平均随访5.6(0.5～9)年,1例出院时有Ⅰ度AVB的患者,于3年后复查显示Ⅱ度Ⅰ型及Ⅱ度Ⅱ型AVB,并安置心脏起搏器治疗。结论:RFCA后发生的迟发性AVB与放电时发生的一过性Ⅲ度AVB有关;经大剂量激素治疗后绝大多数可完全恢复,预后一般良好。     

糖尿病大鼠胃肠动力及肌间神经丛形态学改变

目的 了解糖尿病大鼠胃肠动力障碍时，肌间神经丛有无形态学异常并探讨胃肠功能异常的机制。方法 30只大鼠分成对照组（10只）和糖尿病组（20只），糖尿病组用链脲佐菌素建立大鼠糖尿病模型，4个月后测定两组大鼠胃肠传输速率，并用酶组织化学方法观察回肠肌间神经丛内胆碱能和氮能神经的组织学改变。结果 糖尿病组大鼠胃肠传输速率明显延迟，回肠肌间神经丛内胆碱能神经元密度明显降低（P〈0．01），氮能神经节和氮能神经元的密度均显著升高（P〈0．05和P〈0．01）。结论 糖尿病大鼠小肠肌间神经丛内胆碱能神经减少，氮能神经增多，这可能是导致胃肠传输速率延迟的重要原因，由此引起小肠运动障碍。     

Assessment of Beat-by-Beat Control of Heart Rate by the Autonomic Nervous System: Molecular Biology Techniques Are Necessary, But Not Sufficient

Neural Control of Heart Rate. Vagus nerve activity can change heart rate substantially within one cardiac cycle, and the chronotropic effects decay almost completely within one cardiac cycle after cessation of vagal activity. The ability of the vagus nerves to regulate heart rate beat by beat can be explained in large part by the speed at which the neural signal is transduced to a cardiac response and by the rapidity of the processes that restore the basal heart rate when vagal activity ceases. Currently, the question of whether the cardiac tells can transduce the sympathetic neural signals rapidly enough to implement beatwise regulation is controversial. Emphasis on the speed of the processes that initiate the responses may, however, be misplaced. Instead, the processes that terminate the responses to autonomic neural activity (especially those processes that remove the released neurotransmitters) are probably the main determinants of the ability of the vagal and sympathetic systems to affect beatwise control. The norepinephrine (NE) released from the sympathetic nerve endings is removed from the cardiac tissues much more slowly than is the acetylcholine that is released from the vagal terminals. As a consequence of the potential deleterious effects associated with the slow removal of NE, the cardiac neural control system has evolved such that the sympathetic nerves ordinarily release NE at a slow rate. Hence, changes in sympathetic neural activity can alter cardiac behavior only slightly from beat to beat. Hence, beatwise control of cardiac function would be negligible, regardless of how swiftly the sympathetic nerve impulse is transduced t o a change in cardiac-performance.     

Effect of Renal Denervation on the Development of Cellophane-Wrap Hypertension in Rabbits

The development of hypertension in rabbits with bilateral cellophane wrapping of the kidneys was studied in animals with and without surgical denervatton of the kidneys. Mean arterial pressure was measured before and 14 and 28 days after surgery. After 14 and 28 days of wrapping, mean arterial pressure had increased 12 ± 3 mmHg and 31 ± 3 mmHg in rabbits with innervated kidneys and 7 ± 2 mmHg and 26 ± 2 mmHg in rabbits with denervated kidneys, respectively. The increases in arterial pressure were significantly less in the denervated animals. In sham wrap animals, renal denervation also resulted in significantly lower arterial pressure than in sham wrap+sham denervated rabbits. Noradrenaline concentration of denervated kidneys averaged only 4% of that measured in kidneys subjected to sham denervation. The results show that renal denervation slightly attenuated the degree of hypertension developed following renal wrapping. Since renal denervation produced a similar small decrease in arterial pressure in normotensive rabbits it is suggested that the effect is non-specific and probably due to loss of efferent renal sympathetic nerves.     

Pancreatic polypeptide response to a meal before and after cutting the extrinsic nerves of the upper gastrointestinal tract and the pancreas in the dog

The role of the sympathetic and parasympathetic innervation in the release of pancreatic polypeptide (PP) basally and in response to a meal was studied after stepwise extrinsic denervation of the pancreas and the upper gastrointestinal tract in conscious dogs with gastric fistulae. One set of seven dogs was fed a meat meal (35 g/kg body weight) before and after truncal vagotomy and after truncal vagotomy plus celiac and superior mesenteric ganglionectomy, ie, extrinsic denervation of the pancreas and the upper gastrointestinal tract. In another set of six dogs, only ganglionectomy was performed. Experiments were repeated in the presence of atropine (50 g/kg body weight, given as an intravenous bolus 60 min prior to the meal). Truncal vagotomy significantly (P<0.05) reduced the postprandial 120-min integrated plasma PP response (IPPPR) by 84% as compared to the prevagotomy response. Before truncal vagotomy, atropine significantly reduced the IPPPR by 57%. After truncal vagotomy, atropine completely abolished the residual PP response. Additional celiac and superior mesenteric ganglionectomy did not alter the IPPPR already reduced by truncal vagotomy. With the vagus nerves intact, ganglionectomy alone had no effect on the IPPPR whether or not atropine was given. These findings indicate that (1) the splanchnic nerves do not play a significant role in postprandial PP release and (2) that the vagus nerves are important mediators of the response to a meal. The effect of atropine on postprandial PP release after truncal vagotomy may be due to interruption of short enteropancreatic reflexes, suppression of the intrinsic cholinergic activity of the pancreas, or inhibition of hormonally induced PP release.     

胃电节律失常大鼠胃窦肌间神经丛胆碱能神经的改变

目的：探讨大鼠胃窦肌间神经丛胆碱能神经，氮能神经含量变化与胃电节律失常的关系。方法：63例大鼠随机分为正常对照组，胃电节律失常模型组和白芍组。饲养4周后记录并分析胃电信号，测定胃窦肌间神经丛胆碱能神经含量。结果：模型组胃电节律失常明显增加，胃窦肌间神经丛胆碱能神经含量减少；经白芍治疗后，胃电节律失常明显减少，胃窦肌间神经丛胆碱能神经含量恢复正常。结论：胃窦肌间神经丛的胆碱能神经与胃电节律关系密切，当胆碱能神经减少时，胃电节律失常明显增加。     

Evidence that autonomic mechanisms contribute to the adaptive increase in insulin secretion during dexamethasone-induced insulin resistance in humans

Aims/hypothesis This study examined whether autonomic mechanisms contribute to adaptively increased insulin secretion in insulin-resistant humans, as has been proposed from studies in animals. Methods Insulin secretion was evaluated before and after induction of insulin resistance with or without interruption of neural transmission. Insulin resistance was induced by dexamethasone (15 mg given over 3 days) in nine healthy women (age 67 years, BMI 25.2 ± 3.4 kg/m², fasting glucose 5.1 ± 0.4 mmol/l, fasting insulin 46 ± 6 pmol/l). Insulin secretion was evaluated as the insulin response to intravenous arginine (5 g) injected at fasting glucose and after raising glucose to 13 to15 mmol/l or to >28 mmol/l. Neural transmission across the ganglia was interrupted by infusion of trimethaphan (0.3–0.6 mg kg⁻¹ min⁻¹). Results As an indication of insulin resistance, dexamethasone increased fasting insulin (to 75 ± 8 pmol/l, p < 0.001) without significantly affecting fasting glucose. Arginine-induced insulin secretion was increased by dexamethasone at all glucose levels (by 64 ± 12% at fasting glucose, by 80 ± 19% at 13–15 mmol glucose and by 43 ± 12% at >28 mmol glucose; p <0.001 for all). During dexamethasone-induced insulin resistance, trimethaphan reduced the insulin response to arginine at all three glucose levels. The augmentation of the arginine-induced insulin responses by dexamethasone-induced insulin resistance was reduced by trimethaphan by 48 ± 6% at fasting glucose, 61 ± 8% at 13–15 mmol/l glucose and 62 ± 8% at >28 mmol/l glucose (p < 0.001 for all). In contrast, trimethaphan did not affect insulin secretion before dexamethasone was given. Conclusions/interpretations Autonomic mechanisms contribute to the adaptative increase in insulin secretion in dexamethasone-induced insulin resistance in healthy participants.     

Rat bladder in the early stages of streptozotocin-induced diabetes: adrenergic and cholinergic innervation

Summary The adrenergic and cholinergic innervation of the bladder was studied in streptozotocin-diabetic rats. The presence of hypertrophy and distension in the diabetic bladders necessitates care in assessing changes occurring in the nerves, factors which are also relevant to clinical histochemical studies. Biochemical assays of cholinergic enzymes revealed decreased activities per g wet weight tissue. However, the total activities of choline acetyltransferase and acetylcholinesterase per whole bladder were significantly increased after 2 weeks of diabetes with greater changes by 8 weeks. Total dopamine levels per bladder were significantly higher than in control rats in the 2-week but not the 8-week group of animals; this may indicate an initial increase in adrenergic nerve activity. There was no impairment in the ability of the detrusor muscle to respond to noradrenaline, acetylcholine or to cholinergic nerve stimulation. Shortly after induction of diabetes streptozotocin-treated rats display polyuria. It is proposed that the activity of the bladder is therefore stimulated to allow greater volumes of urine to be passed. The results are discussed in relation to human diabetes mellitus where clinical studies have implicated a neuropathic origin to bladder dysfunction.     

脊神经刺激对星状神经节功能的影响

目的观察低强度脊神经刺激(SCS)对星状神经节功能的影响。方法用随机数字表法将12只成年犬分为两组:实验组6只,用90%阈电压(阈电压定义为刺激胸1-胸2脊神经引起肌肉震颤的最低电压数值)进行低强度SCS,持续6 h;对照组6只,同等强度刺激同水平脊髓节段不会引起肌肉震颤的部位,持续6 h。记录基础状态、2、4和6 h末递增电压刺激左侧星状神经节(LSG)、右侧星状神经节(RSG)时的血压或心率变化。以刺激电压作为横坐标,血压或心率变化的最大百分比作为纵坐标绘出电压-血压反应曲线及电压-心率反应曲线,其中电压-血压反应曲线代表LSG功能曲线,电压-心率曲线则代表RSG功能曲线。结果低强度SCS刺激6 h使电压-血压反应曲线及电压-心率反应曲线逐渐钝化,使同等电压刺激引起的最大血压及最大心率变化逐渐降低;而对照组6 h低强度SCS对LSG的电压-血压反应曲线及RSG的电压-心率反应曲线无明显影响。结论 6 h低强度SCS可以明显抑制LSG及RSG的功能。     

Neuronal control of coronary blood flow

Controversies on acetylcholine-induced increases or decreases in coronary blood flow arise from obvious species differences, the role of endothelium in mediating vascular smooth muscle responses, and the marked negative chronotropic and inotropic effects of acetylcholine. In man, there appears to be a predominant dilation of intact epicardial coronary arteries and a constriction of artherosclerotic segments. However, at present there is no evidence for a vagal initiation of myocardial ischemia. Coronary vascular β-adrenergic receptors mediate dilation, but appear to be functionally insignificant during sympathetic activation. The β-adrenergic mechanism contributing to myocardial ischemia are indirect, mediated by a tachycardia-related redistribution of blood flow away from the ischemic myocardium. α-Adrenergic receptors mediating epicardial coronary artery constriction in experimental studies appear not to be responsible for the initiation of ischemia in patients with angina at rest. However, α-adrenergic constriction of coronary resistance vessels resulting in the precipitation of poststenotic myocardial ischemia was demonstrated in experimental studies and recently confirmed in patients with effort angina. Non-adrenergic, non-cholinergic neurotransmitters exist; however, their role in regulating coronary blood flow remains entirely unclear.     

Innervation of the liver: morphology and function

Abstract: Although it has been known for many years that the liver receives a nerve supply, it is only with the advent of immunohistochemistry that this innervation has been analysed in depth. It is now appreciated not only that many different nerve types are present, but also that there are significant differences between species, especially in the degree of parenchymal innervation. This has stimulated more detailed investigation of the innervation of the human liver in both health and disease. At the same time, functional studies have been underlining the important roles that these nerves play in processes as diverse as osmoreception and liver regeneration. This article briefly reviews current understanding of the morphology and functions of the hepatic nerve supply.