氨氯地平与左旋氨氯地平治疗夜间高血压疗效比较

目的 :观察左旋氨氯地平与氨氯地平治疗夜间高血压患者的疗效及其对血压昼夜节律的影响。　方法 :6 0例轻、中度原发性高血压患者 (必须同时具备夜间血压增高 )随机接受氨氯地平 5mg或左旋氨氯地平 2 .5mg(各30例 )治疗 4周。用 2 4h动态血压监测治疗前后血压的昼夜节律变化。　结果 :氨氯地平和左旋氨氯地平降压疗效显著 ,但二药之间比较无显著差异 (P >0 .0 5 ) ,均不影响血压昼夜节律。　结论 :氨氯地平和左旋氨氯地平治疗有夜间血压增高的轻、中度高血压患者疗效好 ,而且安全     

褪黑素对大鼠体温及活动度昼夜节律的影响

目的　了解外源性褪黑素对大鼠体温及活动度昼夜节律的影响及其可能的调节机制。方法　正常光照条件下,24h连续记录大鼠的体温及活动度的变化,以不同剂量褪黑素在不同的昼夜时间给药观察体温和活动度节律的变化。结果　大鼠的体温及活动度存在昼夜节律性,给药后昼夜节律性不消失;但体温振幅减小,中值降低。黑暗中期给药后,峰值位相显著延迟;活动度振幅增加,中值显著降低,峰值位相延迟。结论　外源性褪黑素不能使体温或活动度的昼夜节律消失,而只是改变昼夜节律的参数。褪黑素可分别调节体温和活动度的昼夜节律,但对活动度的调节作用更为明显。     

似昼夜节律与学习效应对脑事件相关电位P300的影响

目的 探讨昼夜节律和学习效应对脑事件相关电位P300成分的影响。方法 8名被试者在非连续的5d的实验中每天在5个时间点（7：00,12：00,16：00,20：00和0：00）重复相同的听觉Oddball模式测试以诱发脑事件相关电位（ERP）。然后测量各次的ERPP300成分,得到其潜伏期及波幅。结果 P300波幅明显高于下午的波辐。重复测量也使P300波幅从第1个实验日的平均13.0uV降至第5个实验日的9.2uV。P300潜伏期随着重复测试的增加出现了习服,它从第2个实验日的平均350.6ms缩短为第5个实验日的平均343.5ms.结论 似昼夜节律和学习效应对脑事件相关电位P300成分的波幅和潜伏期均有影响。     

慢径路消融改良房室结术中出现的交界性心律之特征

目的：分析房室结慢径路消融术中出现的一过性交界性心律（ＪＲ）的特征。方法：２１例（男６例,女１５例）进行房室结改良术的房室结折返性心动过速患者,术中详细记录释放射频的次数、能量、持续时间、以及出现一过性交界性心律的时间、频率及数目,比较释放射频有效时／无效时出现的一过性交界性心律之特征有无显著性差异。结果：共进行１０６次射频电流释放,其中２１次有效（Ａ组）,８５次无效（Ｂ组）。Ａ组有１９次出现ＪＲ     

Intrinsic burst generation of preinspiratory neurons in the medulla of brainstem-spinal cord preparations isolated from newborn rats

In brainstem-spinal cord preparations isolated from newborn rats, intrinsic burst-generating properties of preinspiratory (Pre-I) neurons in the rostral ventrolateral medulla, which have been suggested to be primary respiratory rhythm-generating neurons, were studied by perforated whole-cell recordings using the antibiotic nystatin. Nystatin causes small pores to be formed in the cells, through which pass small monovalent ions. For blockade of chemical synaptic transmission, perfusate Ca²⁺ concentration was lowered to 0.2 mM and the Mg²⁺ concentration was increased to 5 mM. In Iow-Ca²⁺, high-Mg²⁺ solution (referred to here as low Ca), 10 of 55 Pre-I neurons generated rhythmic bursts (burst type), 14 fired tonically (tonic type), and 31 were silent (silent type). Burst-type neurons showed periodic depolarization of 5–12 mV in low Ca, at a rate of 12±6.5/min. Hyperpolarization of the membrane caused decrease in or disappearance of the periodic depolarization and prolongation of the cycle period. Thus, the burst generations were voltage dependent. The firing frequency of tonictype neurons was 2.3±1.6 Hz and was decreased by hyperpolarization. In 6 of these neurons, the firing patterns changed to burst patterns during continuous hyperpolarization. Membrane depolarization by continuous outward current injection into some silent-type neurons (3 of 11 tested) induced bursting activity. Activity of C4 and Pre-I neurons was completely silent with 0.1–1 M tetrodotoxin (TTX) added to the standard perfusate. In low Ca, burst-type neurons (n=3) were also silent with 1 M TTX perfusion. Inspiratory neurons either became silent (n=4) or fired tonically (n=1) in low Ca. The present study by perforated whole-cell recordings confirmed that some Pre-I neurons possess intrinsic burst-generating properties, which were not attributable to phasic synaptic inputs.     

Melatonin and adjustment to phase shift

The pineal hormone melatonin has clear circadian phase-shifting effects in humans which have recently been formalized as a phase response curve. Its potential use in circadian rhythm disorders has been investigated in field studies of jet lag and shift work and in simulated phase shift. A substantial amount of information indicates that in the majority of subjects it hastens adaptation of both subjective and objective measures to forced shifts in time cues with few reported side-effects. Field studies of its use in adaptation to shift work are sparse and preliminary but the first indications are positive. In some blind subjects with sleep disturbance it can stabilize sleep onset time without necessarily entraining all circadian rhythms and it can advance sleep timing in delayed sleep-phase insomnia. Acute suppression of core body temperature may be an integral part of the phase-shifting mechanism.     

原发性高血压病人血压昼夜节律变化与心率变异的相关分析

为探讨原发性高血压患者的血压昼夜节律的变化与心率变异的关系,对６５例原发性高血压患者进行了２４ｈ动态血压监测,用时域分析法对心率变异性（ＨＲＶ）各项指标进行了检测,并与３８例正常对照比较。结果：代表心率总变异程度的ＳＤＮＮ（２４ｈ正常ＲＲ间期标准差）,ＳＤＡＮＮＩ（２４ｈ５ｍｉｎ平均ＲＲ间期标准差）明显下降（Ｐ＜０．０５）。按照夜间血压下降百分率将原发性高血压病人分为节律消失组、节律正常组,并分别与正常对照组比较,发现节律消失组ＨＲＶ各项指标下降更为显著,ＳＤＮＮ、ＳＤＡＮＮＩ、ＳＤＮＮＩ（２４ｈ５ｍｉｎ正常ＲＲ间期标准差均值）不但显著低于正常对照组（Ｐ＜０．０５）,也显著低于节律正常组（Ｐ＜０．０５）。说明在原发性高血压患者中,节律消失者的心脏自主神经系统功能损害更为严重。     

吉林省吸血蠓昼夜活动节律观察

笔者对吉林省8种优势种群吸血蠓的昼夜活动节律进行了观察.结果表明:华库蠓、孔库蠓、伊库蠓、原野库蠓、亚单带库蠓、淡角库蠓属于晨昏活动型蠓种;明边库蠓属于夜间活动型蠓种;浑江铗蠓属于白天活动型蠓种.     

Melatonin inhibits in vitro serotonergic phase shifts of the suprachiasmatic circadian clock

The suprachiasmatic (SCN) circadian pacemaker generates 24 h rhythms of spontaneous neuronal activity when isolated in an acute brain slice preparation. The isolated pacemaker also retains its capacity to be reset, or phase-shifted by exogenous stimuli. For example, serotonin (5-HT) agonists advance the SCN pacemaker when applied during mid subjective day, while neuropeptide Y (NPY) agonists and melatonin advance the pacemaker when applied during late subjective day. Previous work has demonstrated interactions between NPY and 5-HT agonists, such that NPY can block 5-HTergic phase advances, while 5-HT agonists do not prevent NPY-induced advances. Due to a number of similarities in the actions of melatonin and NPY in the SCN, it seemed possible that melatonin and 5-HT might interact in the SCN as well. Therefore, in this study potential interactions between melatonin and 5-HT agonists were explored. Melatonin inhibited phase advances by the 5-HT agonist, (+)DPAT, and this inhibition was decreased by co-application of tetrodotoxin. Conversely, melatonin was unable to block phase advances by the cyclic AMP analog, 8BA-cAMP. Finally, neither 5-HT agonists nor 8BA-AMP were able to block melatonin-induced phase advances. These results demonstrate a clear interaction between melatonin and 5-HT in the SCN, and suggest that melatonin and NPY may play similar roles with respect to modulating the phase of the SCN circadian pacemaker in rats.