环境线索对戒断期海洛因依赖者神经电生理的影响

目的 了解戒断期海洛因依赖者暴露在吸毒相关环境线索下神经电生理指标的变化特点.方法 采用自身配对设计,指导382例戒断康复期的海洛因依赖者进行放松训练后,观看吸毒相关视频及展示的海洛因模拟物及吸毒用具,同时采用多导联生物反馈仪记录环境线索暴露前后神经电生理指标,评估暴露前后的心理渴求程度,分析心理渴求程度及神经电生理各指标的变化特点.结果 (1)海洛因相关环境线索暴露后,心理渴求程度较暴露前增加[暴露前:(18±22)mm;暴露后:(29±29)mm],肌电[暴露前:(12±7)μV;暴露后:(14±10)μV]及皮肤导电性[暴露前:(6.8±4.3)μS;暴露后:(7.4±4.3)μS]均增加(P<0.01).(2)线索暴露中的脑电各项指标[δ波、θ波、α波、感觉运动节律(SMR)、低β波和高β波的百分率]均低于诱发前(P<0.01～0.05).(3)心理渴求变化与脑电θ波、α波和SMR呈负相关(相关系数为-0.13、-0.12和-0.12);除肌电、δ波外,上述各电生理指标与皮肤导电性之间呈负相关(Pearson相关系数为-0.18～-0.22);余各项指标间呈正相关.结论 海洛因依赖者暴露在吸毒相关环境时,诱发心理渴求反应增强,并引起多项神经电生理指标的变化.     

海洛因依赖者环境线索诱发心理生理反应

目的：了解海洛因依赖者对吸毒相关环境线索诱发反应。方法：对来自自愿戒毒机构的36例刚完成生理脱毒（康复早期）的海洛因依赖者和劳教戒毒机构112例康复期满1年的海洛因依赖者观看吸毒相关视频同时给予海洛因模拟物及吸毒用具刺激,于暴露前后自评渴求程度、情绪以及戒断症状反应;用生物反馈仪自动记录暴露前后的生理反应。结果：环境线索暴露后海洛因依赖者心理渴求、害怕／焦虑、抑郁／悲伤、戒断症状、心率、皮肤导电和肌电增高（P〈0．05）,中性／放松／自然降低（P〈0．05）。自愿戒毒机构康复早期海洛因依赖者环境诱发心率增高,比康复期满一年以上者更明显（P〈0．05）,其余与康复期长短无显著关系。结论：海洛因依赖者戒断康复期的延长并不会使渴求和环境诱发心理生理反应减弱或消褪。     

环境线索对戒断期海洛因依赖者神经电生理的影响

Objective To explore the changes of craving and neuro-electrophysiological reactions under the exposure of heroin-related cues in abstinent heroin dependents.Methods In this self-controlled study,382 abstinent heroin dependent patients watched video of heroin smoking and injecting situations,and in the meantime were exposed to herein simulacrum and apparatus after relaxation exercises.The neuroelectrophysiological reactions were mcagured with a multi-biofeedback instrument before and after the cue exposed.Self-reported craving was also assessed before and after cue exposed.Results The craving were increased[(18±22)mm vs.(29±29)mm,P＜0.01]after cue exposures compared to pre-exposure,EMG[(12±7)μN vs.(14±10)μV,P＜0.01]and SC[(6.8±4.3)μS vs.(7.4±4.3)μS,P＜0.01]also increased.But the percentages of δ,θ,α,SMR,low β,high β decreased compared to that under the cue exposures[8:(10.8±4.7)%vs.(9.7±4.4)%,P＜0.01;0:(6.8±2.0)%vs.(6.3±2.0)%,P＜0.01;α:(4.8±1.8)%vs.(4.5±1.7)%,P＜0.01;SMR:(3.0 ±1.2)%vs.(2.8±1.2)%,P＜0.01;low β:(2.6±1.1)%vs.(2.5±1.1)%,P＜0.01 and high β:(4.6 ±1.5)%vs.(4.5±1.5)%.P＜0.05].Conclusions The results indicate that drug-related cue induce heroin craving and electrophysiological reactions.     

环境线索对戒断期海洛因依赖者神经电生理的影响

Objective To explore the changes of craving and neuro-electrophysiological reactions under the exposure of heroin-related cues in abstinent heroin dependents.Methods In this self-controlled study,382 abstinent heroin dependent patients watched video of heroin smoking and injecting situations,and in the meantime were exposed to herein simulacrum and apparatus after relaxation exercises.The neuroelectrophysiological reactions were mcagured with a multi-biofeedback instrument before and after the cue exposed.Self-reported craving was also assessed before and after cue exposed.Results The craving were increased[(18±22)mm vs.(29±29)mm,P＜0.01]after cue exposures compared to pre-exposure,EMG[(12±7)μN vs.(14±10)μV,P＜0.01]and SC[(6.8±4.3)μS vs.(7.4±4.3)μS,P＜0.01]also increased.But the percentages of δ,θ,α,SMR,low β,high β decreased compared to that under the cue exposures[8:(10.8±4.7)%vs.(9.7±4.4)%,P＜0.01;0:(6.8±2.0)%vs.(6.3±2.0)%,P＜0.01;α:(4.8±1.8)%vs.(4.5±1.7)%,P＜0.01;SMR:(3.0 ±1.2)%vs.(2.8±1.2)%,P＜0.01;low β:(2.6±1.1)%vs.(2.5±1.1)%,P＜0.01 and high β:(4.6 ±1.5)%vs.(4.5±1.5)%.P＜0.05].Conclusions The results indicate that drug-related cue induce heroin craving and electrophysiological reactions.     

环境线索对戒断期海洛因依赖者神经电生理的影响

Objective To explore the changes of craving and neuro-electrophysiological reactions under the exposure of heroin-related cues in abstinent heroin dependents.Methods In this self-controlled study,382 abstinent heroin dependent patients watched video of heroin smoking and injecting situations,and in the meantime were exposed to herein simulacrum and apparatus after relaxation exercises.The neuroelectrophysiological reactions were mcagured with a multi-biofeedback instrument before and after the cue exposed.Self-reported craving was also assessed before and after cue exposed.Results The craving were increased[(18±22)mm vs.(29±29)mm,P＜0.01]after cue exposures compared to pre-exposure,EMG[(12±7)μN vs.(14±10)μV,P＜0.01]and SC[(6.8±4.3)μS vs.(7.4±4.3)μS,P＜0.01]also increased.But the percentages of δ,θ,α,SMR,low β,high β decreased compared to that under the cue exposures[8:(10.8±4.7)%vs.(9.7±4.4)%,P＜0.01;0:(6.8±2.0)%vs.(6.3±2.0)%,P＜0.01;α:(4.8±1.8)%vs.(4.5±1.7)%,P＜0.01;SMR:(3.0 ±1.2)%vs.(2.8±1.2)%,P＜0.01;low β:(2.6±1.1)%vs.(2.5±1.1)%,P＜0.01 and high β:(4.6 ±1.5)%vs.(4.5±1.5)%.P＜0.05].Conclusions The results indicate that drug-related cue induce heroin craving and electrophysiological reactions.     

环境线索对戒断期海洛因依赖者神经电生理的影响

Objective To explore the changes of craving and neuro-electrophysiological reactions under the exposure of heroin-related cues in abstinent heroin dependents.Methods In this self-controlled study,382 abstinent heroin dependent patients watched video of heroin smoking and injecting situations,and in the meantime were exposed to herein simulacrum and apparatus after relaxation exercises.The neuroelectrophysiological reactions were mcagured with a multi-biofeedback instrument before and after the cue exposed.Self-reported craving was also assessed before and after cue exposed.Results The craving were increased[(18±22)mm vs.(29±29)mm,P＜0.01]after cue exposures compared to pre-exposure,EMG[(12±7)μN vs.(14±10)μV,P＜0.01]and SC[(6.8±4.3)μS vs.(7.4±4.3)μS,P＜0.01]also increased.But the percentages of δ,θ,α,SMR,low β,high β decreased compared to that under the cue exposures[8:(10.8±4.7)%vs.(9.7±4.4)%,P＜0.01;0:(6.8±2.0)%vs.(6.3±2.0)%,P＜0.01;α:(4.8±1.8)%vs.(4.5±1.7)%,P＜0.01;SMR:(3.0 ±1.2)%vs.(2.8±1.2)%,P＜0.01;low β:(2.6±1.1)%vs.(2.5±1.1)%,P＜0.01 and high β:(4.6 ±1.5)%vs.(4.5±1.5)%.P＜0.05].Conclusions The results indicate that drug-related cue induce heroin craving and electrophysiological reactions.     

环境线索对戒断期海洛因依赖者神经电生理的影响

Objective To explore the changes of craving and neuro-electrophysiological reactions under the exposure of heroin-related cues in abstinent heroin dependents.Methods In this self-controlled study,382 abstinent heroin dependent patients watched video of heroin smoking and injecting situations,and in the meantime were exposed to herein simulacrum and apparatus after relaxation exercises.The neuroelectrophysiological reactions were mcagured with a multi-biofeedback instrument before and after the cue exposed.Self-reported craving was also assessed before and after cue exposed.Results The craving were increased[(18±22)mm vs.(29±29)mm,P＜0.01]after cue exposures compared to pre-exposure,EMG[(12±7)μN vs.(14±10)μV,P＜0.01]and SC[(6.8±4.3)μS vs.(7.4±4.3)μS,P＜0.01]also increased.But the percentages of δ,θ,α,SMR,low β,high β decreased compared to that under the cue exposures[8:(10.8±4.7)%vs.(9.7±4.4)%,P＜0.01;0:(6.8±2.0)%vs.(6.3±2.0)%,P＜0.01;α:(4.8±1.8)%vs.(4.5±1.7)%,P＜0.01;SMR:(3.0 ±1.2)%vs.(2.8±1.2)%,P＜0.01;low β:(2.6±1.1)%vs.(2.5±1.1)%,P＜0.01 and high β:(4.6 ±1.5)%vs.(4.5±1.5)%.P＜0.05].Conclusions The results indicate that drug-related cue induce heroin craving and electrophysiological reactions.     

环境线索对戒断期海洛因依赖者神经电生理的影响

Objective To explore the changes of craving and neuro-electrophysiological reactions under the exposure of heroin-related cues in abstinent heroin dependents.Methods In this self-controlled study,382 abstinent heroin dependent patients watched video of heroin smoking and injecting situations,and in the meantime were exposed to herein simulacrum and apparatus after relaxation exercises.The neuroelectrophysiological reactions were mcagured with a multi-biofeedback instrument before and after the cue exposed.Self-reported craving was also assessed before and after cue exposed.Results The craving were increased[(18±22)mm vs.(29±29)mm,P＜0.01]after cue exposures compared to pre-exposure,EMG[(12±7)μN vs.(14±10)μV,P＜0.01]and SC[(6.8±4.3)μS vs.(7.4±4.3)μS,P＜0.01]also increased.But the percentages of δ,θ,α,SMR,low β,high β decreased compared to that under the cue exposures[8:(10.8±4.7)%vs.(9.7±4.4)%,P＜0.01;0:(6.8±2.0)%vs.(6.3±2.0)%,P＜0.01;α:(4.8±1.8)%vs.(4.5±1.7)%,P＜0.01;SMR:(3.0 ±1.2)%vs.(2.8±1.2)%,P＜0.01;low β:(2.6±1.1)%vs.(2.5±1.1)%,P＜0.01 and high β:(4.6 ±1.5)%vs.(4.5±1.5)%.P＜0.05].Conclusions The results indicate that drug-related cue induce heroin craving and electrophysiological reactions.     

环境线索对戒断期海洛因依赖者神经电生理的影响

Objective To explore the changes of craving and neuro-electrophysiological reactions under the exposure of heroin-related cues in abstinent heroin dependents.Methods In this self-controlled study,382 abstinent heroin dependent patients watched video of heroin smoking and injecting situations,and in the meantime were exposed to herein simulacrum and apparatus after relaxation exercises.The neuroelectrophysiological reactions were mcagured with a multi-biofeedback instrument before and after the cue exposed.Self-reported craving was also assessed before and after cue exposed.Results The craving were increased[(18±22)mm vs.(29±29)mm,P＜0.01]after cue exposures compared to pre-exposure,EMG[(12±7)μN vs.(14±10)μV,P＜0.01]and SC[(6.8±4.3)μS vs.(7.4±4.3)μS,P＜0.01]also increased.But the percentages of δ,θ,α,SMR,low β,high β decreased compared to that under the cue exposures[8:(10.8±4.7)%vs.(9.7±4.4)%,P＜0.01;0:(6.8±2.0)%vs.(6.3±2.0)%,P＜0.01;α:(4.8±1.8)%vs.(4.5±1.7)%,P＜0.01;SMR:(3.0 ±1.2)%vs.(2.8±1.2)%,P＜0.01;low β:(2.6±1.1)%vs.(2.5±1.1)%,P＜0.01 and high β:(4.6 ±1.5)%vs.(4.5±1.5)%.P＜0.05].Conclusions The results indicate that drug-related cue induce heroin craving and electrophysiological reactions.     

环境线索对戒断期海洛因依赖者神经电生理的影响

Objective To explore the changes of craving and neuro-electrophysiological reactions under the exposure of heroin-related cues in abstinent heroin dependents.Methods In this self-controlled study,382 abstinent heroin dependent patients watched video of heroin smoking and injecting situations,and in the meantime were exposed to herein simulacrum and apparatus after relaxation exercises.The neuroelectrophysiological reactions were mcagured with a multi-biofeedback instrument before and after the cue exposed.Self-reported craving was also assessed before and after cue exposed.Results The craving were increased[(18±22)mm vs.(29±29)mm,P＜0.01]after cue exposures compared to pre-exposure,EMG[(12±7)μN vs.(14±10)μV,P＜0.01]and SC[(6.8±4.3)μS vs.(7.4±4.3)μS,P＜0.01]also increased.But the percentages of δ,θ,α,SMR,low β,high β decreased compared to that under the cue exposures[8:(10.8±4.7)%vs.(9.7±4.4)%,P＜0.01;0:(6.8±2.0)%vs.(6.3±2.0)%,P＜0.01;α:(4.8±1.8)%vs.(4.5±1.7)%,P＜0.01;SMR:(3.0 ±1.2)%vs.(2.8±1.2)%,P＜0.01;low β:(2.6±1.1)%vs.(2.5±1.1)%,P＜0.01 and high β:(4.6 ±1.5)%vs.(4.5±1.5)%.P＜0.05].Conclusions The results indicate that drug-related cue induce heroin craving and electrophysiological reactions.     

急性颈髓损伤对心血管系统影响的临床分析

目的探讨急性颈髓损伤(CSCI)后出现的心血管系统异常情况及其发病机制。方法回顾性对比分析30例CSCI患者与30例非CSCI患者的血压、心率。结果CSCI患者血压、心率明显降低(P均<0.05);颈4以上比颈4以下损伤患者的血压、心率下降更为明显(P均<0.05)。结论急性颈髓损伤后出现心血管系统功能明显异常,血压、心率下降,且其严重度与损伤平面有关。其机制可能为急性颈髓损伤时抑制了体内交感神经系统。     

The effect of the acetylcholine transport blocker vesamicol on central cholinergic pressor neurons

Vesamicol (AH5183) inhibits the uptake of acetylcholine into cholinergic neuronal storage vesicles. Earlier in vitro studies have demonstrated that such inhibition can lead to a failure of transmission, particularly in peripheral cholinergic tissues. The present study was designed to determine whether vesamicol could inhibit central cholinergic transmission in conscious freely moving rats. Central (lateral cerebroventricular) injection of 20 micrograms of vesamicol significantly reduced the hypertensive and bradycardic response to subsequent central injection of physostigmine in spontaneously hypertensive rats. Inhibition of the pressor response was greatest when physostigmine was administered 1 hr after vesamicol. Acetylcholine and choline levels were determined in three brain regions derived from rats treated one hr earlier with either vehicle or vesamicol. Acetylcholine levels were found to be unaltered after vesamicol treatment, although choline levels were significantly higher in two brain regions. These results are consistent with the ability of vesamicol to inhibit the function of central cholinergic cardiovascular regulatory neurons. The mechanism for this inhibition is not related to depletion of total brain acetylcholine content but may be due to depletion of a small critical pool of transmitter.     

利多卡因对颅内动脉瘤夹闭术后患者呛咳、血压和心率的影响

目的 观察静脉注射利多卡因对颅内动脉瘤夹闭术患者麻醉恢复期的呛咳、躁动、血压和心率的影响。方法 前瞻性选择我院2013年8月至2014年5月开颅夹闭术治疗的颅内动脉瘤患者60例,随机分为对照组和试验组,每组30例。两组患者均给予相同药物进行麻醉诱导和麻醉维持。术毕对照组静脉注射生理盐水（0.15 ml/kg）,试验组静脉注射1%利多卡因（0.15 ml/kg）。结果 术后气管导管留置期间和拔管期间,试验组患者咳嗽评分明显低于对照组（P<0.05）,试验组拔管时间、丙泊酚和佩尔地平用量均明显少于对照组（>P<0.05）。气管导管拔管后5 min内,两组收缩压、舒张压和心率均随时间变化显著下降（P<0.05）,但均高于手术结束时（>P<0.05）,且对照组明显高于试验组（>P<0.05）。>结论 静脉注射利多卡因可降低颅内动脉瘤夹闭术患者麻醉恢复期的呛咳和躁动,减少拔管期间的血压和心率波动。     

Role of the anterior region of the third ventricle in the cardiovascular responses produced by systemic injection of a nitric oxide synthase inhibitor

This study examined whether a prior electrolytic lesion of the tissue surrounding the anteroventral third ventricle (AV3V) would affect the increase in mean arterial blood pressure (MAP) and the fall in heart rate (HR) produced by systemic injection of the nitric oxide synthesis (NOS) inhibitor, NG-nitro-L-arginine methyl ester (L-NAME; 25 micromol/kg, i.v.) in conscious rats. L-NAME produced a smaller increase in MAP in AV3V-lesion than in sham-lesion rats (+19+/-3 vs. +40+/-3 mmHg, respectively; P<0.05). In contrast, L-NAME produced similar falls in HR in the AV3V-lesion and sham-lesion rats (-103+/-15 vs. -97+/-8 bpm, respectively; P<0.05). These findings demonstrate that the L-NAME-induced pressor response is dependent upon the integrity of the AV3V region, whereas the L-NAME-induced bradycardia is not.     

Cardiovascular effects and changes in midbrain periaqueductal gray neuronal activity induced by electrical stimulation of the hypothalamus in the rat

The effects of low-intensity electrical stimulation of sites in the hypodalamus and zona incerta (ZI) on mean blood pressure (MBP), heart rate (HR), and neuronal activity in the midbrain periaqueductal gray (PAC) were investigated in rats. Long-lasting depressor responses were elicited from 67 sites in the hypothalamus and ZI. Effects on HR were variable, except for the ZI where bradycardic responses were evoked. The amplitude of the depressor responses was significantly correlated with baseline MBP on stimulation of the dorsomedial hypothalamic nucleus (DMH) or the dorsal hypothalamic area. Extracellular single-unit recordings were made from 94 PAG neurons. Most units were boated in the ventral half of the PAG (62/94), where spontaneous firing rates were significantly higher than in the dorsal half: 12.5 ± 1.4 spikes/s as compared to 6.0 ± 0.9 spikes/s. Changes in PAG neuronal activity to both ipsi- and contralaterel hypothalamic stimulation were observed. Most neurons were inhibited or unresponsive. There was no site specificity: responsive and unresponsive neurons were scattered throughout the PAG. Inhibition was most effectively evoked by stimulation of the DMH (25 out of 39 neurons) and the Zl (9 out of 15 neurons). In most neurons, the inhibition strictly followed the time course of hypothalamic stimulation. The results suggest that PAG as well as nonPAG pathways participate in the hypothalamic control of cardiovascular function.     

Epigenetic changes of serotonin transporter in the patients with alcohol dependence: methylation of an serotonin transporter promoter CpG island

Objective

Psychiatric disorders such as depression, anxiety and alcohol dependence are associated with serotonin metabolism. We assessed the methylation level of the serotonin transporter (5-HTT) promoter region in control and alcohol dependent patients.

Methods

Twenty seven male patients who met the Diagnostic and Statistical Manual of Mental Disorder IV (DSM-IV) criteria for alcohol dependence were compared with fifteen controls. Polymerase chain reaction (PCR) assays of bisulfate-modified DNA were designed to amplify a part of the CpG island in the 5HTT gene. Pyrosequencing was performed and the methylation level at seven CpG island sites was measured.

Results

We found no differences in the methylation patterns of the serotonin transporter linked promoter region (5-HTTLPR) between alcohol-dependent and control subjects.

Conclusion

Our negative finding may be because 5-HTT epigenetic variation may not affect the expression for 5-HTT or there may be other methylation site critical for its expression. To find out more conclusive result, repeating the study in more methylation sites with a larger number of samples in a well-controlled setting is needed.     

The effects of prior chronic stress on cardiovascular responses to acute restraint and formalin injection

Exposure to acute stressors activates both the hypothalamic-pituitary–adrenal (HPA) and cardiovascular systems. Prior chronic stress enhances HPA responses to novel, acute stressors, but whether it alters cardiovascular responsivity to novel, acute stress is unknown. In the present study, we examined mean arterial blood pressure (MAP) and heart rate (HR) to two distinct stimuli, restraint and formalin, following prior exposure to 7 days of intermittent cold. In two sets of control and chronically stressed animals, we measured MAP and HR for 60 min following onset of 30 min restraint and MAP, HR and behavioral responses to intraplantar injection of formalin. Chronic stress raised MAP and HR under resting conditions and elevated HR during, but not following termination of, restraint. These increases in HR during restraint were due to the differences in resting levels of HR, since both control and chronically stressed animals exhibited similar increases from resting levels in HR during restraint. Conversely, chronically stressed animals exhibited lower changes in MAP and HR from resting levels following termination of restraint. Formalin produced the characteristic biphasic pattern of cardiovascular and behavioral responses. Prior chronic stress did not alter behavior, but increased MAP and HR in Interphase and only MAP in Phase 2. The increases in MAP during Interphase and Phase 2 were a result of the elevations in resting levels of MAP, but even when differences in resting levels were taken into account, HR remained elevated in the Interphase in chronically stressed animals. Together, these data demonstrate that prior chronic intermittent cold stress modifies cardiovascular function both under resting conditions and, in very specific ways, under stimulated conditions produced by restraint and formalin. We propose that these modifications are produced by brain regions that are known to regulate cardiovascular function and which are activated by chronic stress.     

The differential contribution of capsaicin-sensitive afferents to behavioral and cardiovascular measures of brief and persistent nociception and to Fos expression in the formalin test

Intraplantar injection of dilute formalin evokes brief (Phase 1) and persistent (Phase 2) increases in primary afferent activity, pain behavior, and cardiovascular responses, and induces spinal cord Fos-like immunoreactivity (Fos-LI). Although previous studies demonstrated that the destruction of small diameter primary afferents with neonatal capsaicin treatment decrease formalin-evoked nociception, these studies only evaluated behavioral responses, and did not distinguish between Phase 1 and 2. To address these questions, we simultaneously evaluated formalin-evoked pain behavior (flinching of the afflicted paw), cardiovascular responses (heart rate and mean arterial pressure), and lumbar spinal cord Fos expression in control rats and in rats treated with capsaicin (100 mg/kg) one day postpartum. We found that neonatal capsaicin-treated rats, compared to controls, exhibited similar cardiovascular responses and slightly less flinching behavior during Phase 1. During Phase 2, however, capsaicin-treated rats exhibited 59% less flinching and 45% smaller heart rate responses. Also, in capsaicin-treated rats, we counted 59% fewer Fos-labeled neurons in the spinal cord. These results indicate that capsaicin-sensitive afferents contribute to formalin-evoked behavioral and cardiovascular responses and to spinal cord neuronal responses. The differential effect of neonatal capsaicin on nociception during Phase 1 and Phase 2 suggests that sensitization mechanisms during Phase 1 do not contribute to the magnitude of nociceptive responses during Phase 2.     

Effects of gender on the central actions of neuropeptide Y and norepinephrine on vasopressin and blood pressure in the rat

Neuropeptide Y (NPY) and norepinephrine are co-localized in the noradrenergic projection from the A₁ nucleus of the medulla to the vasopressinergic magnocellular neurons of the supraoptic and paraventricular nuclei. Because this pathway is involved in the control of vasopressin release, we have examined the possibility that NPY and norepinephrine interact in this control. Because the stimulation of vasopressin release by the intracerebroventricular (i.c.v.) administration of norepinephrine is greater in male than in female rats, the experiments were carried out in conscious male rats and in female rats in the proestrous and non-proestrous phases of the estrous cycle. NPY (940 pmol i.c.v.) caused small sustained increases in plasma vasopressin concentrations that were greater in proestrous than in non-proestrous females and males. Norepinephrine i.c.v. increased plasma vasopressin levels transiently and to a greater extent in females than males. When NPY and norepinephrine were given together, the pattern of the vasopressin response was similar to that of norepinephrine alone. The magnitude of this response in males and proestrous females did not differ from that to norepinephrine alone; in non-proestrous females the response was twice that to norepinephrine alone. In non-proestrous rats, NPY also enhanced the pressor response to norepinephrine. Thus, NPY interacts centrally with norepinephrine in vasopressin release and cardiovascular function and this effect is dependent upon gender and phase of the estrous cycle.     

Effects of cold exposure on autonomic changes during the last rapid eye movement sleep transition and morning blood pressure surge in humans

BackgroundVarious studies have linked the occurrence of cardiovascular events and low ambient temperatures as well as the morning blood pressure surge (MBPS). We hypothesized that low ambient temperatures produce a higher sympathetic change during the last rapid eye movement (REM) sleep transition and that this may play an important role in cold-related cardiovascular events.MethodsAll experiments were carried out on 12 healthy male adults, aged 24.00 ± 0.74 years, who participated in two experimental conditions randomly (>1 day apart): warm (23 °C) and cold (16 °C). Blood pressure (BP) was measured every 30 min for 24 h by autonomic ambulatory BP monitoring. The electroencephalograms, electrocardiograms, ambient temperature, near-body temperature, and physical activity were recorded by miniature polysomnography for 24 h.ResultsThe cold conditions resulted in: (i) higher MBPS than under warm conditions; (ii) significant and greater sympathetic index changes during the sleep–wake transition than during cover-to-uncover and supine-to-sit position tests; (iii) the non-REM–REM transition-related sympathetic elevation during the cold conditions being significantly higher in late sleep period than in early sleep period; (iv) at 1 h prior to morning awakening, the value of total power of heart rate variability changes being significantly negatively correlated with the changes of near-body temperature; and (v) significantly higher arousal index and shorter average interval of REM periods than in warm conditions.ConclusionCold exposure elevates the amplitude of MBPS and is associated with late sleep stage transition sympathetic activation, which might have important implications for cold-related cardiovascular events.