绞股蓝总甙对多柔比星致膈肌毒性的保护作用

以跨膈压 ,膈肌诱发电位及膈肌中丙二醛(MDA)和超氧化物歧化酶 (SOD)为指标 ,同时电镜观察膈肌组织超微结构改变 ,研究绞股蓝总甙 (GP)对多柔比星 (Dox)膈肌毒性的保护作用 .结果表明1 0 mg·kg-1Dox使跨膈压 ,膈肌诱发电位幅度降低 ,膈肌中 MDA增加 ,SOD活性降低 ,电镜下肌小节断裂溶解 ,线粒体肿胀 ,嵴减少 . 1 0 0 mg· kg-1GP可抑制上述变化 .结果提示 ,GP对 Dox致膈肌毒性有保护作用     

慢性阻塞性肺疾病急性加重期患者的膈神经电生理研究

目的：探讨慢性阻塞性肺疾病急性加重期(AECOPD)合并呼吸衰竭患者膈神经运动传导(PNC)及磁刺激膈肌运动诱发电位(dMEP)的特点。方法：借助于Keypoint4肌电诱发电位仪和Magpro Compact型磁刺激器对20例因呼吸衰竭而行机械通气的AECOPD患者进行PNC检测和dMEP检测。选取20例同期健康体检者为对照组。结果：与对照组比较,AECOPD组脱机前PNC潜伏期延长,波幅对数值减低,经C7棘突磁刺激dMEP潜伏期、经皮层磁刺激dMEP潜伏期和中枢运动传导时间(CMCT)延长,经C7棘突磁刺激dMEP波幅对数值减低(P<0.01),经皮层磁刺激dMEP波幅对数值差异无统计学意义(P>0.05)。AECOPD组13例患者脱机后复检,PNC潜伏期及波幅对数值、经C7棘突磁刺激dMEP潜伏期及波幅对数值、经皮层磁刺激dMEP波幅对数值与对照组相比差异情况同脱机前,而经皮层磁刺激dMEP潜伏期、CMCT与对照组差异无统计学意义(均P>0.05)。结论：AECOPD患者可存在膈神经和(或)膈肌功能不全及呼吸中枢运动传导功能异常,PNC及磁刺激dMEP联合应用对评价AECOPD患者膈神经、膈肌及呼吸中枢运动传导功能状态有一定参考价值。     

不同频率电刺激膈肌对治疗慢性阻塞性肺病临床研究

目的:探讨不同频率电刺激膈肌对治疗慢性阻塞性肺病(COPD)患者血清超氧化物歧化酶(SOD)活力变化。方法:选择住院患者96例,随机分为3组:40V组、60V组及100V组。(1)3组患者病情缓解1周后,停止所有治疗包括氧疗,采用膈肌起博器治疗,每组均30min/次,2次/日,14d为1个疗程;(2)采用黄嘌吟氧化酶法测定,清晨空腹采血4ml送检,红细胞滤过指数(FI)采用核孔滤膜法,采血后即刻测定FI和37℃温孵化24h后测定FI指标;(3)计量资料组间比较采用t检验,组间采用方差分析,进一步两两比较采用Fisher's LSD法(α=0.05)。结果:(1)40V组及60V组:治疗后血清SOD活力均明显高于治疗前(P0.05),红细胞滤过指数(FI)有显著性下降(P0.01);(2)100V组治疗前后相近(P0.05);(3)血清SOD活力及红细胞滤过指数(FI)治疗前3组差异不明显(P0.05),治疗后40V组及60V组明显高于100V组。结论:100V组结果表明较大频率脉冲幅度刺激膈肌神经,不能增强膈肌运动,亦不能提高血浆SOD浓度,反而会加重膈肌疲劳和呼吸功能障碍。因此,选择低频及超低频电刺激方法对恢复膈肌疲劳性呼吸功能障碍患者很重要。     

牛磺酸对阿霉素致膈肌毒性的保护作用

目的研究牛磺酸对阿霉素致隔肌毒性的保护作用。方法家兔１８只,分３组：①对照组：静脉注射生理盐水（ＮＳ）×５ ｄ;②ＮＳ＋阿霉素组：静脉注射ＮＳ×５ ｄ;③牛磺酸＋阿霉素组：静脉注射牛磺酸 １００ ｍｇ·ｋｇ－１ × ５ ｄ。 ２、３组于末次注射后 ２ ｈ,静脉注射阿霉素 １０ ｍｇ·ｋｇ－１组注射等量ＮＳ。２４ｈ后,麻醉动物,测量跨膈压（Ｐｄｉ）、膈肌诱发电位（ＤＥＰ）。同时测定膈肌组织中丙二醛（ＭＤＡ）含量和超氧化物歧化酶（ＲＪＤ活性。电镜观察细胞器改变。结果阿霉素（ １０ ｍｇ· ｋｇ－１）可使跨膈压（ Ｐｄｉ）、膈肌诱发电位（ＤＥＰ）幅度降低（ Ｐ＜ ０． ０５）;膈肌中 ＭＤＡ含量增加, ＳＪＤ活性降低（Ｐ＜０．０５）,肌小节和线粒体形态改变。而牛磺酸１００ｍｇｋｇ－１可抑制上述现象。结论牛磺酸对阿霉素致膈肌毒性有保护作用。     

咖啡因对低氧高碳酸性大鼠膈肌疲劳的影响

膈肌疲劳(diaphragmatic fatigue),指膈肌在负荷下活动而导致其产生力量和(或)速度的能力下降,这种能力下降可通过休息而恢复[1], 它是呼吸衰竭发生发展的重要病理机制之一.咖啡因曾被发现能提高反复电刺激所致疲劳膈肌的收缩力[2],但它对更接近COPD(Chronic obstructive pulmonary disease)患者膈肌疲劳病理状态的低氧高碳酸性疲劳膈肌的作用,尚未见报道,本实验探讨咖啡因在此种膈肌疲劳模型中的作用.     

床旁超声测量膈肌移动度指导学龄前儿童全麻术后拔管的探讨

目的 探讨床旁超声测量膈肌移动度对学龄前儿童全麻术后深麻醉拔管的指导意义。方法 入选2020年1月-2022年12月收住曲靖市第一人民医院行全麻气管插管四肢手术的学龄前患儿97例,根据患儿拔管结局分为拔管后无并发症组(C组)和拔管后有并发症组(F组),记录患儿临床资料,床旁超声测量术前、术后自主呼吸恢复时、拔管后即刻、拔管后10min、20min、30min的膈肌移动度,及相应时间点的患儿生命体征、潮气量,围术期呼吸相关并发症发生情况、Ramsay镇静评分,手术时间和复苏室停留时间。对比2组间观察数据的差异,绘制术后各时间点膈肌移动度恢复比率的受试者工作曲线。结果 2组间基线资料无显著性差异(P均>0.05)。术后自主呼吸恢复时、气管拔管即刻、拔管后10min、20min膈肌移动度及恢复比率比较均有统计学差异(P<0.05),自主呼吸恢复时膈肌移动度恢复比率的曲线下面积最大(AUC=0.69,P=0.003),灵敏度81.8%,特异度58.1%。拔管时膈肌移动度恢复比率的曲线下面积次之(AUC=0.68,P=0.006),灵敏度95.5%,特异度38.7%。结论 围术期借助...     

HI-6对正常及梭曼抑制大鼠离体膈神经-膈肌标本收缩功能的影响

目的　探讨HI 6对抗梭曼中毒所致呼吸抑制重活化作用外的其他可能作用机制。方法　采用MS 30 2三道生理记录仪 ,建立大鼠离体膈神经 膈肌收缩标本 ,观察HI 6对梭曼中毒膈神经 膈肌标本收缩功能的影响。结果　①梭曼 (2mg·L- 1)中毒后 ,膈肌收缩功能明显下降 ,中毒 10min内强直收缩曲线下面积下降至最低点 ,且在 3h内无明显恢复。②梭曼中毒前给予不同浓度的HI 6 (0 .0 1,0 .1,1.0mmol·L- 1) ,发现HI 6 (0 .1,1.0mmol·L- 1)对梭曼中毒所致膈肌强直收缩具有明显保护作用 ,且保护作用随着浓度的增加逐渐增强。③梭曼中毒后再给予HI 6 (0 .0 1,0 .1,1.0mmol·L- 1) ,发现 0 .0 1mmol·L- 1HI 6对中毒大鼠离体膈肌收缩功能无任何拮抗作用 ;当浓度增至 0 .1mmol·L- 1时 ,对膈肌强直收缩有一定的拮抗作用 ,但无统计学意义 ;但 1.0mmol·L- 1HI 6可显著对抗梭曼中毒所致膈肌收缩功能下降。结论　HI 6对梭曼中毒所致大鼠离体膈神经 膈肌收缩功能抑制具有明显拮抗作用 ,提示HI 6对抗梭曼中毒所致呼吸抑制作用机制存在酶保护作用外的直接生理对抗作用     

膈肌起搏研究的新进展

膈肌起搏是通过功能性电刺激(FES)刺激膈神经引起膈肌收缩,从而达到改善通气之目的。近20年来发展较快,尤其近几年国内开发研制了体外膈肌起搏器(EDP),本文就膈肌起搏的新进展综述如下。1 膈肌起搏的生理基础膈肌是主要的呼吸肌,位于胸腹之间,在平静呼吸时是完成呼吸工作的主要动力来源。正常呼吸情况下,通气是一种机械运动,呼吸运动依靠膈肌和肋间肌的收缩和舒张带动肺的扩张和收缩,从而维持着正常通气功能。肠肌下移1cm,潮气量可增加350ml,下移1.5cm,潮气量增加可达500ml,由膈肌舒缩而完成的通气量约占平静呼吸时通气量的3/4～4/5,表明膈肌在通气中起着重要作用。     

机械通气慢性阻塞性肺疾病患者皮质-膈肌通路的电生理评价

目的:探讨机械通气慢性阻塞性肺疾病(COPD)患者膈神经运动传导(PNC)及磁刺激膈肌运动诱发电位(dMEP)的特点.方法:选取10例常规机械通气COPD患者(上机时间≤7 d)和10例长期机械通气COPD患者(上机时间＞7 d),健康体检者10例为对照组,分别行PNC和dMEP检测.结果:3组间脱机前后PNC、经C7棘突dMEP、经皮质dMEP潜伏期及波幅对数值差异均有统计学意义(P＜0.01或P＜0.05);3组间脱机前后中枢运动传导时间(CMCT)差异有统计学意义(P＜0.01),其中脱机前2组COPD患者与对照组相比CMCT延长(P＜0.01),2组COPD患者间CMCT差异无统计学意义(P＞0.05);脱机后长期机械通气组与常规机械通气组相比CMCT延长(P＜0.01),而脱机后常规机械通气组与对照组相比CMCT差异无统计学意义(P＞0.05).结论:机械通气COPD患者存在不同程度的皮质-膈肌通路功能障碍,长期机械通气可加重其功能障碍,PNC和dMEP检测有助于明确机械通气COPD患者呼吸功能障碍的原因.     

阿霉素对兔膈肌的毒性作用

目的 探讨阿霉素对膈肌的毒性作用。方法 家兔随机分为对照组和阿霉素组,分别注射阿霉素和等量的生理盐水,２４ｈ后测膈肌诱发电位（ＤＥＰ）,数据经ｔ检验。制作膈肌标本,电镜观察超微结构的变化。结果 ①阿霉素能显降低膈诱发电位幅度,与对照组相比,Ｐ〈０．０１。②阿霉素可致膈肌细胞损伤,表现为肌小节Ｚ线排列不整齐、紊乱,部分Ｚ线模糊、消失,线粒体嵴管状,空泡变性,见板层状结构。结论 阿霉素对兔膈肌有毒性     

在不均匀牵拉的离体大鼠膈肌标本上梭曼的突触前和突触后作用

在离体大鼠膈肌上制备了一种不均匀牵拉肌肉以制动,便于用微电极记录终板电位(EPP)的标本(INSMP),避免了常规制动方法带来的制动药物、台氏液Ca~(2+),Mg~(2+)浓度改变或钳压肌肉导致膜电位(MP)下降的种种干扰。INSMP的MP和小终板电位(MEPP)正常,EPP幅度高达30mV以上,是研究药物对接头作用的较好标本。在INSMP上,梭曼(5.5μM)使MEPP频率加快,串刺激(50Hz)诱发的平均串EPPs幅度及其平均ACh 量子含量减少80％和77％。小剂量三碘季铵酚和六烃季铵可部分对抗梭曼的作用。梭曼引起强直收缩抑制主要原因为终板区蓄积的ACh作用于突触前N受体、负反馈地抑制ACh 量子释放;次要原因为作用突触后N受体、使其对ACh敏感性降低。     

The inhibitory effect of cadmium on neuromuscular transmission in the rat.

Cadmium (0.125-1 mM) was found to inhibit the isometric response of the isolated rat hemidiaphragm during indirect stimulation, but not during direct stimulation. This effect of cadmium (1 mM) was completely reversed by ethyleneglycol bis-(aminoethyl)-N,N,N',N'-tetra-acetic acid (2 mM) or by L-cysteine (2 mM) but only partially by increased calcium. Cadmium (10 micronM) significantly reduced the quantal release of transmitter in the isolated phrenic diaphragm and a concentration of 0.1 mM frequently caused a complete failure of the endplate response after 30 min. The effect of cadmium on neuromuscular transmission could not be readily reversed by washing with cadmium-free solution. Miniature endplate potential frequency and amplitude were not significantly affected by cadmium (0.1 or 0.5 mM). The results suggest that the effect of cadmium on the isolated phrenic nerve-diaphragm is due largely to inhibition of calcium function at presynaptic nerve terminals.     

Haloperidol-induced within-session response decrement patterns and catalepsy in rats: behavioural dissociation

The typical antipsychotic haloperidol is known to induce extra-pyramidal side-effects (EPS). Catalepsy in rats is generally regarded as a valid model for detecting the EPS liability of compounds in humans. Together with its antipsychotic and cataleptogenic actions, haloperidol causes an attenuation of instrumental responding which becomes larger in the course of a session: a within-session response decrement. The present study compared the time-course of haloperidol-induced catalepsy, measured by a bar test, to the haloperidol-induced within-session response decrements, measured by operant behaviour under a fixed ratio 10 schedule of reinforcement. Rats were trained to press a lever on a Fixed Ratio 10 schedule of food reinforcement during sessions of 15 min. When responding was stable, saline or haloperidol in 0.03 mg/kg, 0.1 mg/kg, or 0.3 mg/kg was administered intra-peritoneally either 30, 90 or 180 min prior to behavioural testing. The number of lever presses, food tray visits and latency to press the lever and to visit the food tray were analysed in five successive blocks of 3 min. Catalepsy was tested 30, 60, 90, 120, and 180 min. after injection, by placing a rat with its forepaws on a horizontal bar. The latency to remove both forepaws from the bar was scored. Within-session response decrements were present at 0.1 mg/kg and at 0.3 mg/kg, from 30 min after administration onward. At these doses, latency to press the lever was increased after 30 and 90 min, but not significantly after 180 min. Latency to visit the tray was affected only after 30 min, at 0.3 mg/kg. Haloperidol induced a dose-dependent increase in catalepsy from 60 min onwards, with maximal effect after 120 min. A dissociation between the time-course of occurrence of within-session response decrement and the cataleptogenic action of haloperidol, as well as between the latter and both latency measures, was found. Consequently, the present data suggest that within-session response decrements are not obviously caused by catalepsy-related impairments.     

Change in flash visual evoked potentials in New Zealand albino rabbits after sub-tenon’s anesthesia

Context: The occurrence of amaurosis during ophthalmic anesthesia is well known. The reason for this manifestation has not been studied.

Purpose: To investigate the effect of sub-tenon’s anesthesia on visual conduction in rabbit eyes.

Methods: Fifteen right eyes of 15 New Zealand albino rabbits were included. 2% lidocaine hydrochloride and 0.75% bupivacaine hydrochloride (1?ml, 1:1 mixture) was injected in the sub-tenon’s space of 8 eyes while the control group (n?=?7) was injected with 1?ml physiological saline. Flash visual evoked potentials (FVEP) were performed with Roland reti-scan system before and, 5?min, 15?min, and 5 days after injection. The natural pupillary diameter and minimal pupillary diameter with light reflex were recorded.

Results: In the anesthesia group, N1 latency, P1 latency, and P1 amplitude were 17.13?±?1.13?ms, 28.25?±?1.83?ms, 13.45?±?4.36?μv respectively before injection; 21.75?±?3.06?ms, 29.63?±?2.67?ms, 7.24?±?4.64?μv at 5?min after injection; 22.25?±?1.39?ms, 29.50?±?2.51?ms, 7.54?±?4.47?μv at 15?min after injection, and, 17.75?±?0.71?ms, 28.13?±?2.42?ms, 13.17?±?4.08?μv 5 days after injection. When compared with baseline, N1 latency at 5?min and 15?min after injection showed prolongation (p?=?0.019 and p?=?0.001, respectively). Likewise, P1 amplitude decreased at 5?min and 15?min after injection (p?<?0.001, p?<?0.001, respectively). Both N1 latency and P1 amplitude recovered 5 days after the injection. Pupillary light reflex (PLR) constriction amplitude was 35.42% and 0.00% before and at 5?min after injection (p?=?0.012). After 5 days it recovered to 33.33%. The FVEP and PLR constriction amplitude did not change significantly after injection in the control group.

Discussion: Sub-tenon’s anesthesia was associated with changes in the FVEP and pupullary light reflex in rabbit eyes in our study.

Conclusions: The data from this study suggested that sub-tenon’s anesthesia could reversibly block visual conduction in rabbit’s eyes.     

Neurophysiological studies of L-acetylcarnitine administration in man

Systemic administration of L-acetylcarnitine HCl (LAC) increases in human subjects the amplitude of visual evoked potentials (VEPs) obtained with patterned elements of 7.5 min of visual angle, of steady-state VEPs obtained with intermittent luminous stimulation, of EEG theta, alpha and beta bands. The latency of the "cognitive" P300 potential obtained with an auditory "oddball" paradigm was also reduced by LAC injection, while the amplitude of this potential was increased. These results were obtained in control volunteers and in patients affected by different forms of dementias. The modifications induced by LAC appear 10-15 min after the i.v. injection and last for 50-90 min. These results parallel previously described findings of animal experiments and suggest an effect of LAC on cholinergic neurotransmission.     

Diesel exhaust particulates affect cell signaling,mucin profiles,and apoptosis in trachea explants of Balb/C mice

Particulate matter from diesel exhaust (DEP) has toxic properties and can activate intracellular signaling pathways and induce metabolic changes. This study was conducted to evaluate the activation of extracellular signal‐regulated kinase (ERK) and c‐Jun N‐terminal kinase (JNK) and to analyze the mucin profile (acid (AB⁺), neutral (PAS⁺), or mixed (AB/PAS⁺) mucus) and vacuolization (V) of tracheal explants after treatment with 50 or 100 μg/mL DEP for 30 or 60 min. Western blot analyses showed small increases in ERK1/2 and JNK phosphorylation after 30 min of 100 μg/mL DEP treatment compared with the control. An increase in JNK phosphorylation was observed after 60 min of treatment with 50 μg/mL DEP compared with the control. We did not observe any change in the level of ERK1/2 phosphorylation after treatment with 50 μg/mL DEP. Other groups of tracheas were subjected to histological sectioning and stained with periodic acid‐Schiff (PAS) reagent and Alcian Blue (AB). The stained tissue sections were then subjected to morphometric analysis. The results obtained were compared using ANOVA. Treatment with 50 μg/mL DEP for 30 min or 60 min showed a significant increase (p < 0.001) in the amount of acid mucus, a reduction in neutral mucus, a significant reduction in mixed mucus, and greater vacuolization. Our results suggest that compounds found in DEPs are able to activate acid mucus production and enhance vacuolization and cell signaling pathways, which can lead to airway diseases. © 2014 Wiley Periodicals, Inc. Environ Toxicol 30: 1297–1308, 2015.     

Pathophysiology of soman intoxication in primates

Adult baboons were monitored during intravenous infusion of Soman (1,2,2-trimethylpropyl ester, phosphonofluoridate). Three groups of animals were studied. Two groups were anesthetized with sodium pentobarbital (initial dose, 20 mg/kg), instrumented for measurement of systemic blood pressure (BP), pulmonary artery pressure, cardiac output (CO), ECG, ventilatory flow, translaryngeal pressure (PTL), transdiaphragmatic pressure (Pdi), transpulmonary pressure (PTP), diaphragm EMG, and efferent phrenic nerve traffic (Eph). One group received no Soman and served as controls. In the other group, Soman was infused over 10 min at doses of 13.1, 8.21, 4.92, or 3.3 micrograms/kg. The onset of intoxication occurred within 7-8 min (before the end of the 10-min infusion), manifested by muscular fasciculations, stridorous breathing, copious secretions, and atrioventricular arrhythmias. Mean BP decreased to 30 mm Hg by the combination of decreased CO and decreased vascular resistance. There was a dose-related response in the onset and duration of these effects. Apnea occurred in most animals and coincided with cessation of the Eph signal. Stimulation of the diaphragm via the phrenic nerve following apnea yielded Pdi values unchanged from baseline, indicating an intact neuromuscular apparatus. All animals required ventilatory support. Some surviving animals exhibited severe behavior changes. The third group of animals was studied without anesthesia. Instrumentation was performed 3 days before using a tether system for the measurement of BP, CO, and ECG, and an arterial line for blood withdrawal. Soman was infused over 10 min at a dose of 13.1 micrograms/kg. The onset of intoxication occurred within 2-3 min, manifested by hyperactivity, severe muscle fasciculations which simulated grand-mal convulsions, stridorous respiratory sounds, copious secretions, and cardiac arrhythmias. Apnea and severe lactic acid acidosis developed in all animals and all required ventilatory assistance. None recovered spontaneous ventilation at the end of 4 hr.     

Effects of L-arginine on penicillin-induced epileptiform activity in rats

It has been suggested that nitric oxide (NO) is involved in the pathophysiology of epilepsy. Data are, however controversial because it is not clear whether NO has pro- or anticonvulsant effects. The aim of this study was to investigate the effects of NO on penicillin G-induced epileptiform activity. The left cerebral cortex was exposed by craniotomy in urethane-anesthetized Wistar rats. The epileptic activity was produced by intraperitoneal injection of penicillin G (3 million U/kg, i.p.). The ECoG (electrocorticogram) activity was displayed on a four-channel recorder. At 39.7 +/- 5.4 min after penicillin administration, large amplitude sharp waves appeared in the ECoG. Mean spike frequency and mean spike amplitude were calculated as 29.5 +/- 3.2/min and 865 +/- 91 microV, respectively, at the 55th min. 7-Nitroindazole (60 mg/kg, i.p.) injection 30 min before penicillin G administration significantly reduced the latency of epileptiform activity. Intracerebroventricular administration of L-arginine (300 microg/2 microl, i.c.v.) and sodium nitroprusside (100 microg/2 microl, i.c.v.) suppressed epileptiform activity. Saline (2 microl) and D-arginine (300 microg/2 microl, i.c.v.) administration into the cerebral ventricle were completely ineffective on epileptiform activity (P<0.01). These findings suggest that NO may be an endogenous antiepileptic substance.