Reduced oxidative muscle metabolism in chronic fatigue syndrome

The purpose of this study was to determine if chronic fatigue syndrome (CSF) is characterized by abnormalities in oxidative muscle metabolism. Patients with CFS according to Centers for Disease Control (CDC) criteria (n = 22) were compared to normal sedentary subjects (n = 15). CFS patients were also tested before and 2 days after a maximal treadmill test. Muscle oxidative capacity was measured as the maximal rate of postexercise phosphocreatine (PCr) resynthesis using the ADP model (V_max) in the calf muscles using ³¹P magnetic resonance spectroscopy. V_max was significantly reduced in CFS patients (39.6 ± 2.8 mmol/L/min, mean ± SE) compared to controls (53.8 ± 2.8 mmol/L/min). Two days postexercise there was no change in resting inorganic phosphate (Pi)/PCr or V_max in the CFS patients (n = 14). In conclusion, oxidative metabolism is reduced in CFS patients compared to sedentary controls. In addition, a single bout of strenuous exercise did not cause a further reduction in oxidative metabolism, or alter resting Pi/PCr ratios. © 1996 John Wiley & Sons, Inc.     

Relation between in vivo and in vitro measurements of skeletal muscle oxidative metabolism.

The relationships between in vivo (31)P magnetic resonance spectroscopy (MRS) and in vitro markers of oxidative capacity (mitochondrial function) were determined in 27 women with varying levels of physical fitness. Following 90-s isometric plantar flexion exercises, calf muscle mitochondrial function was determined from the phosphocreatine (PCr) recovery time constant, the adenosine diphosphate (ADP) recovery time constant, the rate of change of PCr during the initial 14 s of recovery, and the apparent maximum rate of oxidative adenosine triphosphate (ATP) synthesis (Q(max)). Muscle fiber type distribution (I, IIa, IIx), citrate synthase (CS) activity, and cytochrome c oxidase (COX) activity were determined from a biopsy sample of lateral gastrocnemius. MRS markers of mitochondrial function correlated moderately (P < 0.05) with the percentage of type IIa oxidative fibers (r = 0.41 to 0.66) and CS activity (r = 0.48 to 0.64), but only weakly with COX activity (r = 0.03 to 0.26, P > 0.05). These results support the use of MRS to determine mitochondrial function in vivo.     

推拿对一次性离心运动后延迟性肌肉酸痛的影响

背景：推拿是运动性疲劳防治的常用手段之一,但有关推拿防治延迟性肌肉酸痛疗效的客观评价较少。 目的：评价推拿对一次性离心运动后延迟性肌肉酸痛的影响。 设计、时间及地点：对比观察,于2008-04/07在南京中医药大学完成。 对象：将30名健康男性学生按照条件对等原则随机分成对照组和运动前推拿组、运动后推拿组共3组,每组10名。 方法：运动前推拿组学生于训练前在左上肢进行30 min的推拿,推拿结束5 min后开始训练。运动后推拿组学生于训练后30 min在左上肢进行30 min的推拿,并在此后的3 d内按规定的时间继续接受推拿治疗,30 min/次,1次/d。对照组学生仅参加训练,不做任何的准备活动或整理活动,也不接受任何治疗。 主要观察指标：观察训练前、训练后即刻、训练后24,48,72 h测定肌肉酸痛程度和持续时间、最大等长收缩力量、臂围、肘关节的屈伸度,训练前1 h、训练后即刻、训练后24,48 h血清肌酸激酶的变化。 结果：与对照组相比,运动前推拿组、运动后推拿组的肌肉酸痛持续时间明显缩短,酸痛的程度明显减轻(P < 0.01,P < 0.05),运动后72 h的肌肉最大等长收缩力量的恢复明显(P < 0.01),运动后72 h的血清肌酸激酶升高幅度明显降低。运动前推拿组运动后即刻的肘关节屈曲程度变化明显小于对照组(P < 0.05),运动后推拿组在运动后72 h的肘关节伸直程度的恢复明显优于对照组(P < 0.05);运动前推拿组、运动后推拿组的臂围变化与对照组无明显差异。 结论：运动前推拿能一定程度预防延迟性肌肉酸痛,减轻延迟性肌肉酸痛的严重程度,而运动后推拿能一定程度促进延迟性肌肉酸痛的恢复。     

Improved Cerebral Vasoreactivity After Statin Administration in Healthy Adults

BACKGROUND AND PURPOSE: Significant improvements of cerebral vasomotor reactivity during statin treatment were found in patients with cerebral small-vessel disease. The authors analyzed the cerebrovascular CO(2) reactivity before and after statin administration in healthy adults using a case-control study design. METHODS: The mean cerebral blood flow velocity (CBFV) of both middle cerebral arteries and the vasomotor reserve capacity (VMRC) were measured by repeated and simultaneous bilateral transcranial Doppler sonography in 25 healthy adults (7 men, mean age 28.8 years [95% confidence interval (CI): 25.7; 31.9]) before, during (days 1, 3, 7, and 14), and after administration of 40 mg pravastatin for 14 days as compared to 10 healthy control persons (4 men, mean age 30.6 years [95% CI: 22.9; 38.3]). The VMRC was calculated off-line as the percentage change of CBFV per 1% increase in end-tidal CO2 by a blinded investigator. RESULTS: In the statin group, 5 persons were excluded from further analysis. In the remaining 20 volunteers, the authors observed a highly significant effect of statin administration on VMRC (P = .002). The VMRC was significantly increased after statin administration on day 7 as compared to the initial value (3.03 [95% CI: 2.67; 3.38] vs 2.64 [95% CI: 2.41; 2.86]; P = .04). The effect was most pronounced in patients with lower initial VMRC values. In the control group, the VMRC did not differ significantly from baseline at different time intervals. CONCLUSIONS: The findings indicate an improvement of cerebral vasoreactivity even after short-term statin administration in healthy adults. However, this effect was related to baseline vasoreactivity.     

Motor-evoked potentials in response to fatiguing grip exercise in multiple sclerosis patients.

OBJECTIVE: This study examined central and peripheral effects of fatiguing exercise (3 min maximal grip) in healthy controls (n=10) and multiple sclerosis (MS) subjects with weakness, MS-W (n=16) and normal motor function, MS-NM (n=16) in the studied extremity.Method: Transcranial magnetic stimulation (TMS) was used to assess resting and facilitated motor-evoked potentials (MEPs) of abductor pollicus brevis (APB) and flexor carpi radialis (FCR) muscles before and after fatiguing exercise. Exercise-induced depletion and recovery of phosphocreatine (PCr) were measured using (31)P magnetic resonance spectroscopy ((31)PMRS) in FCR. RESULTS AND CONCLUSION: MS subjects demonstrated significantly lower peak force and a faster decline in force than controls. Contralateral muscle activation (hand grip) before the fatigue protocol resulted in significantly increased MEP amplitudes in all groups. Contralateral hand grip following fatiguing exercise resulted in significantly higher MEP amplitudes in controls and MS-NM subjects, but not MS-W subjects. Fatiguing exercise resulted in prolonged central motor conduction time (CMCT) in MS subjects, but not controls. No group differences in PCr depletion or resynthesis were observed. All groups demonstrated significant post-exercise depression (PED) of MEP amplitude that persisted beyond the time course of PCr recovery, indicating fatigue was central in origin. MS subjects were less able than controls to increase cortical excitability using contralateral muscle activation following fatiguing exercise, possibly indicating impaired conduction in the corpus callosum.     

Mitochondrial impairment of human muscle in Friedreich ataxia in vivo

Friedreich ataxia occurs due to mutations in the gene encoding the mitochondrial protein frataxin. This (31)P magnetic resonance spectroscopy study on the calf muscle of Friedreich ataxia patients provides in vivo evidence of a severe impairment of mitochondrial function. Mitochondrial adenosine triphosphate resynthesis was studied by means of the post-exercise recovery of phosphocreatine. After ischemic exercise in calf muscles of all patients, phosphocreatine recovery was dramatically delayed. Time constants of recovery correlated with mutations of the frataxin gene, the age of the patients, and disease duration. (31)P magnetic resonance spectroscopy represents the first expedient tool for monitoring therapeutic trials in Friedreich ataxia non-invasively.     

音乐游戏运动疗法对高龄轻度认知障碍患者干预效果的研究

目的 探讨音乐游戏运动疗法对高龄轻度认知障碍（mild cognitive impairment,MCI）患者功能独立 性的影响。 方法 纳入2017年1月-2018年12月于上海市普陀区人民医院老年科住院的60例65～95岁的MCI患者, 随机分为观察组和对照组,观察组患者开展一周5次、每次40 min、持续6周的音乐游戏运动疗法,对 照组采用常规健康教育。采用功能独立性评定量表（functional independence measure,FIM）对患者治疗 前及治疗6周效果进行总体评价。 结果 观察组（30例,实际完成28例）与对照组（30例,实际完成30例）一般情况和治疗前FIM得分 差异无统计学意义。治疗后观察组FI M中运动功能（P =0.006）、认知功能（P =0.001）和总分（P =0.001） 优于对照组。观察组治疗后FIM中运动功能（P＜0.001）、认知功能（P＜0.001）和总分（P＜0.001）均高 于本组治疗前。对照组治疗后FIM得分与治疗前差异无统计学意义。 结论 音乐结合游戏运动疗法对高龄MCI患者是一项有效的非药物治疗方法,能延缓MCI进程,提高 患者运动功能及认知功能。     

Serum neuron-specific enolase in the major subtypes of status epilepticus

OBJECTIVES: To determine the relative magnitudes of neuron-specific enolase (NSE) levels after complex partial status epilepticus (SE), absence SE, generalized convulsive SE, and subclinical generalized convulsive SE (frequently referred to as acute symptomatic myoclonic status epilepticus). BACKGROUND: NSE is a marker of acute brain injury and blood-brain barrier dysfunction, which is elevated in SE. METHODS: Serum NSE levels were drawn in 31 patients 1, 2, 3, and 7 days after SE. Patients were classified as acute symptomatic or remote symptomatic, and the duration and outcome of SE were determined and correlated with the peak NSE level. RESULTS: NSE was elevated significantly in all four subtypes of SE, but NSE levels were highest in complex partial and subclinical SE. The mean peak NSE level for the complex partial SE group was 23.88 ng/mL (n = 12), 21.5 ng/mL for absence SE (n = 1), 14.10 ng/mL for the generalized convulsive SE group (n = 12), and 37.83 ng/mL for the subclinical SE group (n = 6), all of which was significantly higher than normal control subjects (5.02 ng/mL). Outcome was significantly different between the three groups (p = 0.0007), and was significantly worse for subclinical SE (p = 0.0005, subclinical versus generalized convulsive SE). CONCLUSION: Serum NSE levels were highest in complex partial and subclinical generalized convulsive SE. The extremely high levels of NSE in subclinical SE reflect the severity of the acute neurologic insults and poor outcome common to subclinical SE. High NSE levels in complex partial SE reflects the long duration of SE in this subgroup, and potential for brain injury.     

Sertraline for prevention of depression recurrence in diabetes mellitus: a randomized, double-blind, placebo-controlled trial

CONTEXT: In patients with diabetes mellitus, depression is a prevalent and recurrent problem that adversely affects the medical prognosis. OBJECTIVE: To determine whether maintenance therapy with sertraline hydrochloride prevents recurrence of major depression in patients with diabetes. DESIGN: A randomized, double-blind, placebo-controlled, maintenance treatment trial. Patients who recovered from depression during open-label sertraline treatment continued to receive sertraline (n = 79) or placebo (n = 73) and were followed up for up to 52 weeks or until depression recurred. SETTING: Outpatient clinics at Washington University, St Louis, MO, the University of Washington, Seattle, and the University of Arizona, Tucson. PATIENTS: One hundred fifty-two patients with diabetes (mean age, 52.8 years; 59.9% female; 82.9% with type 2 diabetes) who recovered from major depression (43.3% of those initially assigned) during 16 weeks of open-label treatment with sertraline (mean dose, 117.9 mg/d). INTERVENTION: Sertraline continued at recovery dose or identical-appearing placebo. MAIN OUTCOME MEASURES: The primary outcome was length of time (measured as the number of days after randomization) to recurrence of major depression as defined in DSM-IV. The secondary outcome was glycemic control, which was assessed via serial determinations of glycosylated hemoglobin levels. RESULTS: Sertraline conferred significantly greater prophylaxis against depression recurrence than did placebo (hazard ratio = 0.51; 95% confidence interval, 0.31-0.85; P = .02). Elapsed time before major depression recurred in one third of the patients increased from 57 days in patients who received placebo to 226 days in patients treated with sertraline. Glycosylated hemoglobin levels decreased during the open treatment phase (mean +/- SD glycosylated hemoglobin level reduction, -0.4% +/- 1.4%; P = .002). Glycosylated hemoglobin levels remained significantly lower than baseline during depression-free maintenance (P = .002) and did not differ between treatment groups (P = .90). CONCLUSIONS: In patients with diabetes, maintenance therapy with sertraline prolongs the depression-free interval following recovery from major depression. Depression recovery with sertraline as well as sustained remission with or without treatment are associated with improvements in glycosylated hemoglobin levels for at least 1 year.     

大强度离心运动大鼠不同时相骨骼肌结构及血白细胞介素6、肌酸激酶、肌酸激酶同工酶的变化

背景：运动预处理可在一定程度上减轻运动性骨骼肌微损伤,从而避免延迟性肌肉酸痛的发生。目前应用白细胞介素6和CK-MM评定骨骼肌微细损伤还较缺少实验性研究。 目的：观察运动预处理对大鼠大强度离心运动后不同时相骨骼肌结构损伤及血液白细胞介素6、肌酸激酶和CK-MM变化的影响。 设计、时间及地点：随机对照动物实验,2006/2007在成都体育学院动物实验室完成。 材料：成年健康雌性SD大鼠80只,体质量(231.3±12.44) g。每组又随机分别分为运动前和运动后即刻、运动后24,48,72 h 5个亚组,每组8只。 方法：无预处理组：除对运动前组外其他大鼠进行一次速度19~21 m/min,坡度为-16°的90 min的跑台运动。运动预处理组：进行2周离心跑台训练,2周后,除运动前组外,其他大鼠进行一次性跑台运动,运动方式同无预处理组。 主要观察指标：一次性离心运动后即刻、24,48和72 h观察比目鱼肌结构及血液白细胞介素6、肌酸激酶、CK-MM的变化。 结果：运动后两组大鼠比目鱼肌均出现损伤性改变,尤以无预处理组更为明显,且以运动后24~48 h较为严重。无预处理组运动后即刻血浆白细胞介素6显著增高,随后逐渐下降,72 h再次显著增高。运动预处理组运动后即刻略降低,随后逐渐升高,于48 h达峰值。运动后运动预处理组血浆白细胞介素6水平低于无预处理组。运动前运动预处理组肌酸激酶和CK-MM均低于无预处理组。运动后无预处理组、运动预处理组两组肌酸激酶和CK-MM先升后降,除运动后72 h 外,运动预处理组CK和CK-MM水平及变化幅度低于无预处理组。 结论：运动预处理有助于减轻离心运动导致的骨骼肌超微结构损伤及运动应激所引起的相关血液指标变化。肌酸激酶和CK-MM活性水平的个体差异较大,更适用于个体自身的纵向比较。     

Canine X-linked muscular dystrophy studied with in vivo phosphorus magnetic resonance spectroscopy.

Duchenne muscular dystrophy (DMD) is an X-linked disease characterized by progressive muscle weakness and degeneration. Dystrophin is the product of the missing gene in this disorder. However, the cause of the dystrophic process is not understood. Transient muscle injury is normally seen after muscle exercise, and may be a necessary process in muscle growth and preservation. We, therefore, chose to evaluate the role of exercise in Duchenne dystrophy by studying the canine X-linked animal model (CXMD). These dogs also lack dystrophin and have clinical signs similar to humans. Exercise was initiated by electrical stimulation, and muscle metabolism was monitored with phosphorus magnetic resonance spectroscopy (P-MRS). Dogs with CXMD had abnormal muscle pathology and markedly elevated serum CK. The inorganic phosphate (Pi) to phosphocreatine (PCr) ratio was increased in CXMD dogs at rest compared with normal dogs (Pi/(Pi + PCr) = 0.166 +/- 0.054 for CXMD and 0.073 +/- 0.017 for normals, mean +/- SE). No changes in resting ATP, pH, phosphomonoesters (PME), and phosphodiesters (PDE) were seen. The mean Pi/(Pi + PCr) and pH values during stimulation were normal in the CXMD dogs. Two to three days after electrical stimulation, resting Pi/(Pi + PCr) ratios were significantly increased in the CXMD dogs (0.127 +/- 0.029 compared with 0.172 +/- 0.054, mean +/- SD). Normal dogs showed no increase in Pi/(Pi + PCr) following stimulation. There was a 50-fold greater increase in serum CK in CXMD compared with normal dogs following exercise. These results indicate greater muscle injury in CXMD muscle, and suggest that in the absence of dystrophin, exercise-induced muscle injury may play a role in the dystrophic process.     

Prolactin levels in cerebrospinal fluid of patients with infantile spasms

Infantile spasms are an age-related epileptic syndrome of infancy and are characterized by the combination of clusters of epileptic spasms and specific electroencephalographic findings. The etiology and the pathogenesis of the disease is still unclear. Prolactin has been thought to be specifically related to epileptic seizures. To investigate the possible mechanism of prolactin secretion in infantile spasms cerebrospinal fluid prolactin levels were examined. Fifteen patients with infantile spasms (10 females and five males), 3-16 months of age, were evaluated and compared with age- and sex-matched control subject. Cerebrospinal fluid samples for prolactin were obtained before and after treatment. The mean prolactin levels in the cerebrospinal fluid of the patients before therapy (3.25 +/- 1.48 ng/mL) was higher than the control group (2.38 +/- 0.89 ng/mL), and the difference between the two groups was statistically significant (P < 0.001). The mean prolactin level in the cerebrospinal fluid of the patients after therapy (4.69 +/- 1.47 ng/mL) was demonstrated to be higher than the mean prolactin level before therapy (3.25 +/- 1.48 ng/mL) and the difference between the two groups was statistically significant (P = 0.037). Elevation of cerebrospinal fluid prolactin levels before and after treatment in patients with infantile spasms provided evidence that the cerebrospinal fluid prolactin level is related with neuronal injury.     

姜黄素对癫痫持续状态后海马内质网应激相关分子表达的影响

目的探讨姜黄素对癫痫持续状态（SE）后海马内质网应激（ERS）标志分子免疫球蛋白结合蛋白（BiP）和ERS相关促凋亡分子如生长停滞、DNA损害可诱导基因153（GADD153）表达的影响。方法将90只SD大鼠随机分人SE组、姜黄素组和对照组。建立氯化锂一匹罗卡品大鼠SE模型。应用半定量逆转录-聚合酶链反应（RT-PCR）动态观察SE后海马BiP和GADD153的转录状况。结果（1）与对照组相比，SE组SE后2、4、6、24hBiPmRNA表达升高（P〈0．01），6h达高峰，24h开始下降（P〈0．01），72h恢复至正常水平；姜黄素组BiP mRNA表达的动态变化同SE组类似，但显著低于SE组（P〈0．05或0．01）。（2）与对照组比，SE组SE后2、4、6、24、72hGADD153mRNA显著上调（P〈0．01），SE后2h达高峰，24h开始下降（P〈0．01）。姜黄素组仅于SE后2、4hGADD153mRNA表达明显高于对照组（P〈0．01），且较SE组低（P〈0．01）。结论姜黄素有可能成为在体抑制ERS的有效药物；减轻ERS、抑制GADD153表达可能是姜黄素在SE后发挥神经元保护作用的重要机制。     

踏车锻炼对慢性阻塞性肺疾病患者运动耐力和中枢驱动的影响

目的 探讨踏车锻炼对慢性阻塞性肺疾病(COPD)患者运动耐力和中枢驱动的影响.方法 选择南方医科大学珠江医院呼吸内科自2009年10月至2010年10月收治的中、重度COPD缓解期COPD患者22例,其中康复组(12例)接受12周中等强度踏车运动训练,对照组(10例)不接受训练.在训练前后分别进行常规肺通气功能、弥散功能和肺容量测定以及运动心肺功能测试及高强度持续恒定功率运动试验,监测运动过程中呼吸流量、容量和膈肌肌电的变化.比较患者试验前后运动耐力和呼吸困难评分的变化.结果 康复组患者锻炼后运动时间比锻炼前延长,峰运动功率增加,差异均有统计学意义(P＜0.05);等时间点呼吸频率(RR)、分钟通气量(VE)、平均吸气流速(VT/Ti)、膈肌电电压的均方根(RMS)、Borg评分较锻炼前下降,差异均有统计学意义(P＜0.05); COPD患者△Borg分别与△VE、△VT/Ti、△RMS呈正相关关系(P＜0.05).结论 下肢运动训练可显著改善COPD患者的运动耐力,降低COPD患者在相同运动强度下的通气需求和中枢驱动,改变了COPD患者的呼吸应答方式,从而减轻了COPD患者呼吸困难的主观感觉.     

Statin-associated changes in skeletal muscle function and stress response after novel or accustomed exercise

Introduction: The most common side effect of statins, myopathy, is more likely in exercisers. We investigated the interaction of statin treatment with novel vs. accustomed exercise on muscle function, heat shock protein (Hsp) expression, and caspase activation. Methods: Mice received daily cerivastatin or saline for 2 weeks, with/without wheel running (RW) (novel/sedentary). Accustomed groups completed 2 weeks of RW before statins. At 4 weeks, plantarflexor isometric force, Hsp25, αB‐crystallin, caspase‐3 and ‐9, and plasma creatine kinase (CK) were quantified. Results: Statins reduced force in sedentary and novel groups, compared with saline, by 15% and 27%, respectively. Muscle fatigability increased 21% and 30% with statins compared with saline in sedentary and novel groups, respectively. Accustomed exercise prevented statin‐associated force loss and increased fatigability. CK did not correlate with functional outcomes. RW increased Hsp protein in all groups. Conclusion: Our results suggest that exercise prior to statin treatment can protect against decrements in muscle function. Muscle Nerve 2011     

不同麻醉深度对抑郁症电休克治疗后学习记忆的影响

目的观察抑郁症在不同麻醉深度下行电休克治疗的疗效及对学习记忆的影响。方法75例初次接受电休克治疗的抑郁症患者,随机分为A、B、C三组,每组25例。A组:单次静脉推注丙泊酚1.5 mg/kg后实施电休克;B组:丙泊酚泵注维持深麻醉(脑电双频指数<45)下电休克;C组:丙泊酚泵注维持临床麻醉深度(脑电双频指数=45～60)下电休克。于电休克治疗前、治疗后24 h和1周末以17项汉密尔顿抑郁量表和韦氏记忆量表评估抑郁症状及学习记忆功能。结果与C组比较,A组、B组呼吸恢复时间、意识恢复时间、治疗室观察时间均延长(P<0.05)。三组患者电休克治疗后24 h(F=5.04,P<0.01)及1周末(F=4.05,P<0.05)汉密尔顿抑郁量表评分较治疗前均降低,而在各时间点评分三组之间差异无统计学意义。与治疗前比较,三组患者ECT后24 h长时记忆均降低(P<0.05),而ECT后24 h和1周后患者短时记忆、即刻记忆均升高(P<0.05),且B组、C组短时记忆、即刻记忆高于A组(P<0.05)。结论临床麻醉深度下实施电休克治疗可有效缓解抑郁症状,且患者的短期记忆在治疗后可得到早期改善,有利于患者早期康复,更适于电休克的麻醉。     

Late-onset distal muscular dystrophy affecting the posterior calves

Miyoshi myopathy, caused by mutations in the membrane protein dysferlin, is the most common muscular dystrophy that presents in the posterior calves. Its onset is before the age of 30 years and it is associated with marked elevations of serum creatine kinase (CK). In contrast, little is known about calf myopathies with onset after the age of 30, and it is not clear whether such patients have a dysferlinopathy. We describe five patients with a myopathy predominantly affecting the calf muscles, with onset after the age of 30. Muscle tissue was analyzed by immunoblot for dystrophin and dysferlin. All five had normal dysferlin but one had a dystrophinopathy. Serum CK levels ranged from 3 to 15 times the upper limit of normal. In contrast, all of 13 patients presenting before age 30 with calf weakness had a dysferlinopathy. Thus, isolated calf atrophy and weakness with onset after age 30, and associated with serum CK levels that are only moderately elevated, represents a distinct myopathy phenotype. Most of these cases are sporadic, although the overall phenotype appears genetically heterogeneous and dysferlinopathy is uncommon.     

Myoglobin is a sensitive marker of increased muscle membrane vulnerability

Summary Changes in muscle proteins in serum after exercise were studied to evaluate the use of such proteins as indicators of increased muscle membrane vulnerability. Seventy-one women were asked to perform bicycle exercise for 45 min at a moderate load; four proteins (creatine kinase — CK, myoglobin — Mb, aldolase — Ald and pyruvate kinase — PK) were measured in serum up to 24 h after exercise. Twenty-one women were carriers of Duchenne's muscular dystrophy (DMD); these are known to show an elevated serum CK activity at rest, as well as an increased CK response after exercise. Fifty women without a family history of neuromuscular disease were tested to obtain normal values: they showed a small peak (18%) of CK activity 8h after exercise, and an even smaller peak of Mb (9%) 1h after exercise. The mean post-exercise increase for both CK and Mb in the 21 DMD carriers was significantly higher than in controls; the maximum of Mb, on average 70% of baseline levels, was reached 1h after exercise and was higher than that for CK (48%), which was reached 8 h after exercise. It is concluded that myoglobin levels after exercise are a good index of increased vulnerability of the muscle membrane.     

Atorvastatin reduces thrombin generation after percutaneous coronary intervention independent of soluble tissue factor

INTRODUCTION: Statins were previously shown to suppress cellular tissue factor (TF) in vitro. Here, we investigated the effect of atorvastatin on the TF-pathway and thrombin generation after coronary angioplasty and stenting in vivo. MATERIALS AND METHODS: A cohort of 30 patients with coronary artery disease (CAD) was randomised to treatment with either none (n=10), 10 mg (n=10) or 80 mg (n=10) atorvastatin per day for the postinterventional period of 6 months starting the day before percutaneous coronary intervention (PCI). Fasting blood samples were collected on admission and after 6 weeks and 6 months of statin therapy to determine sTF, free tissue factor pathway inhibitor (TFPI) and prothrombin fragment F1.2 by immunoassay. RESULTS: Soluble TF (sTF) significantly correlated with thrombin generation as measured by prothrombin fragment F1.2 at baseline. This correlation was lost 6 weeks and 6 months after initiation of statin therapy. In vivo, F1.2 was significantly lowered after 6 months of statin therapy by both, low dose (0 vs. 10 mg: 1.3+/-0.3 vs. 0.7+/-0.2 ng/ml; P<0.05) and high dose (0 vs. 80 mg: 1.2+/-0.3 vs. 0.6+/-0.2 ng/ml; P=0.01) atorvastatin compared to control. However, sTF and free TFPI did not change significantly with atorvastatin therapy when compared to baseline or control. CONCLUSIONS: Our results demonstrate reduced in vivo generation of thrombin six months after percutaneous coronary intervention and statin therapy independent of sTF and free TFPI.