The effects of a reduced exercise duration taper programme on performance and muscle enzymes of endurance cyclists

Summary The influence of tapering on the metabolic and performance parameters in endurance cyclists was investigated. Cyclists (n = 25) trained 5 days · week^–1, 60 min·day^–1, at 75–85% maximal oxygen consumption (VO_2max) for 8 weeks and were then randomly assigned to a taper group: 4D (4 days;n = 7), 8D (8 days;n = 6), CON (control, 4 days rest;n = 6), NOTAPER (non-taper, continued training;n = 6). Muscle biopsy specimens taken before and after training and tapering were analysed for carnitine palmityltransferase (CPT), citrate synthase, ß-hydroxyacyl CoA dehydrogenase (HOAD), cytochrome oxidase (CYTOX), lactate dehydrogenase, glycogen and protein. Significant increases inVO_2max (6%), a 60-min endurance cycle test (34.5%), oxidative enzymes (77–178%), glycogen (35%) and protein (34%) occurred following training. After the taper, HOAD and CPT decreased 25 % (P<0.05) and 26% respectively, in the CON. Post-taper CYTOX values were different (P<0.05) for 4D and 8D compared with CON. Muscle glycogen levels were increased (P<0.05) after tapering in the 4D, 8D and CON, but decreased in NOTAPER. Similarly, power output at ventilation threshold was significantly increased in the 4D (27.4 W) and 8D (27 W) groups, but decreased (22 W) in the NOTAPER. These findings suggest that tapering elicited a physiological adaptation by altering oxidative enzymes and muscle glycogen levels. Such an adaptation may influence endurance cycling during a laboratory performance test.     

葡萄糖酸镁灌胃对大鼠异丙肾上腺素心肌损伤的影响

用大鼠异丙肾上腺素心肌损伤模型,研究了葡萄糖酸镁胃内给药的心肌保护作用。结果表明,葡萄糖酸镁胃内给药能减少异丙肾上腺素所致的心肌细胞Mg~(2+)丢失和Ca~(2+)聚积,减轻心肌组织脂质过氧化损害,抑制细胞内乳酸脱氢酶的释放,并能显著地减轻异丙肾上腺素引起的心肌肥大或/和水肿等病理损伤。证实了葡萄糖酸镁胃肠道给药具有一定的心肌保护作用,为其临床应用提供了实验依据。     

Influence of heparin on fibrinogen and D-dimer plasma levels in acute myocardial infarction treated with streptokinase

The purpose of this study was to investigate whether, to whatextent, and through which mechanisms intravenous heparin, administeredbefore and after streptokinase, affects the plasma levels ofD-dimer and fibrinogen in myocardial infarction. Data concerningmortality and incidence of coronary recanalization in patientsreceiving heparin and thrombolytic therapy after acute myocardialinfarction are controversial; furthermore, the mechanisms throughwhich heparin acts in combination with thrombolytic therapyare unclear. Thirty-eight patients with acute myocardial infarctiontreated with streptokinase were considered. Nineteen of themreceived, immediately before the beginning of thrombolytic treatment,a bolus of heparin (100 U. kg¹ intravenously) and, 2 h later,intravenous heparin in doses raising the partial thromboplastintime to 2-2.5 times the normal value (Group 1); the remaining19 did not receive anticoagulant treatment (Group 2). Multipledeterminations of plasma D-dimer and fibrinogen levels wereobtained in all patients before, and in the seven days followingthrombolytic treatment. Six hours after streptokinase, fibrinogendecreased from 304 ± 34 to 61 ± 34 mg. dt¹ inGroup 1 and from 312 ± 29 to 38 ±21 mg. dt¹ inGroup 2 (P<002 versus Group 1). The same difference betweengroups persisted at the 12th and at the 18th hour. D-dimer values,from 0-5 ± 01 \ig. dl¹ in Group 1 and 04 ±01 fig.dt¹ in Group 2, increased at the 1st hour to 37.2 ± 36.5fig. dt¹ and 52.2 ± 39.8 µg. dl¹, respectively.A peak value was reached in both groups at the 6th hour, whichwas followed by a slow decrease. A significant difference betweenthe two groups (P<0.05) was observed at the 1st, 2nd, 4thand 6th hour. An inverse correlation between maximal changesof fibrinogen and of D-dimer was found in both groups (r= 0.89,P<0.001 in Group 1; r=-0.81, P<0.001 in Group 2). The relationship between D-dimer and fibrinogen variations afterstreptokinase and changes induced by heparin, support the hypothesisthat the decrease of fibrinogen, following thrombolysis, isnot only the consequence of its direct degradation, but alsothe result of its transformation by streptokinase into fibrin,fibrin cross-linked (with facilitation of thrombogenic condition)and then into the stable catabolite, D-dimer. These data confirma thrombogenic effect of streptokinase therapy; this tendencycan be limited by prompt use of high doses of heparin.     

异丙酚预处理对大鼠离体心脏缺血-再灌注损伤的影响

目的 探讨异丙酚预处理对心肌缺血-再灌注(I-R)损伤的作用及其机制。方法 成年雄性 SD 大鼠18只，随机分为对照组(C组)、I-R 组、50μmol/L 异丙酚预处理组(P组)，每组6只。建立Langendorff 离体心脏灌流模型，平衡35min 后 I-R 组和 P 组均停灌30min，然后复灌120min。其中 P 组停灌前用含50μmol/L 异丙酚的 K-H 液灌流10min，并用无异丙酚的 K-H 液冲洗10min。C 组不停灌，也不用异丙酚处理。灌流结束后，制备心肌组织匀浆，测定 NO 含量、总 NOS 及超氧化物歧化酶(SOD)活性，用免疫组化 SABC 染色检测诱导型 NOS(iNOS)蛋白与血红素氧化酶-1(HO-1)蛋白表达水平，同时行光镜及透射电镜观察。结果病理学显示 C 组正常，I-R 组心肌组织严重损伤，P 组轻度损伤；与C 组相比，I-R 组和 P 组 iNOS、HO-1蛋白表达量和 iNOS 活性均升高，cNOS 活性均降低(P<0.05或0.01)；I-R 组总 NOS 活性和 NO 含量、Cu.Zn-SOD、Mn-SOD 和总 SOD 活性均降低(P<0.05或0.01)，但P 组无变化(P>0.05)。与 I-R 组比较，P 组除 iNOS 活性不变外，其余指标均升高(P<0.05或0.01)。结论 异丙酚预处理对心肌 I-R 损伤具有保护作用，其机制在于抑制或清除氧自由基以降低氧化应激水平，并通过恢复 cNOS 活性而增加 NO 的含量。     

罗比卡因与布比卡因硬膜外麻醉剖宫产术时心电图及心肌酶的变化

目的　比较硬膜外麻醉剖宫产术时罗比卡因和布比卡因对心电图及心肌酶的影响。方法　择期剖宫产手术病人 30例 ,硬膜外麻醉时Ⅰ组 (15例 )用 0 5 %罗比卡因 ,Ⅱ组 (15例 )用0 5 %布比卡因。观察麻醉手术期间心电图P R、QRS波间期以及肌酸磷酸激酶 (CK)和同工酶 (CK MB)的变化 ,同时观察麻醉镇痛、肌松效果和不良反应。结果　两组病人P R、QRS波间期均在正常范围内 (P >0 0 5 )。两组病人CK术后 2 4h值明显高于术前 (P <0 0 5 ) ,但反映心肌受损特异性较高的CK MB则无明显变化 (P >0 0 5 ) ,两组间亦无差异 (P >0 0 5 )。麻醉效果及不良反应两组间无差异。结论　硬膜外麻醉时罗比卡因与布比卡因对心电图及心肌酶影响无明显差异     

红花注射液治疗冠心病心绞痛、心肌缺血临床观察

目的:观察红花注射液治疗冠心病心绞痛、心肌缺血的临床疗效。方法:选择126例冠心病心绞痛、心肌缺血的病例,分红花组及丹参组,疗程两周,详细记录治疗前后的临床表现、心电图、血糖、血脂、血液流变学检查的变化。结果:红花、丹参均可明显改善冠心病心肌缺血相应的临床症状和心电图改变,以红花较显著。红花还有降血糖、血脂作用,显著改善血液流变指标。结论:红花注射液是治疗冠心病心绞痛、心肌缺血的理想药物。     

内皮素在评价不阻断升主动脉低温室颤对心肌保护作用中的应用

①目的探讨体外循环条件下低温室颤技术对心肌的保护作用。②方法14只健康成年犬随机分为两组，低温停跳组(n=7)与低温室颤组(n=7)，分别检测两组手术前、手术1、2小时和复跳后1小时4个时间点血内皮素(ET)的水平。③结果室颤组ET水平明显低于停跳组。④结论通过内皮素水平的变化，说明体外循环条件下低温室颤技术是一种安全、有效的心肌保护方式，优于传统低温停跳技术。     

美托洛尔对心肌梗死兔自主神经重构的影响

目的探讨β受体阻滞剂美托洛尔治疗对心肌梗死后心脏自主神经重构的改善作用。方法通过结扎新西兰大白兔冠状动脉前降支制作心肌梗死模型,随机分成心肌梗死 美托洛尔组[(10mg/(kg·d),治疗组)、心肌梗死组(模型组)和假手术组。8周后所有成活兔均进行统一的电生理检查,诱发室性心律失常。并处死实验动物,取心肌采用免疫组织化学的方法观察心室神经纤维的形态、密度及生长活性。结果模型组室性心律失常诱发率明显高于假手术组(58.3%比16.7%,P<0.001),而美托洛尔治疗后其诱发率降至8.3%。模型组梗死灶周S100及GAP43阳性神经纤维密度分别达到3889±521μm2/mm2和3090±622μm2/mm2,明显高于假手术组(1727±304μm2/mm2和718±177μm2/mm2;P均<0.01),且神经纤维空间分布紊乱;而治疗组梗死灶周S100及GAP43阳性神经纤维密度降至2725±283μm2/mm2和1922±508μm2/mm2,与模型组比差异均有统计学意义(P<0.05),且神经形态及分布更类似于假手术组,非梗死左心室游离壁心肌梗死后密度上调的S100及GAP43阳性神经纤维经美托洛尔治疗后也明显下降(P<0.05)。结论美托洛尔可改善心肌梗死动物模型的神经重构,从而可能预防心肌梗死后室性心律失常的发生。     

Ankle-brachial index and extent of atherothrombosis in 8891 patients with or at risk of vascular disease: results of the international AGATHA study.

AIMS: AGATHA (a Global Atherothrombosis Assessment) was designed to assess the extent of atherothrombosis and the use of the ankle-brachial index (ABI) in vascular patients. The principal hypotheses were that (1) in diseased patients, a low ABI was related to the number and site of vascular beds affected and (2) in at-risk patients without disease, a low ABI was related to the number of risk factors present. METHODS AND RESULTS: Patients were recruited consecutively by 482 clinicians in 24 countries and the ABI measurement was performed at a single visit. Of 8891 patients recruited, 1792 were defined as at risk and 7099 as with disease. Of the with-disease patients, 65.2% had one arterial bed affected, 27.6% two and 7.1% all three. Abnormal ABI (< or =0.9) was present in 30.9% of at-risk and 40.5% of with-disease patients. A lower ABI was weakly associated with an increasing number of risk factors in at-risk patients (r=-0.056, P=0.02) and with the site and number of arterial beds affected in with-disease patients (P<0.001). CONCLUSION: This large international study confirms that atherothrombotic disease often occurs at more than one site. The ABI is related to the risk factor profile and to the site and extent of atherothrombosis.     

Reinfusion potassium blood cardioplegia versus cold blood reinfusion alone in elective revascularization

The purpose of this study was to determine if the addition of potassium to reinfusion cold blood cardioplegia (CBC) offers an advantage over cold blood alone. Forty patients matched for age, left ventricular function, extent of coronary disease and number of vessels bypassed were prospectively randomized. Each patient received an initial dose of CB C (10 cc/kg) with potassium. Group I patients (n=23) received subsequent infusions of CBC (5 cc/kg) containing potassium while Group II patients (n=17) received cold blood only. The cross-clamp time, mean infusate volume and temperature were not significantly different in the two groups. Following reperfusion, the cardiac index and the CPK isoenzyme release at 0.5, 1, 8, and 12 h after cross-clamp release were not significantly different between the groups. The postoperative appearance of new Q-waves, inotropic agent requirement, and reversal of the lactate dehydrogenase (LDH) isoenzyme ratio were also not significantly different in the two groups. The study demonstrated that following initial arrest with potassium, cold blood is equally as effective as potassium blood cardioplegia in protecting the ischemic myocardium.