田径运动员最大摄氧量和无氧功测试中血乳酸的应用

目的:研究田径运动员最大摄氧量和Wingate测试后血乳酸的变化,分析血乳酸对测试结果的意义。方法:测试田径短跑运动员36例和中长跑运动员29例的最大摄氧量和Wingate无氧功,以及测试后的血乳酸值。结果:最大摄氧量测试后血乳酸数值为9～11mmol/L左右,摄氧量与乳酸值没有直接相关关系,但不同项目之间有一定的差异;Wingate测试后血乳酸数值一般大于12mmol/L,测试的主要评价指标与乳酸值都有较高的相关关系。结论:血乳酸值对于最大摄氧量测试意义不大,但对于Wingate测试可以作为一项辅助评价指标。     

Monitoring myocardial reperfusion injury with NADH fluorometry.

Using NADH fluorometry to monitor myocardial metabolism, the mechanism of reperfusion injury was investigated after the delivery of an experimental reperfusate. Using an isolated working heart preparation, rat hearts underwent 15 min of global ischemia at 37 degrees C. Following the ischemic insult, an oxygenated enriched reperfusion solution was given for 5 min. The hearts were then returned to a working state and aortic flow recorded to evaluate recovery. NADH levels were monitored throughout the experiment with a fluorometer and glycogen, AMP, ADP, and ATP were measured biochemically pre- and postischemia, after reperfusion and after recovery. In this study, reperfusion injury was best abated by an enriched reperfusate. Our results indicate the mechanism for this amelioration is not high-energy phosphate replenishment. Rather, as indicated by NADH fluorescence, the hearts attain an intermediate level of metabolism that permits glycogen to be restored and functional recovery to be improved.     

Skeletal Muscle Adaptations to Physical Training in Type II (Non-insulin-dependent) Diabetes Mellitus

Seven middle-aged men with manifest type II diabetes mellitus underwent an endurance training programme for 10–15 weeks. The maximal aerobic capacity, as well as the endurance capacity, was improved by 10% (p<0.05). The intramuscular glycogen store increased by more than 80% (p<0.05) from 350 μmol/g dw (dry weight), and the activities of citrate synthase and 3-hydroxy-acyl-CoA dehydrogenase increased by more than 50% (p<0.05) and 30% (p<0.05). The activity of glycogen synthase was decreased by approximately 20% (p<0.05), whereas lactate dehydrogenase remained unchanged. Capillaries/fibre and fibre area increased by more than 50% (p<0.05) and 30% (p<0.05) leaving the area of supply constant. Training did not influence fasting blood lipids and glucose, glycosylated hemoglobin, oral glucose tolerance, and insulin response to an oral glucose load measured 72 hours post-exercise. It is concluded that patients with manifest type II diabetes, as normoglycaemic individuals, adapt to physical training. However, no persistent effect on glucohomeostasis and lipaemia is produced by short-term training in the diabetic patients.     

ANGIOTENSIN CONVERTING ENZYME (ACE) INHIBITORS AND KININ METABOLISM: EVIDENCE THAT ACE INHIBITORS MAY INHIBIT A KININASE OTHER THAN ACE

1. Angiotensin converting enzyme (ACE) converts angiotensin I to angiotensin II, and also metabolizes bradykinin-(1–9) to bradykinin-(1–7) and bradykinin-(1–7) to bradykinin-(1–5). Increases in endogenous kinin levels may contribute to the therapeutic effects of ACE inhibitors. 2. ACE inhibitors increase vascular levels of both bradykinin-(1–9) and its ACE cleavage product bradykinin-(1–7), at doses below the threshold for ACE inhibition, leading to the proposal that ACE inhibitors may also inhibit a non-ACE kininase which cleaves both kinin peptides; this non-ACE kininase may be the major pathway of kinin metabolism in the vasculature and some other tissues. 3. In support of this proposal, ACE inhibitors potentiate bradykinin-(1–9) effects at doses which have little or no effect on ACE activity, as indicated by angiotensin I conversion to angiotensin II. ACE inhibitors also potentiate the actions of ACE-resistant kinin analogues, which may be susceptible to metabolism by a non-ACE kininase. 4. Identification and characterization of the putative non-ACE kininase which is inhibited by ACE inhibitors may reveal novel approaches to the tissue-specific modulation of kinin levels.     

Disposition of antipyrine in patients with extensive metastatic liver disease

Summary In the present study the effect of metastatic liver disease on hepatic drug metabolism has been examined by studying the pharmacokinetics of antipyrine and the urinary excretion of antipyrine and its three major metabolites (4-hydroxyantipyrine, norantipyrine, and 3-hydroxymethylantipyrine) in 12 patients with extensive metastatic liver disease, and in 12 matched healthy controls.In the patients total liver volume, the volume of the liver parenchyma, and the volume of the liver metastases were determined by computed tomography. The volume of liver metastases always exceeded 35% of the total liver volume.There were no significant differences between the patients and controls in plasma half-life, plasma clearance, or apparent volume of distribution of antipyrine.The cumulative urinary excretion of antipyrine and its three major metabolites was significantly lower in patients [44 (18)%] than in controls [71 (8)%]. The excretion of antipyrine itself was unchanged and the decrease in cumulative excretion was due to reduced excretion of the three metabolites.The results show that the activity of the hepatic mixed function oxidases was not impaired even in patients with extensive metastatic liver disease. This may be because liver metastases do not cause a corresponding reduction in the volume of normal hepatic parenchyma. The decreased urinary excretion of the three major metabolites of antipyrine, which are mainly glucuronidated, may have been due to an alteration in the process of conjugation.     

继发性骨质疏松防治的研究

目的总结继发性骨质疏松预防与治疗的经验及提出见解.方法用钙代谢平衡的方法研究了钙代谢的基本情况,比较了补钙与不补钙在若干种生理状态对骨密度的影响,总结继发性骨质疏松的病因及对其采取不同方法的治疗经验.结果中国人膳食含钙量属于正常范围低水平状态,与适宜摄入量(AI)比较是不足的,在一定的生理状态下应予补钙.缺钙是原发性骨质疏松与继发性骨质疏松的不利因素.氟中毒骨病、糖尿病、性腺功能减退、肿瘤、糖皮质激素过多和甲亢均有其各别的病理生理,导致继发性骨质疏松,防治方法各异.结论从胚胎至老年都应防治骨质疏松.不同情况采取方法各异,但有效.     

Scopolamine abolishes cerebral blood flow response to somatosensory stimulation in anesthetized cats: PET study

The effect of the cholinergic blocker, scopolamine on the cerebral blood flow (CBF) response to vibrotactile stimulation of a fore paw was studied using high-resolution positron emission tomography and H₂¹⁵O in 5 pentobarbital-anesthetized cats. Before scopolamine injection, the CBF response to the stimulation was found in the contralateral somatosensory cortex (mean ratio (contralateral/ipsilateral) control: stimulated1.02 ± 0.02: 1.17 ± 0.05; P < 0.01). After intravenous injection of scopolamine (0.35 mg/kg), the CBF response was abolished. However, the cerebral metabolic rate of glucose (CMRGlu) response to the same stimulation was unchanged after scopolamine injection in the same cats. We concluded that scopolamine abolishes the CBF response but not neuronal response to stimulation. We suggest that cholinergic mechanisms may play an important role for mediating CBF coupling to neuronal activity during physiological stimulation.     

维生素K4、维生素D2对绝经妇女骨折早期骨代谢的影响

为探讨不同剂量水平的维生素K4及维生素D对绝经妇女骨折早期骨代谢的影响。选择年龄60~84岁(72.17±1.216岁),绝经女性骨折病人35例,随机分为4组,分别给予不同剂量的维生素K4及维生素D口服,实验进行20天。通过观察患者服药前后血清钙、血清磷、血清碱性磷酸酶、血清凝血酶原时间及血清骨钙素值的变化,综合评价维生素K、维生素D对老年妇女骨折早期骨代谢的影响。结果显示,不同剂量水平维生素K4、维生素D对绝经妇女骨折早期骨代谢的影响不同,有统计学意义。维生素K4对骨代谢的影响作用超过维生素D,并随剂量水平不同而差异有显著性。但维生素K4、维生素D对骨代谢的影响无交互作用。表明维生素D、维生素K4能促进骨折早期骨代谢,对骨折愈合有一定促进作用,且维生素K的作用强于维生素D。     

Anthracycline-induced cardiotoxicity: Overview of studies examining the roles of oxidative stress and free cellular iron

The risk of cardiotoxicity is the most serious drawback to the clinical usefulness of anthracycline antineoplastic antibiotics, which include doxorubicin (adriamycin), daunorubicin or epirubicin. Nevertheless, these compounds remain among the most widely used anticancer drugs. The molecular pathogenesis of anthracycline cardiotoxicity remains highly controversial, although the oxidative stress-based hypothesis involving intramyocardial production of reactive oxygen species (ROS) has gained the widest acceptance. Anthracyclines may promote the formation of ROS through redox cycling of their aglycones as well as their anthracycline-iron complexes. This proposed mechanism has become particularly popular in light of the high cardioprotective efficacy of dexrazoxane (ICRF-187). The mechanism of action of this drug has been attributed to its hydrolytic transformation into the iron-chelating metabolite ADR-925, which may act by displacing iron from anthracycline-iron complexes or by chelating free or loosely bound cellular iron, thus preventing site-specific iron-catalyzed ROS damage. However, during the last decade, calls for the critical reassessment of this “ROS and iron” hypothesis have emerged. Numerous antioxidants, although efficient in cellular or acute animal experiments, have failed to alleviate anthracycline cardiotoxicity in clinically relevant chronic animal models or clinical trials. In addition, studies with chelators that are stronger and more selective for iron than ADR-925 have also yielded negative or, at best, mixed outcomes. Hence, several lines of evidence suggest that mechanisms other than the traditionally emphasized “ROS and iron” hypothesis are involved in anthracycline-induced cardiotoxicity and that these alternative mechanisms may be better bases for designing approaches to achieve efficient and safe cardioprotection.     

Effects of complete heart block on myocardial function, morphology, and energy metabolism in the rat.

AIMS: Severe sustained bradycardia may cause acute and possibly chronic congestive heart failure (CHF). The aim of this study was to investigate acute and chronic effects of complete heart block (CHB) on cardiac function, morphology, and creatine (Cr) metabolism. METHODS AND RESULTS: CHB was induced in male Sprague-Dawley rats (approximately 250 g, n = 11) by means of electrocautery applied to the region of AV node and were compared with controls (n = 15). The rats were investigated at 1, 3, and 12 weeks after CHB induction with transthoracic echocardiography. Invasive haemodynamic assessment of left and right ventricular pressures was performed at 12 weeks. After the sacrifice, the hearts were freeze-clamped for analysis of myocardial Cr, and high energy phosphometabolites. The efficacy of operative procedure was 54%. The peri-operative mortality rate was 20%. Heart rate (HR) decreased by approximately 50% (P < 0.01) while stroke volume (SV) increased 2.5 times (P < 0.01) in the CHB rats. Cardiac index remained unchanged. The rats with CHB grew normally and were in no apparent distress. Filling pressures in left and right ventricles were normal. The CHB rats developed marked cardiomegaly with biventricular dilatation and eccentric left ventricular hypertrophy (P < 0.01). There was no change in the myocardial content of Cr and high energy phosphometabolites. CONCLUSION: Rats with CHB are compensating for reduction in HR with increased SV without haemodynamic and biochemical characteristics of CHF. This model may be useful to study the effects of CHB and bradycardia on myocardial structure, function, electrophysiology, and metabolism as well as for studies of cell therapy for reparation of AV conductance.