Effect of dipyridamole on myocardial adenosine metabolism and coronary flow in hypoxia and reactive hyperemia in the isolated perfused guinea pig heart.

The effect of dipyridamole on adenosine metabolism and coronary flow in the hypoxic intact myocardium was studied in normal and hypertrophied isolated perfused guinea pig hearts. The presence of dipyridamole in the normal guinea pig heart resulted in a significant increase in the level of tissue adenosine (67%) with a concomitant increase in coronary flow (85%) and a decrease in the rate of adenosine release (18%) from the myocardium during perfusion with normoxic and hypoxic solutions. Directional changes in hypertrophied hearts were the same as for normal hearts. Tissue levels of adenosine in normal dipyridamole-treated hearts during normoxic perfusion were significantly increased above those of untreated hearts at the peak of reactive hyperemia (× 1.5), after 30 s of aortic occlusion (× 2.3) and during steady state flow (× 2.0). Furthermore, the presence of dipyridamole in normal hearts during reactive hyperemia, produced by 30 s of aortic occlusion, increased the volume and duration of coronary flow by 44% and 75%, respectively. These findings are in accord with the hypothesis that adenosine is a mediator of coronary flow and that dipyridamole potentiates the vasodilator effect of endogenous as well as exogenous adenosine.     

Effect of adenosine on the relaxation of coronary arteries at varying pH values

Summary The efficiency of adenosine to relax the bovine coronary arterial strips increased significantly by lowering the bath pH from 7.4 to 6.8 (CO₂ or HCO ₃ ^– ). The large vessels (3–4 mm O.D.) relaxed with greater significance at higher concentrations of adenosine, whereas small vessels (0.5–0.7 mm O.D.) relaxed better at low concentrations of adenosine. Theophylline and 8-phenyltheophylline competitively inhibited the effect of adenosine. 8-phenyltheophylline was found to be a better antagonist than theophylline. Furthermore, binding assays with 2-³H adenosine displayed a single species of binding sites. The K_d was 3×10^–6 M and 4×10^–6 M, while B_max was 48 and 19 pmoles/mg protein for small and large vessels, respectively. The antagonistic effect of theophylline and 8-phenyltheophylline was not affected by pH variations. It is concluded that relaxation of coronary arteries by adenosine is affected by pH variations.This work was supported by HL27339     

The effect of adenosine on myocardial metabolism and oxygen consumption in the isolated dog heart preparation

The effects of adenosine on myocardial metabolism and oxygen consumption were examined in the isolated supported dog heart preparation (ISHP) perfused at a constant coronary blood flow. Heart rate was controlled by right atrial pacing. Coronary arterial and venous blood samples were collected and oxygen content, lactate, glucose and free fatty acid levels were determined. From arterialvenous differences and coronary blood flow, oxygen consumption and substrate uptake were determined. A 3 min intracoronary infusion of adenosine (50 and 100 μg/min) produced a significant dose-dependent decrease in MV?O₂ while increasing glucose uptake and decreasing the uptake of lactate. The decrease in oxygen consumption, the increase in glucose uptake and the decrease in the uptake of lactate were all found to be dependent on the initial MV?O₂. These findings suggest that, in addition to its putative role as a regulator of coronary vascular resistance, adenosine might also exert important metabolic effects on the heart.     

Relationship between coronary flow and adenosine release during severe and mild hypoxia in the isolated perfused rat heart with special reference to time-course change

Summary The contribution of endogenous adenosine to coronary vasodilation induced by global myocardial hypoxia was examined. In isolated rat hearts perfused by means of Langendorff's technique, the relationship between chronological changes in coronary flow and adenosine release during hypoxia was analyzed. The oxygenation level of myoglobin (MbO₂), myocardial oxygen uptake, lactate release, and left ventricular pressure (LVP) was also measured. Adenosine was determined by radio-immunoassay, and the MbO₂ levels by the optical method. Severe hypoxia (20% O₂+75% N₂+5% CO₂) increased coronary flow, adenosine release, and lactate release and decreased both myocardial oxygen uptake and LVP. Mild hypoxia (50% O₂+45%N₂+5%CO₂) also increased coronary flow, adenosine release, and lactate release, while it affected neither myocardial oxygen uptake nor LVP. These results suggest that the oxygen supply is compensated by an increase in coronary flow in mild hypoxia, whereas this does not occur in severe hypoxia. Changes in MbO₂ were the reverse of those in coronary flow during severe hypoxia, confirming that a decrease in intracellular oxygen correlates well with an increase in coronary flow. The pattern of changes in adenosine release, however, was not identical with that in coronary flow in severe and mild hypoxia, indicating that there is no significant relationship between coronary flow and adenosine release in either severe or mild hypoxic hearts. These findings suggest that adenosine is not the only metabolic mediator of regulation of coronary flow in hypoxic hearts.     

Transmural inhomogeneity of extracellular [K+] and pH and myocardial energy metabolism in the isolated rat heart during acute global ischemia; dependence on gaseous environment

We investigated in the isolated rat heart the influence of the gas surrounding the globally ischemic heart on transmural inhomogeneity of energy metabolism, extracellular K+ accumulation, and change of extracellular pH. Hearts were made ischemic in 100% N2 (N2-ischemia), 100% O2 (O2-ischemia) or 100% CO2 (CO2-ischemia). We measured: 1) Midmural, subepicardial, and epicardial changes of extracellular [K+] and pH during successive 6-min periods of global ischemia, and 2) content of creatinephosphate (CrP) in consecutive tissue sections of 100 microns, from the subepicardium after 10 min of ischemia. A) During O2-ischemia both extracellular [K+] and change of pH in the subepicardium are significantly less than in the midmyocardium. During N2-ischemia only minor differences exist in [K+] and pH between the subepicardium and the midmyocardium. During CO2-ischemia midmural and subepicardial [K+] are similar to those during N2-ischemia. The midmural change of pH resembles that during N2-ischemia; subepicardial change of pH, however, was slightly larger. Midmural changes in [K+] and pH were not influenced by the nature of the surrounding gas. B) After 10 min of O2-ischemia a gradient of tissue content of CrP extends from the epicardium (CrP about 30 mumoles/g dry weight) to a distance of about 1000 microns (CrP 1 mumoles/g dry weight). In N2- and CO2-ischemia a CrP gradient is absent; CrP is appreciably less than 1 mumoles/g dry weight at any distances from the epicardium. C) We conclude that diffusion of O2 into the myocardium and of CO2 from the myocardium affects transmural gradients of [K+], pH, and energy metabolism during ischemia. Local availability of O2 increases the capacity of the ischemic tissue to generate high energy phosphates and mitigates ischemia-induced changes of transsarcolemmal ion gradients.     

Effects of continuous positive airway pressure on endothelial function and circulating progenitor cells in obstructive sleep apnoea: A randomised sham-controlled study

Objective

Obstructive sleep apnoea (OSA) is characterised by reoccurring apnoeas and hypopneas, causing repetitive hypoxia and reoxygenation, and is associated with endothelial dysfunction and reduced levels of circulating progenitor cells (CPCs). The potential to improve endothelial function and CPC levels in people with OSA by preventing hypoxic episodes with Continuous Positive Airway Pressure (CPAP) was investigated in a sham-controlled CPAP study.

Methods

Men with moderate-to-severe OSA (mean ± SD: age = 49 ± 12 y, apnoea hypopnea index (AHI) = 37.6 ± 16.4 events/h, body mass index = 31.5 ± 5.7 kg/m²) who were CPAP naïve without diabetes mellitus were randomised in a 12-week double-blind sham-controlled parallel group study to receive either active (n = 25) or sham (n = 21) CPAP. CPCs, isolated from blood, were measured by flow cytometry and by co-staining cultured cells (7 days) with acetylated low-density lipoprotein (acLDL) and lectin. Endothelial function was assessed by peripheral arterial tonometry (PAT).

Results

Compared to sham, CPAP significantly decreased AHI (mean between-group difference − 36.0 events/h; 95%CI, − 49.7 to − 22.3, p < 0.0001) after 12 weeks. Despite this improvement in AHI, CPAP had no effect on change in CPC levels (including CD34⁺/KDR⁺ (565 cells/mL; − 977 to 2106, p = 0.45), CD34⁺/KDR⁺/CD45⁻ (37.0 cells/mL; − 17.7 to 85.7, p = 0.13), acLDL⁺/lectin⁺ (− 43.1 cells/field, − 247 to 161, p = 0.67)) or change in endothelial function (0.27; − 0.14 to 0.67, p = 0.19) compared to sham therapy.

Conclusions

Despite the improvement in OSA parameters and ablation of apnoeic events by CPAP, CPC counts and endothelial function in men with moderate-to-severe OSA were not significantly improved after 12 weeks of therapeutic CPAP when compared to sham control.     

pH值对呼吸道分离肺炎克雷伯菌抗药性及生物膜形成能力的影响

目的探讨pH值对呼吸道分离肺炎克雷伯菌的抗药性及生物膜形成能力的影响,为临床抗感染治疗提供理论依据。方法在第三军医大学西南医院呼吸科住院患者的痰液标本中分离12株肺炎克雷伯菌(K1-K12)。在不同pH值(5.5、6.5和7.5)条件下微量肉汤稀释法检测肺炎克雷伯菌的最低抑菌浓度(MIC);菌落计数法检测细菌黏附能力;96孔板结晶紫染色法测定细菌的生物膜形成能力。采用SPSS 17.0软件进行数据分析。计量资料以均数±标准差(±s)表示,组间比较采用t检验。结果头孢他啶对肺炎克雷伯菌的MIC随着pH值降低而降低;左氧氟沙星对肺炎克雷伯菌的MIC随着pH值降低而增加;庆大霉素对肺炎克雷伯菌的MIC与pH变化没有相关性。与pH 5.5相比,pH 6.5条件下大部分细菌的黏附性和生物膜形成能力显著增高(P0.05),而pH 7.5条件下所有细菌的黏附性和生物膜形成能力均显著增高(P0.05)。结论不同pH值环境可以改变肺炎克雷伯菌药物敏感性和生物膜形成能力。     

Insulin receptors on isolated heart cells: Effect of temperature and hydrolytic enzymes

Summary Isolated muscle cells from adult rat heart have been used to study the effect of temperature and enzymic digestion on the binding of¹²⁵I-labelled insulin. Equilibrium binding studies were performed at both 4 and 37°C, using insulin concentrations ranging from 2.5×10^–11 mol/l to 10^–6 mol/l. The empty site affinity constant decreased by 51% from 1.0×10⁸ l/mol at 4°C to 4.9×10⁷ l/mol at 37°C, whereas the total receptor concentration remained unaltered at both temperatures. The rate of dilution induced dissociation was enhanced by the presence of native insulin at 37°C, confirming the presence of negative cooperativity among the receptor sites at physiological temperatures.Treatment of isolated heart cells with trypsin and -galactosidase led to a decrease in specific binding of¹²⁵I-labelled insulin. Myocytes treated with neuraminidase exhibited a significant increase in insulin binding, which was shown to be due to an increase in insulin-receptor affinity.These studies provide new information on the molecular characteristics of insulin receptors in the heart muscle.

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Zusammenfassung Isolierte Herzmuskelzellen von adulten Ratten wurden benutzt, um den Einfluß von Temperatur und enzymatischer Andauung auf die Bindung von¹²⁵I-markiertem Insulin zu untersuchen. Âquilibriums-Bindungsstudien wurden bei 4 und 37°C mit Insulinkonzentrationen im Bereich von 2,5×10^–11 mol/l bis 10^–6 mol/l durchgeführt. Die empty site-Affinitätskonstante verringerte sich um 51% von 1,0×10⁸ l/mol bei 4°C auf 4,9×10⁷ l/mol bei 37°C, während die Gesamtkonzentration der Rezeptoren bei beiden Temperaturen unverändert blieb. Die Geschwindigkeit der Verdünnungs-induzierten Dissoziation vergrößerte sich in Gegenwart von nativem Insulin bei 37°C, was das Vorhandensein von negativer Kooperativität zwischen den Rezeptorstellen bei physiologischen Temperaturen bestätigt.Die Behandlung von isolierten Herzzellen mit Trypsin und -Galactosidase führte zu einer Verringerung der spezifischen Bindung von¹²⁵I-markiertem Insulin. Myozyten, die mit Neuraminidase behandelt wurden, zeigten eine signifikante Erhöhung der Insulinbindung, was auf einer Erhöhung der Affinität des Insulinrezeptors beruhte.Diese Untersuchungen liefern neue Informationen zur molekularen Charakteristik der Insulinrezeptoren im Herzmuskel.

     

Effect of adenosine and adenosine analogs on [14C]aminopyrine accumulation by rabbit parietal cells

Adenosine receptors that modulate adenylate cyclase activity have been identified recently in a number of tissues. Adenosine A₂ receptor is stimulatory to adenylate cyclase, whereas adenosine A₁ receptor is inhibitory to adenylate cyclase. We investigated the effect of adenosine and its analogs on [¹⁴C]aminopyrine accumulation by rabbit parietal cells. Rabbit gastric mucosal cells were isolated by enzyme digestion. Parietal cells were enriched by nonlinear percoll gradients. [¹⁴C]Aminopyrine accumulation was used as an indicator of acid secretion. The effect of 2-chloroadenosine on histamine-stimulated [¹⁴C]aminopyrine accumulation was studied. The effects ofN-ethylcarboxamideadenosine, 2-chloroadenosine, stable analogs of adenosine, and adenosine on [¹⁴C]aminopyrine accumulation were assessed. Cyclic AMP content of parietal cells was determined by radioimmunoassay. Histamine and carbachol, known secretagogues, stimulated [¹⁴C]aminopyrine accumulation. 2-Chloroadenosine did not suppress histaminestimulated [¹⁴C]aminopyrine accumulation. 2-Chloroadenosine,N-ethylcarboxamideadenosine, and adenosine dose dependently increased [¹⁴C]aminopyrine accumulation. The order of potency wasN-ethylcarboxamideadenosine > 2-chloroadenosine > adenosine. 8-Phenyltheophylline and theophylline, adenosine-receptor antagonists, or cimetidine did not have significant effects on the increase of AP uptake induced by 2-chloroadenosine. Coadministration of dipyridamole, an adenosine uptake inhibitor, augmented the effect of adenosine on [¹⁴C]aminopyrine accumulation. 2-Chloroadenosine,N-ethylcarboxamideadenosine, and adenosine each induced a significant increase in cellular cyclic AMP. We conclude that there may be adenosine A₂ receptors on rabbit parietal cells which modulate gastric acid secretion.     

Blockade of histamine H2 receptors protects the heart against ischemia and reperfusion injury in dogs

We have previously reported that histamine H(2) blockers may be cardioprotective in patients with chronic heart failure. Since both endogenous histamine and histamine H(2) receptors are present in heart tissue, we tested the hypothesis that the blockade of histamine H(2) receptors mediates protection against reversible or irreversible ischemia and reperfusion injury. In open-chest dogs, the left anterior descending coronary artery was occluded for 90 minutes, followed by reperfusion for 6 hours. Administration of famotidine and cimetidine from 10 minutes before occlusion until after 1 hour of reperfusion reduced infarct size (17.0 +/- 4.1% and 17.8 +/- 2.9% vs. 36.9 +/- 5.9% of the solvent group, respectively) Famotidine administration only during the reperfusion period for 1 hour also attenuated infarct size (22.5 +/- 3.5%). There were no differences in either area at risk or collateral flow among the groups. In another set of experiments, we decreased coronary perfusion pressure in dogs so that the coronary blood flow decreased to 50% of the non-ischemic level. In such conditions, we observed the increases in histamine release compared with non-ischemic conditions (0.04 +/- 0.03 to 0.28 +/- 0.13 ng/ml, p < 0.05). Famotidine improved anaerobic myocardial metabolism gauged by both lactate extraction ratio and myocardial oxygen consumption. We conclude that the blockade of histamine H(2) receptors mediates improvements in the anaerobic myocardial metabolism, and thus protects against ischemia and reperfusion injury.     

冠脉慢性闭塞病变再通对心脏功能的影响

目的:评价冠脉慢性闭塞病变再通对患者心功能的影响。方法:对冠脉造影证实的冠脉≥1支慢性闭塞的35例患者,采用冠脉介入治疗(PCI:PTCA加支架植入术)或冠脉旁路移植术(CABG),使再血管化,比较治疗前和治疗后3～6个月患者的临床心功能状态和左室射血分数(LVEF)的改变。结果:22例患者行PCI治疗,13例患者行CABG。平均随访4.2个月。治疗后临床心功能状态改善2级以上者27例(77.1％),改善1级者6例(17.1％),无改善者2例(5.8％),总有效率94.2％。LVEF较术前显著改善(术前51.6％±5.8％,术后62.2％±11.3％,P<0.01)。结论:PCI和CABG开通慢性闭塞冠脉能够改善患者的心功能和LVEF。     

Effects of deferoxamine on H2O2-induced oxidative stress in isolated rat heart

During myocardial reperfusion injury, iron has been implicated in the Fenton based generation of hydroxyl radical, ·OH, leading to further organ injury. Although previous studies have investigated the protective effect of iron chelators including deferoxamine (DFX) in myocardial reperfusion injury, there is little information regarding the role of iron chelation during oxidative stress produced by H₂O₂ on the heart. Isolated hearts from male Sprague-Dawley rats were retrograde-perfused with Krebs-Henseleit solution at 5 ml/min. After a 60-min equilibration, oxyradical challenge was instituted by the addition of H₂O₂ (200–600 M) to the perfusate for 60 min. A subgroup of animals received DFX (400 M) in the perfusate prior to challenge with 400 M H₂O₂. Contractility was continuously monitored; perfusate samples for glutathione (GSH) and lactate dehydrogenase (LDH) estimations were collected at 30-min intervals. Headspace ethane, an indicator of lipid peroxidation, was estimated at 30-min intervals by gas chromatography. Control hearts maintained contractility during the perfusion period. H₂O₂ perfusion caused a dose dependent decrease in myocardial contractility; DFX pretreatment was partialy protective. Headspace ethane slowly accumulated in control hearts; perfusion with H₂O₂ caused dose dependent increase in ethane accumulation indicative of enhanced lipid peroxidation. GSH and LDH in the perfusate remained low in control hearts. In contrast, H₂O₂ treated hearts had a dose dependent inclease in the efflux of GSH and LDH which was markedly increased by perfusion with 600 M H₂O₂. Pretreatment with DFX did not significantly reduce GSH or LDH efflux from hearts perfused with peroxide. While H₂O₂ perfused with peroxide. While H₂O₂ perfusion causes a dose dependent decrease in myocardial contractility with a corresponding increase in headspace ethane release with GSH & LDH efflux indicative of oxidative stress, concurrent treatment with DFX reduces myocardial dysfunction and ethane generation. However, sublethal damage of plasma membrane still continues as reflected by continuous enhancement of LDH efflux, possibly indicating involvement of other reactive species besides hydroxyl radical.     

腺病毒转染的肝细胞生长因子对冠心病患者外周造血干细胞的动员作用

目的 探讨经冠状动脉内注射腺病毒（adenovirus,Ad,）转染人肝细胞生长因子（HGF）对严重冠状动脉狭窄患者外周造血干细胞的动员作用。方法 本研究人选18例冠心病患者,分为两组：给药组9例,经冠状动脉注入Ad5-HGF;对照组9例,经冠状动脉注入同等量的生理盐水。所有患者均于冠状动脉造影术前、术后6h、24h及6天抽取外周血,并应用流式细胞仪单克隆荧光抗体标记法检测其外周造血干细胞表面抗原CD34^＋、CD38^＋及CD117^＋。结果 给药组术后6h的CD34^＋明显高于对照组（0,104±0．082比0．022±0．012,P=0．021）,0h、24h及6天的CD34^＋两组之间差异无统计学意义;给药组术后6天的CD117^＋明显高于对照组（0．058±0．058比0．012±0．009,P=0,034）,差异有统计学意义,其余时间点两组间差异均无统计学意义;CD38^＋在各时间点两组间差异均无统计学意义。结论 经冠状动脉内注射转染A5-HGF可能在短时间内引起外周造血干细胞的动员。动员外周造血干细胞可能是HGF参与血管新生和器官组织损伤修复及抗凋亡、改善心功能的一个重要机制。     

养心生脉颗粒辅助治疗老年冠心病并发慢性心力衰竭效果观察

目的观察养心生脉颗粒辅助治疗老年冠心病(CHD)并发慢性心力衰竭(CHF)的临床效果。 方法将2017年1月至2018年6月郏县第二人民医院收治的92例老年CHD并发CHF患者纳入研究,采用随机数表法将其分为A组和B组,各46例。A组患者接受常规治疗,B组患者加服养心生脉颗粒。对比两组患者治疗前后LVEDD、LVESD、LVESV、LVEF等心功能指标,统计两组患者治疗总有效率和不良反应发生率。 结果治疗后B组患者LVEDD、LVESD、LVESV水平低于A组,LVEF水平高于A组,组间差异有统计学意义(P<0.05);B组治疗总有效率(93.48%)高于A组(80.43%),组间差异有统计学意义(P<0.05);两组患者治疗期间均未出现明显不良反应。 结论养心生脉颗粒辅助治疗老年CHD并发CHF临床效果较好,可有效改善患者心功能,且不会增加用药风险,具有较高的临床推广价值。     

Effect of solanine on the membrane potential of mitochondria in HepG2 cells and [Ca^2＋]i in the cells

AIM: To observe the effect of solanine on the membrane potential of mitochondria in HepG2 cells and [Ca2 ]i in the cells, and to uncover the mechanism by which solanine induces apoptosis. METHODS: HepG2 cells were double stained with AO/EB, and morphological changes of the cells were observed using laser confocal scanning microscopy (LCSM). HepG2 cells were stained with TMRE, and change in the membrane potential of mitochondria in the cells were observed using LCSM. HepG2 cells were double stained with Fluo-3/AM, and change of [Ca2 ]i in the cells were observed using LCSM. HepG2 cells were double stained with TMRE and Fluo-3/AM, and both the change in membrane potential of mitochondria and that of [Ca2 ]i in the cells were observed using LCSM. RESULTS: Cells in treated groups showed typical signs of apoptosis. Staining with TMRE showed that solanine could lower membrane potential; staining with Fluo-3/AM showed that solanine could increase the concentration of Ca2 in tumor cells; and those of double staining with TMRE and Fluo-3/AM showed that solanine could increase the concentration of Ca2 in the cells at the same time as it lowered the membrane potential of mitochondria. CONCLUSION: Solanine opens up the PT channels in the membrane by lowering the membrane potential, leading to Ca2 being transported down its concentration gradient, which in turn leads to the rise of the concentration of Ca2 in the cell, turning on the mechanism for apoptosis.     

The role of carbon dioxide and the influence of pH on the insulin stimulated glucose metabolism of isolated cells from rat adipose tissue

Summary The role of CO₂ and the influence of pH on the insulin-stimulated glucose metabolism of cell suspensions from rat adipose tissue were investigated in a Trisbuffered system. CO₂ was assimilated in presence of glucose, fructose or pyruvate in the medium. The fixed CO₂ is mainly localized in the C-1 position of lactate. Insulin enhances the turnover rates only when cells are incubated in glucose-containing medium. The influence of the extracellular CO₂ concentration on CO₂ fixation, on glucose oxidation, and on the transfer of glucose-6-¹⁴C to lipid compounds follows saturation kinetics. The same metabolic reactions show a defined maximum at an extracellular pH of 7.5. On both sides of the pH-peak the turnover rates decrease very rapidly.

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Die Rolle von Kohlendioxid und der Einfluß des pH auf den durch Insulin stimulierten Glucosestoffwechsel isolierter Fettzellen von Ratten

Zusammenfassung In einem mit Tris gepufferten System wurden die Rolle des CO₂ und der Einfluß des pH auf den insulinstimulierten Glucosemetabolismus von Zellsuspensionen des Rattenfettgewebes untersucht. CO₂ wird bei Anwesenheit von Fructose, Glucose oder Pyruvat im Medium assimiliert. Das fixierte CO₂ ist hauptsächlich in der C-1-Position der Milchsäure lokalisiert. Insulin erhöht die Umsatzraten nur bei der Inkubation in einem glucosehaltigen Medium. Der Einfluß der extracellulären CO₂-Konzentration auf die CO₂-Fixierung, auf die Glucoseoxidation und auf den Übergang von 6-¹⁴C-Glucose in die Verbindungen der Lipidfraktion läßt sich durch Substratsättigungskurven beschreiben. Die gleichen Stoffwechselreaktionen zeigen ein ausgeprägtes pH-Maximum bei pH 7.5. Beiderseits der Gipfelpunkte fallen die Kurven steil ab.

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Le rôle de l'anhydride carbonique et l'influence du pH sur le métabolisme du glucose stimulé par l'insuline, des cellules isolées du tissu adipeux de rat

Résumé Les auteurs ont étudié le rôle du CO₂ et l'influence du pH sur le métabolisme du glucose stimulé par l'insuline, de suspensions de cellules du tissu adipeux de rat, dans un système tampon Tris. Le CO₂ était assimilé en présence de glucose, de fructose ou de pyruvate dans le milieu. Le CO₂ fixé est localisé principalement dans la position C-1 du lactate. L'insuline augmente les vitesses de renouvellement seulement lorsque les cellules sont incubées dans un milieu contenant du glucose. L'influence de la concentration extracellulaire en CO₂ sur la fixation du CO₂, sur l'oxydation du glucose et sur la transformation du glucose-6-¹⁴C en composés lipidiques suit des cinétiques de saturation. Les mêmes réactions métaboliques montrent un maximum caractérisé à un pH extracellulaire de 7.5. Des deux côtés du pH maximum, les vitesses de renouvellement décroissent très rapidement.

     

他汀类药物对不同类型冠心病患者外周血中内皮祖细胞数量的影响

目的：研究他汀类药物对不同类型冠心病患者外周血中内皮祖细胞（EPCs）数量的影响。方法：选择127例冠心病患者,分为急性心肌梗死（AMI）介入治疗组（A组,45例）,AMI保守治疗组（B组,29例）,不稳定型心绞痛组（C组,31例）,稳定型心绞痛组（D组,22例）,入院后均给予阿托伐他汀治疗;同时选择30例非冠心病患者作为非冠心病对照组,不给予阿托伐他汀治疗。上述所有患者在入院即刻、14d、30d采血,检测患者外周血中CD133标记的EPCs数量。结果：冠心病各组及非冠心病对照组患者外周血中均有EPCs（CD133）的表达,与入院即刻相比,冠心病各组患者服用阿托伐他汀后EPCs（CD133）的表达在14d和30d后明显上升[A组：（0.015±0.016）%比（0.411±0.361）%比（0.472±0.384）%,B组：（0.009±0.010）%比（0.250±0.031）%比（0.413±0.035）%,C组：（0.421±0.814）%比（1.065±2.014）%比（1.325±2.321）%,D组：（1.387±0.021）%比（2.153±0.167）%比（3.052±0.086）%],P均〈0.05;非冠心病对照组患者EPCs（CD133）的表达在14d和30d后无明显变化（P〉0.05）。结论：他汀类药物能增加冠心病患者外周血内皮祖细胞数量。