炮制对黄芩抗氧化作用的影响

目的　研究炮制对黄芩中黄芩苷的含量和抗氧化作用的影响。方法　高效液相色谱法测定黄芩苷含量 ,并采用体外氧自由基和羟自由基生成系统 ,评价其抗氧化作用。结果　炒制和酒制略有降低黄芩中黄芩苷的含量 ,炒炭显著地降低了黄芩苷含量。炒黄芩、酒黄芩并不影响清除次黄嘌呤 黄嘌呤氧化系统中产生的超氧阴离子 (O·-2 )的能力 ,而显著地降低清除Fen ton反应生成的羟自由基 (·OH)能力。炭黄芩作用更弱。结论　黄芩炮制品中黄芩苷含量和抗氧化作用存在一定的差异性。     

肾炎灵颗粒剂对慢性原发性肾小球疾病氧自由基代谢的影响

目的 :探讨肾炎灵颗粒剂治疗慢性肾炎、难治性肾病综合征的作用机理。方法 :以肾炎灵颗粒剂治疗慢性肾炎和难治性肾病综合征 ,检测治疗前后患者的过氧化脂质 (LPO)、血浆和红细胞的超氧阴离子和SOD活性。结果 :肾炎灵颗粒剂能明显降低患者的过氧化脂质 (LPO)、血浆和红细胞的超氧阴离子 ,提高SOD活性。结论 :肾炎灵颗粒剂调整慢性肾炎、难治性肾病综合征患者的氧自由基代谢 ,可能是其临床疗效作用机理的一个组成部分。     

心可舒对心肌顿抑的保护作用及机制研究

探讨心可舒对心肌顿抑的保护作用及其机制。 18只家兔随机分为假手术组 (SH组 )、缺血 /顿抑组 (IS组 )和心可舒处理组 (XKS组 )。开胸结扎兔左冠状动脉前降支 2 0min ,然后松扎 6h。动态观察心可舒对ECG及心功能的影响 ,同时测定血清及心肌组织中SOD活性和MDA的含量及心肌组织中ATP的含量。结果 ,与IS组比较 ,心肌缺血再灌注后 ,XKS组左室内压力上升和下降速率及左室内压峰值明显增高 (P <0 0 1) ,血清及心肌组织中SOD活性升高 (P <0 0 1) ,MDA含量降低 (P <0 0 1) ,心肌组织中ATP含量明显增高 (P <0 0 1)。心可舒可改善左室收缩和舒张功能 ,改善心肌能量代谢 ,清除氧自由基 ,对心肌顿抑有良好的保护作用     

Superoxide dismutase ameliorates impaired nitric oxide synthase-dependent dilatation of the basilar artery during chronic alcohol consumption

The goals of this study were to determine whether chronic alcohol consumption impairs nitric oxide synthase-dependent reactivity of the basilar artery and to determine a potential mechanism which might account for the effects of alcohol on the basilar artery. Sprague-Dawley rats were fed liquid diets with or without alcohol for 8 weeks. Using intravital microscopy, we measured the diameter of basilar artery in response to nitric oxide synthase-dependent agonists (acetylcholine and bradykinin) and a nitric oxide synthase-independent agonist (nitroglycerin). Topical application of acetylcholine (0.1 and 1 microM) and bradykinin (1 and 10 nM) produced dose-related dilatation of the basilar artery in non-alcohol-fed and alcohol-fed rats. However, the magnitude of vasodilatation in response to acetylcholine and bradykinin was significantly less in alcohol-fed rats compared to non-alcohol-fed rats. Dilatation of the basilar artery in response to nitroglycerin was similar in non-alcohol-fed and alcohol-fed rats. Next, we examined whether impaired responses of the basilar artery in alcohol-fed rats in response to acetylcholine and bradykinin may be related to the production of oxygen radicals. We found that topical application of superoxide dismutase (150 U/ml) significantly improved impaired receptor-mediated nitric oxide synthase-dependent dilatation of basilar artery in alcohol-fed rats. However, superoxide dismutase did not alter responses of the basilar artery to nitroglycerin in alcohol-fed rats, and did not alter responses of the basilar artery to nitric oxide synthase-dependent or -independent agonists in non-alcohol-fed rats. Our findings suggest that chronic consumption of alcohol impairs nitric oxide synthase-dependent dilatation of a large cerebral artery which may be related to the receptor-mediated release of oxygen radicals to inactivate nitric oxide.     

Response dynamics of entorhinal cortex in awake, anesthetized, and bulbotomized rats

The steady-state rate of glucose oxidation through the mitochondrial TCA cycle (V(TCA)) was measured in acid extracts of 10- and 30-day-old cerebral cortex of rats receiving [1-13C]glucose intravenously and in neocortical slices superfused in vitro with the same isotope. TCA cycle flux was determined for each age group based on metabolic modeling analysis of the isotopic turnover of cortical glutamate and lactate. The sensitivity of the calculated rates to assumed parameters in the model were also assessed. Between 10 and 30 postnatal days, V(TCA) increased by 4.3-fold (from 0.46 to 2.0 micromol g(-1) min(-1)) in the cortex in vivo, whereas only a 2-fold (from 0.17 to 0.34 micromol g(-1) min(-1)) increase was observed in neocortical slices. The much greater increase in glucose oxidative metabolism of the cortex measured in vivo over that measured in vitro as the cortex matures suggests that function-related energy demands increase during development, a process that is deficient in the slice as a result of deafferentiation and other mechanisms.     

Vasopressin induced cyclooxygenase dependent superoxide generation contributes to K(+) channel function impairment after brain injury

This study determined if vasopressin generates superoxide anion (O⁻₂) in a cyclooxygenase dependent manner and if such production contributes to impairment of dilation to activators of ATP sensitive K⁺ (K_ATP) and calcium sensitive K⁺ (K_ca) channels following fluid percussion brain injury (FPI) in newborn pigs equipped with closed cranial windows. Superoxide dismutase (SOD) inhibitable nitroblue tetrazolium (NBT) reduction was determined as an index of O⁻₂ generation. Under non-brain injury conditions, topical vasopressin (40 pg/ml, the concentration present in CSF following FPI) increased SOD inhibitable NBT reduction from 1±1 to 25±4 pmol/mm². Indomethacin, a cyclooxygenase inhibitor, blunted such NBT reduction (1±1 to 5±1 pmol/mm²), while the vasopressin antagonist, l-(β-mercapto-β β-cyclopentamethylene propionic acid) 2-(o-methyl)-Tyr-AVP (MEAVP) blocked NBT reduction. MEAVP and indomethacin also blunted the NBT reduction observed after FPI. Under non-brain injury conditions, vasopressin (40 pg/ml) coadministered with the K_ATP and K_ca channel agonists, cromakalim and NS1619 (10⁻⁸, 10⁻⁶ M) diminished dilation to these K⁺ channel agonists while indomethacin partially prevented such impairment (13±1 and 23±1 vs. 4±1 and 10±2 vs. 8±1 and 19±1% for cromakalim in untreated, vasopressin, and vasopressin plus indomethacin treated piglets, respectively). Cromakalim and NS1619 induced pial artery dilation was attenuated following FPI, while indomethacin or MEAVP preadministration partially prevented such impairment (13±1 and 23±1, sham control; 1±1 and 4±1, FPI; 8±1 and 16±3%, FPI–indomethacin pretreated for responses to cromakalim 10⁻⁸, 10⁻⁶ M, respectively). These data show that vasopressin increased O⁻₂ production in a cyclooxygenase dependent manner and contributed to this production after FPI. These data also show that vasopressin blunted K_ATP and K_ca channel mediated cerebrovasodilation in a cyclooxygenase dependent manner. These data suggest that vasopressin induced cyclooxygenase dependent O⁻₂ generation contributes to K_ATP and K_ca channel function impairment after FPI.     

比较多巴胺与去甲肾上腺素对感染性休克血流动力学和氧代谢的影响

目的比较多巴胺与去甲肾上腺素对感染性休克患者血流动力学和氧代谢的影响。方法44例早期感染性休克患者经过充足的液体复苏使肺动脉楔压(PAWP)维持在1.6～2kPa之间,随机分为多巴胺组(Dopa组)和去甲肾上腺素组(NE组)。分别加用多巴胺或去甲肾上腺素,使平均动脉压(MAP)维持>10.7kPa。分别测定并计算应用多巴胺或去甲肾上腺素前(T0)、用药后1h(T1)、4h(T2)、8h(T3)、16h(T4)、24h(T5)和48h(T6)各个时间点的血流动力学指标[包括心率(HR)、外周血管阻力指数(SVRI)、心脏指数(CI)、肺动脉楔压(PAWP)及平均肺动脉压(MPAP)]和氧和指标[包括氧供指数(DO2I)、氧耗指数(VO2I)及氧摄取率(O2ext)]。结果(1)用药后2组同一时间点的HR、CI相比,NE组显著低于Dopa组(P<0.05);NE组的SVRI明显高于Dopa组(P<0.05)。(2)Dopa组的DO2I比NE组明显增加(P<0.05),NE组的VO2I、O2ext和Dopa组同一时间点相比明显增高(P<0.05)。结论对于早期感染性休克患者,去甲肾上腺素比多巴胺能更好的维持血流动力学稳定,它可以增加脏器灌注,提高O2ext,改善氧代谢。     

乐胃饮对脾虚型IBS兔胃肠激素及氧自由基的影响

[目的]观察中药复方乐胃饮对脾虚型IBS免胃肠激素及氧自由基的影响，探讨乐胃饮治疗脾虚型1BS的可能作用机制。[方法]两月龄白毛黑眼兔（WHBE免）36只，雌雄各半，随机分为6纽：正常纽、模型组、香砂六君丸组、丽珠肠乐组、乐胃饮低剂量组、乐胃饮高剂量组。除正常组外，其余WHBE兔采用湿热环境应激联合番泻叶灌胃加饥饱失常复合方法致脾虚泄泻型IBS模型。从模型复制的中期开始各用药组预防给药，至造模结隶。观察各组一般情况，测定血清NO、NOS、MDA、SOD含量及结肠黏膜组织中SP含量。[结果]模型组WHBE免血清NO、NOS、MDA含量、结肠黏膜SP阳性表达较正常组均显著升高（P〈0．01或P〈0．05），血清SOD活力明显降低（P〈0．01）。药物干预后，乐胃饮高剂量组血清NO含量较模型组明显降低（P〈0．01）；除乐胃饮低剂量组外，余用药组血清NOS活力、血清MDA含量与模型组比较均明显降低（P〈0．01或P〈0．05）、血清SOD活力明显增加（P〈0．01或P〈0．05）；各用药组结肠黏膜SP阳性表达较模型组均明显降低（P〈0．01或P〈0．05）。[结论]乐胃饮能有效调节脾虚型IBS兔胃肠激素的异常分泌及氧自由基的异常表达，这是乐胃饮治疗脾虚型IBS的可能作用机制。     

Insulin-like growth factor binding protein-3 proteolysis and growth of athyreotic infants in the first weeks of life

To gain a better understanding of the growth of athyreotic newborns in the first weeks of life, we evaluated auxological parameters and determined the serum levels of growth hormone (GH), insulin-like growth factor I (IGF-I) and free IGF-I, and IGF-binding protein-3 (IGFBP-3) in 15 hypothyroid infants (10 females) at a mean age of 25 d of life, immediately before the beginning of L-thyroxine therapy, and at 3 and 6 mo of life. Fourteen normal infants (9 females) of the same age were studied as controls. IGFBP-3 proteolytic activity was evaluated in 8 patients and in 8 controls at 25 d and 6 mo of life. There was no significant difference concerning weight and length between the patients and controls at birth, 25 d, 3 and 6 mo of life. The blood GH, IGF-I and IGFBP-3 levels were significantly lower in patients at diagnosis than in controls of the same age (p < 0.01 for all parameters), as well as IGFBP-3 studied by Western blotting. At diagnosis, the patients' free IGF-I level was within the control range, but the free IGF-I percentage of total IGF-I was higher than in the controls (p < 0.01). IGFBP-3 proteolytic activity was found to be greater in the patients (p < 0.01). At 6 mo of life, after therapy, none of these parameters was different from those of the controls. CONCLUSION: Increased IGFBP-3 proteolytic activity in our patients at diagnosis, favouring IGF-I bioavailability, could account for normal free IGF-I levels and in turn for their normal growth pattern during the first weeks of life and before the start of treatment.     

Complex level alterations of the 2<Emphasis Type="Italic">f</Emphasis><Subscript>1</Subscript>−<Emphasis Type="Italic">f</Emphasis><Subscript>2</Subscript> distortion product due to hypoxia in the guinea pig

It is controversially discussed inasmuch acute hearing disorders might originate from impaired cochlear circulation. Hypoxia-specific alterations of inner ear parameters measurable in patients with acute sensorineural hearing loss would therefore be of great interest. Aim of this study was to characterize hypoxia-related alterations of the 2f ₁−f ₂ distortion product. Nine guinea pigs were anaesthetized by i.m. administration of Midazolam, Medetomidin and Fentanyl. For introduction of hypoxia, the spontaneously breathing animals were offered a gas mixture of N₂O and O₂ containing either 21 or 12–13% O₂. Distortion product otoacoustic emissions (DPOAEs) were continuously monitored at f ₂ = 16 kHz; f ₂/f ₁ = 1, 2; DP-definition = 2f ₁−f ₂; L ₁ = 65 dB and L ₂ = 55 dB, while inhaled oxygen was switched from 21 to 12–13% and back. Oxygen saturation (SaO₂) was continuously monitored. Data from an hypoxic interval were only used for further data processing if DPOAE levels were stable before and after hypoxia. Six hypoxic intervals in five animals fulfilled the stability criterion. During the hypoxic interval with the highest measured SaO₂ (75%), no alterations of DPOAE levels were observed. During the remaining five hypoxic intervals, when SaO₂ ranged between 57 and 70%, DPOAE levels were on average lower with an increased standard deviation compared to mean pre-hypoxic levels. Mean decrease correlated with the decrease of SaO₂ (r = 0.90, P = 0.014). Alterations followed a characteristic time course—when hypoxia was started, DPOAE levels exhibited a short increase before they decreased and remarkably destabilized. After re-oxygenation DPOAE levels showed a pronounced level decrease, while SaO₂ already had recovered to pre-hypoxic values. After reaching a minimum, DPOAE levels slowly recovered to pre-hypoxic values. The decrease of DPOAE levels during hypoxia and the post-hypoxic level alterations have similarly been described by other authors before, while the distinct destabilization and transiently increased DPOAE levels have not been explicitly mentioned. A micromechanical mechanism that might explain a transient level increase and the post-hypoxic DPOAE level changes is discussed.