土党参多糖对小鼠耐缺氧能力的影响

目的探讨土党参多糖(CJP)对小鼠耐缺氧能力的影响。方法把KM小鼠分为给药组和空白组,建立小鼠亚硝酸钠所致缺氧、常压缺氧以及缺血缺氧再灌注模型,观察小鼠在缺氧条件下存活时间以及常压缺氧条件下小鼠耗氧量,检测小鼠缺血缺氧再灌注后血红蛋白及红细胞含量变化。结果 CJP低、中、高3个剂量组与空白组比较,存活时间在亚硝酸钠所致缺氧条件下,分别延长了17.48%,21.22%,30.70%;常压缺氧条件下分别延长了4.63%、10.36%、17.87%;3个剂量组小鼠单位时间耗氧量比空白组明显降低(P<0.05);缺血缺氧再灌注后给药组血红蛋白及其红细胞含量增加。结论土党参多糖能够提高小鼠耐缺氧的能力。     

神经生长液的脑保护作用研究

目的研究现代中药复方制剂神经生长液(NGD)的脑保护作用.方法①采用小鼠常压耐缺氧实验,观察小鼠从断氧到死亡的时间.②采用小鼠不完全性脑缺血后再灌注模型,比较各组脑含水率及脑组织SOD活性与MDA含量.③采用电磁流量计测量大鼠脑血流量.结果高剂量NGD能显著延长缺氧情况下小鼠的存活时间,降低脑含水率,增高脑组织SOD活性,降低MDA含量.中、高剂量NGD能明显增加大鼠脑血流量.结论 NGD有一定的脑保护作用,其作用机制与增强神经元耐缺氧能力,降低脑耗氧量,减轻缺血导致的脑水肿,增强脑组织SOD活性,降低MDA含量,增加脑血流,降低脑血管阻力等有关.     

癫痫宁胶囊的药理及毒性研究

采用最大电休克发作（ＭＥＳ）法，戊四氮最小阈发作（ＭＥＴ）法，协同巴比妥作用法以及小鼠耐缺氧法，观察癫痫宁对动物惊厥催眠及耐缺氧的影响，同时还观察对小鼠的毒性作用。实验表明，癫痫宁４．５ｇ·ｋｇ－１能对抗小鼠的ＭＥＳ和ＭＥＴ，能增强巴比妥类药物的催眠作用以及延长小鼠常压耐缺氧存活时间，且毒性甚小。     

银丹心脑通胶囊对小鼠常压耐缺氧能力的影响

目的观察银丹心脑通胶囊对小鼠常压耐缺氧能力的影响。方法将48只小鼠随机分为银丹心脑通胶囊高、中、低剂量组及空白对照组,每天灌胃1次,连续给药7 d。末次给药后1 h,通过小鼠常压耐缺氧存活时间观察银丹心脑通胶囊的耐缺氧功能。结果与空白对照组比较,银丹心脑通胶囊高、中、低剂量组均能延长常压耐缺氧小鼠的存活时间(P<0.05)。结论银丹心脑通胶囊能提高动物的耐缺氧能力。     

大黄酚抗衰老作用的实验研究

目的 探讨大黄酚对小鼠抗衰老的作用。方法 采用避暗实验，观察大黄酚对学习记忆的影响；通过常压耐缺氧、断头耐缺氧、亚硝酸钠中毒造成的缺氧以及负重游泳实验，观察大黄酚对小鼠缺氧及耐力的影响；以AlCl3造成急性衰老小鼠模型，观察大黄酚对小鼠血中超氧化物歧化酶（SOD）活性的影响。结果 大黄酚能明显改善记忆障碍、提高小鼠耐力、并且能明显提高急性衰老小鼠血中SOD活性。结论 大黄酚具有一定的抗衰老作用。     

运动训练对老年痴呆小鼠的改善作用

目的 考察运动训练对老年痴呆小鼠学习记忆障碍的影响,并探讨其作用机制.方法　昆明种小鼠采用被动转笼法训练4 w后,采用Morris水迷宫法测试小鼠学习记忆能力;比色法检测脑组织中超氧化物歧化酶(SOD)活性及丙二醛(MDA)含量,HE染色观察海马组织形态学改变;BI-2000图像分析系统测定小鼠微循环;采用耐缺氧实验观察小鼠耐缺氧能力.结果 与空白对照组比较,模型组小鼠定向游泳实验潜伏期显著延长(P< 0.05),SOD活力显著降低,MDA含量显著升高(P<0.05),海马神经元变性、脱落,耐缺氧存活时间显著延长;与模型组比较,运动训练对上述指标均有显著改善作用.与空白对照组比较,运动训练显著改善微循环、提高耐缺氧能力.结论 运动训练能不同程度地改善小鼠学习记忆障碍,其作用机制可能与运动能提高小鼠清除自由基能力、改善微循环、提高耐缺氧能力有关.     

江苏地产白首乌C21甾苷抗衰老作用研究

目的研究江苏地产白首乌C21甾苷(C21 steroidal glycoside,CSG)抗氧化、耐缺氧、抗疲劳等抗衰老作用。方法以维生素E[VE,100mg/(kg.d)]为对照,观察CSG低、中、高剂量组[10mg/(kg.d)、20mg/(kg.d)、40mg/(kg.d),即CL、CM、CH组]对小鼠常压耐缺氧试验,负重游泳试验和D-半乳糖(D-gal)亚急性衰老模型小鼠的影响。测定小鼠常压耐缺氧和负重游泳时间,取血清、心、肝、脑组织,黄嘌呤氧化酶法测定超氧化物歧化酶(SOD)活性,硫代巴比妥酸法测定丙二醛(MDA)含量,ELISA法检测端粒酶活性。结果与正常对照组相比,CSG和VE能够延长健康小鼠常压耐缺氧和负重游泳时间,提高D-gal模型小鼠血清、心、肝、脑SOD活性,降低MDA含量;中、高剂量CSG组小鼠血清端粒酶活性升高;CSG低、中、高剂量组及VE组小鼠心脏端粒酶活性均升高(P<0.01);CSG及VE对小鼠肝及脑组织端粒酶活性无影响。结论CSG能拮抗自由基损伤,提高健康小鼠常压耐缺氧和负重游泳时间,提高D-gal衰老模型小鼠血清、心、肝、脑组织SOD活性,减少MDA含量,提高心脏组织中端粒酶活性。具有抗氧化、延缓衰老、抗疲劳作用。     

松果菊苷抗氧化作用研究

目的 研究管花肉苁蓉中松果菊苷(echinacoside,ECH)抗氧化、耐缺氧、抗疲劳等抗衰老作用.方法 以维生素E[VE,100mg/(kg*d)]为对照,观察低、中、高剂量[10mg/(kg*d)、20mg/(kg*d)、40mg/(kg*d)]ECH对正常健康小鼠和D-半乳糖亚急性衰老模型小鼠的影响.测定正常小鼠常压耐缺氧和负重游泳时间,检测衰老小鼠血清中超氧化物歧化酶(SOD)活性,丙二醛(MDA)含量,放射免疫法测定外周血白介素-2(IL-2)含量.计算亚急性衰老模型小鼠的脾指数和胸腺指数.结果 ECH和VE能够延长健康小鼠常压耐缺氧和负重游泳时间(P＜0.01);ECH和VE能提高衰老小鼠血清SOD活性(P＜0.01),降低血清MDA含量(P＜0.01),升高外周血IL-2含量(P＜0.05),增加脾指数(P＜0.01)和胸腺指数(P＜0.01).结论 ECH能拮抗自由基损伤,提高健康小鼠常压耐缺氧和负重游泳时间,增加脾指数和胸腺指数,具有抗氧化,增强免疫力,延缓衰老,抗疲劳作用.     

海带多糖对小鼠动脉血气影响及抗疲劳作用

目的　研究海带多糖 (Laminaria Japonica polysaccharides,LJP)的耐缺氧作用及其抗疲劳作用。方法　按 1 0 mg· kg- 1 · d- 1 、2 0 mg· kg- 1· d- 1、50 mg· kg- 1· d- 1、1 0 0 mg· kg- 1· d- 1不同剂量的海带多糖灌胃受试小鼠 ,连续 1 0 d,进行抗疲劳及密闭缺氧试验。结果　海带多糖能显著的提高受试小鼠负重游泳时间和常压缺氧下存活时间 ,并能升高受试小鼠的血红蛋白 ;使氧合血红蛋白解离 ,促进氧的释放。结论　海带多糖能提高缺氧小鼠组织对氧的利用 ,增强小鼠的耐缺氧、抗疲劳能力     

郁金防治急性缺氧小鼠脑损伤的机制

目的 探讨郁金对急性缺氧小鼠脑损伤的保护作用及其机制.方法 用郁金水煎剂低、中、高剂量(10、20、40 g/kg)连续灌胃6 d,利用常压密闭耐缺氧和断头实验复制小鼠急性缺氧模型,检测脑组织超氧化物歧化酶(SOD)活性、丙二醛(MDA)及一氧化氮(N0)含量;利用bcl-2、caspase-3抗体进行脑组织免疫组化染色.结果 与模型组比较,各剂量组均能不同程度地提高缺氧小鼠脑组织SOD活性,减少其MDA和NO含量,使caspase-3蛋白表达下调而bcl-2表达上调.结论 郁金水煎剂减轻急性缺氧小鼠脑组织损伤的机制可能与其减轻氧化应激损伤及抑制脑细胞凋亡有关.     

Effect of pentobarbital on spontaneous recovery from hypoxic apnoea in mice

The effect of pentobarbital anaesthesia on spontaneous recovery from hypoxic apnoea (autoresuscitation) was investigated in SWR/J mice. Experiments were performed in 17 to 23 day old animals, in which the mechanism often fails, and in adults, in which it is usually successful. Mice, matched for age and weight, were injected with pentobarbital (62.5 mg/kg) or saline. Hypoxic apnoea was induced with 97% N2-3% CO2 and air given at its onset. To determine whether the effect of pentobarbital depended on hypothermia, we performed experiments in 17-23-day-olds with and without maintenance of body temperature. In the 'hypothermic' experiments one of 27 mice given pentobarbital died, compared with 10 of 22 controls (P less than 0.005). In the 'isothermic experiments', none of 15 mice given pentobarbital died, compared to 7 of 13 controls (P less than 0.005). All adults in both groups survived. Pentobarbital had a different effect on eupnoea and gasping: resting ventilation was depressed but gasp ventilation increased, and the duty cycle of gasps but not eupnoeic breaths was altered. Pentobarbital may facilitate autoresuscitation because gasping is unimpaired but oxygen consumption and lactate production are reduced, allowing cardiac function and cerebral survival until PO2 is restored.     

Rostral medullary respiratory neuronal activities of decerebrate cats in eupnea, apneusis and gasping.

Eupnea is generated by mechanisms within the pons and medulla. Following removal of pons or exposure to anoxia, gasping is elicited. Eupnea and gasping are markedly different ventilatory patterns. The genesis of gasping is dependent upon rostral medullary neuronal activities. To generate the gasp, these activities should commence before the phrenic burst. In decerebrate, vagotomized, paralyzed and ventilated cats, eupnea was altered to gasping in anoxia. Rostral medullary neuronal activities had inspiratory, expiratory and phase-spanning patterns in eupnea. During gasping, some inspiratory neuronal activities commenced before the phrenic gasp; these same neurons had commenced activities after the onset of the eupneic phrenic burst. Expiratory and phase-spanning neurons did not discharge. Neuronal activities which are consonant with a role in the neurogenesis of gasping had very different discharge patterns in eupnea. Results support the concept that medullary mechanisms for gasping are incorporated in the ponto-medullary circuit responsible for the neurogenesis and expression of eupnea.     

Protective effects of selenium on ultrastructural changes in heart muscles with experimental free-glucose and anoxia in organ culture]

Fetal hearts taken from the 16th to 18th day of pregnant mice were cultured in MEM + 0.5 microgram/ml of sodium selenite [Na2SeO3] (MEMS), and in MEM alone with oxygen for 24 hours, and then the two groups of hearts were exposed to 10, 15, 20, 30, 40, 60 min and a long term of anoxia in glucose-free MEMS and glucose-free MEM respectively. Results showed that the survival and beating of the cultured fetal mouse hearts with experimental free-glucose and anoxia were prolonged by selenium. The application of lanthanum as a marker demonstrated that the permeability function of myocardial cell membrane and mitochondrial membrane of early experimental anoxia were protected by selenium. By using electron microscopy when structural damages occurred, it was shown that the time of occurrence of irreversible injuries could be postponed by selenium. From the fact that ribosomes increased in the cell of selenium-treated hearts, we concluded selenium may play a promotive role in the synthesis of protein in experimental free-glucose and anoxic conditions.     

Ethanol exposure during pregnancy persistently attenuates cranially directed blood flow in the developing fetus: evidence from ultrasound imaging in a murine second trimester equivalent model

Background: Ethanol (EtOH) consumption during pregnancy can lead to fetal growth retardation, mental retardation, and neurodevelopmental delay. The fetal brain initiates neurogenesis and vasculogenesis during the second trimester, and depends on maternal‐fetal circulation for nutrition and growth signals. We used high‐resolution in vivo ultrasound imaging to test the hypothesis that EtOH interferes with fetal brain‐directed blood flow during this critical developmental period. Methods: Pregnant mice were lightly anesthetized on gestational day 12 with an isoflurane/oxygen mixture. We assessed the effect of single and repeated binge‐like maternal EtOH exposures at 3 g/kg, administered by intragastric gavage or intraperitoneal injection, on maternal circulation and fetal umbilical, aortic, internal carotid, and middle cerebral arterial circulation. Results: Binge maternal EtOH exposure, regardless of exposure route, significantly reduced fetal arterial blood acceleration and velocity time integral (VTI), from umbilical to cerebral arteries, without a change in fetal heart rate and resistivity indices. Importantly a single maternal binge EtOH exposure induced persistent suppression of fetal arterial VTI for at least 24 hours. Repeated binge episodes resulted in a continuing and persistent suppression of fetal VTI. Qualitative assessments showed that maternal EtOH exposure induced oscillatory, nondirectional blood flow in fetal cerebral arteries. Maternal cardiac and other physiological parameters remained unaltered. Conclusions: These data show that binge‐type maternal EtOH exposure results in rapid and persistent loss of blood flow from the umbilical artery to the fetal brain, potentially compromising nutrition and the maternal/fetal endocrine environment during a critical period for neuron formation and angiogenesis in the maturing brain.     

Protection from anoxic myocardial injury in fetal mouse heart culture by selenium

Fetal hearts taken from the 17 day pregnant mice were cultured in minimum essential medium (MEM) + 0.5 ug ml of Na2SeO, and in MEM alone with oxygen for 24 h, and then the hearts in groups were exposed to 15, 20, 30, 40 min, 1 h, 3h and long term of anoxia respectively. The results showed that the survival and beating of the cultured fetal mouse hearts with anoxia were prolonged by selenium. Using lanthanum as a marker, we found that after 20 min of anoxia, this electroopaque marker remained extracellular in the selenium-treated hearts, however, intracellular lanthanum could be found in the control hearts, entering selectively into the swelling mitochondria. During the same period of anoxia, ACPase reaction products could be only found in the lysosomes and in the Golgi complex in the selenium-treated hearts, but a lot of reaction products deposited in cytoplasm in the control hearts. By electron microscopy, at 40 min of anoxia, there were swelling of mitochondria, with cristae partially lost and plasma-membrane changed and so on. Generally normal ultrastructure was observed in the selenium-treated hearts at 40 min of anoxia. The cytoplasm was rich in ribosomes and the sarcoplasmic reticulum with a rough face. There events showed that cellular membrane and membrane-bound organelles appeared to be well protected target by the selenium. Therefore, selenium may play an important role in the synthesis of protein.     

Fluorocarbon emulsion as a blood substitute: cerebral microcirculation and related parameters

Mice were exchange transfused with a fluorocarbon emulsion (FC-80). Their hematocrits were reduced to levels of 10–15. The survival time of these animals was significantly longer than that of control mice transfused with dextrose-saline, or saline alone, provided they were kept on 100% O₂. Survival was related to the capacity of FC-80 blood, over a wide range of HCT, to carry larger amounts of oxygen than did normal blood, provided both bloods were drawn from mice breathing 100% O₂. Fluorescein transit time through the cerebral microcirculation was normal or slightly accelerated in the majority of FC-80 mice. Acceleration may have been due to reduced “blood” viscosity. A relationship was found between microcirculatory viability as judged by transit time, and the continued capacity of the brain to respond to anoxia with a rise in NADH. Thus all mice with normal or reduced transit times displayed reversible increases in brain NADH levels when they were rendered anoxic while a small group of mice with prolonged fluorescein transit, tended to display NADH levels which failed to rise when O₂ was reduced in the inspired air. Many FC-80 mice displayed reversible decreases in brain PO₂ levels when inspired O₂ was reduced. Pentylenetetrazol activated the EEG of FC-80 mice. The EEG activity was reversibly reduced when the animals were briefly exposed to room air or N₂. These data suggest that fluorocarbon emulsions can support brain microcirculation, oxygenation and electrical activity in vivo, a result which is consonant with the observations of others who have performed in vitro experiments, or observed long-term survival.     

Prognosis of congestive heart failure and predictors of mortality

The interaction of physiologic variables that appear to be predictive of prognosis in patients with severe congestive heart failure was examined in a series of 139 patients referred to a heart failure service. Left ventricular ejection fraction, peak oxygen consumption during a progressive maximal exercise test and resting plasma norepinephrine concentration were identified as the strongest univariate predictors of prognosis. Examination of their interaction was accomplished by stratifying each variable into quartiles and then pooling quartiles for bivariate analysis. The data demonstrate that ejection fraction has the most profound effect on survival calculated from maximal oxygen consumption and norepinephrine concentration, but that each of the variables provides additional independent prognostic information when added to survival estimated from any of the other variables. Therefore, ventricular function, exercise tolerance and sympathetic nervous system activation appear to provide independent insight into the prognosis of patients with heart failure.     

The prediction of maximal oxygen consumption from a continuous exercise treadmill protocol

This study investigated the hypothesis than an individual's maximal oxygen consumption can be realistically predicted by the maximal time achieved in the Balke treadmill protocol. The oxygen consumption in the final minute of exercise of 1,025 normal men who performed a maximal effort in the Balke protocol were linearly regressed on their maximal treadmill time using a least-squares fit technique. In addition, the men were grouped by heart rate response, and regression equations plus (0.95, 0.95) tolerance limits were computed for each subgroup. A regression equation was also computed for an additional 127 men who had multiple bags of expired air collected approaching maximal effort. It was demonstrated that the tolerance limits are so wide that maximal oxygen consumption can be only grossly estimated by treadmill time. Thus, other factors than maximal oxygen consumption must be operating in determining treadmill performance.