缺氧和酵母多糖对清醒山羊肺动脉压和肺内液体的影响

作者采用山羊慢性肺淋巴瘘模型,观察了缺氧和酵母多糖活化的血浆对清醒山羊肺动脉压、肺血管壁通透性和肺组织间液形成的影响。缺氧时肺动脉压显著升高,这可能是肺毛细血管前肌性小动脉收缩的结果。为缺氧动物输入酵母多糖活化的血浆,肺动脉压在缺氧增高的基础上又有短暂升高,接着出现肺血管扩张,缺氧性肺动脉增压反应受抑。酵母多糖活化的血浆可致山羊肺微血管壁受损,缺氧(模拟4000米高原)并未加重其损伤。     

慢性缺氧对大鼠肺动脉和主动脉舒缩反应的影响

大鼠经模拟高原5000m缺氧15d后,右肺动脉对Ach所致的舒张反应显著减弱,对5-HT所致的收缩反应显著增强,胸主动脉则无这种变化。结果提示,慢性缺氧对肺血管和体血管血管反应性的不同影响可能是高原缺氧环境下肺动脉压升高、体动脉压下降或不变的重要原因之一。     

急性和慢性间断缺氧对血内组织胺含量的影响

一般认为猪的肺血管对缺氧收缩反应较敏感,但缺氧引起猪的肺动脉增压反应与血组织胺之间的关系尚未见报导。因而。本文用猪作为实验对象,观察急性和慢性间断缺氧时,肺动脉和股动脉血内组织胺含量的变化,试图阐明血组织胺在猪的缺氧性肺动脉压增压反应中的作用。雄性猪15只,体重20～49.5公斤,随意分为两组。甲组(9只)为急性缺氧组。以戍基     

缺氧和空气栓塞对清醒山羊肺动脉增压反应及肺内液体交换的影响

作者采用山羊慢性肺淋巴瘘方法,观察缺氧、空气栓塞单独和复合作用,对清醒山羊肺动脉压、肺微血管壁通透性和肺内液体交换的影响。实验结果表明:①缺氧所致的成年山羊肺动脉压增高,可能是毛细血管前阻力血管收缩的结果。成年山羊在模拟4000m高原缺氧1小时,未致肺微血管壁通透性增高;②肺血管空气栓塞可致肺动脉压和微血管壁通透性增高;③缺氧和空气栓塞复合作用时,肺动脉增压反应的幅度并非两者单独作用的叠加;④空气栓塞引起的肺血管壁通透性增高未为缺氧所加重。     

异搏停对急性缺氧肺动脉增压反应的影响

急性缺氧对猪的血液动力学影响,尚未见有报导。缺氧引起肺动脉高压是肺心病、高原心脏病、高原肺水肿发病重要环节。因此找寻降低肺动脉压药物具有一定临床意义。本文研究猪在不同的模拟高原时肺动脉压变化和异搏停(Verapamil)对急性缺氧肺血管增压反应的作用。 11只雄性猪,体重为20～49.5公斤,在麻醉下进行右心导管。首先测定平原肺和股动脉     

硝苯吡啶对幼猪缺氧性肺动脉压增高和右心室肥大的影响

在本实验中,观察了缺氧(模拟4000米高原)和在缺氧条件下注入硝苯吡啶溶液对幼猪(n=18)血流动力学指标和血液气体参数的影响。结果表明:1.缺氧时,肺动脉平均压(Psa)和肺血管阻力(PVR)显著增高,颈总动脉压(Psa)和总外周阻力(TPR)亦增高,心输出量(CO)则无明显改变,2.在4000米模拟高原注入硝苯吡啶(40μg/kg,IV)溶液后,Psa和PVR显著下降,Psa和TPR亦下降,CO明显增加;3.每天肌注两次硝苯吡啶(40mg/kg/次)溶液的幼猪,经过慢性间断性缺氧(模拟4000米高原,8小时/天,共30天)后,右心室并无明显肥大。实验结果说明硝苯吡啶能防治猪的缺氧性肺动脉高压及慢性间断性缺氧引起的右心室肥大。     

猪在慢性间断缺氧后循环机能对再次缺氧的反应以及异搏停的影响(摘要)

猪在慢性间断缺氧30天后,其循环机能对再次缺氧的反应,以及异搏停(Verapamil)对此种反应的影响,在国内外文献中尚未见报导。雄性幼猪10只,体重21.0～41.5公斤。每天在低压舱内减压至模拟4,000米高原停留8小时,共30天。第31天在戊基巴比妥钠麻醉下于平原(300米)用水银检压计观测股动脉压,经右心导管用水检压计测定肺动脉的平均压和中心静脉压,用染料(T1824)稀释法测定心输出量。于部分猪用四导生理记录仪(SJ—41型四导生理记录仪,上海医用电子仪器厂)通过电血压计和压力换能器描记肺动脉的收缩和舒张压。计算体循环血管的总阻力、肺     

尼群地平对缺氧性右心室肥大和心肌血流量的影响

高原慢性缺氧和阻塞性肺疾病均可引起肺动脉高压和右心室肥大。本文探讨钙阻断剂尼群地平能否预防和治疗缺氧性肺动脉高压、右心室肥大和对心功能及心肌血流量的影响。 Wistar大白鼠任意分四组:(1)对照组;(2)慢性缺氧组:其中11只减压30天,9只减压60天。(3)尼群地平预防组:于减压舱同时口服尼群地平,其中10只为10mg/     

缺氧对肺动脉压的影响(文摘)

国外学者曾用吸入低氧混合气体和把动物送入高原的方法研究过急性和慢性缺氧对肺动脉压影响,而国内对这方面工作研究较少。本文观察不同种的平原动物在不同摸拟高原和世居高原动物的肺动脉压和血气变化并寻找降低肺动脉压的药物。 18只雄性平原狗,体重为11～15公斤。12只雄性高原世居狗(3865m),体重为10～17公斤。11只平原雄性猪,体重20～49.5公斤。4只高原世居猪(3658m),体重30～40公斤,在麻醉下进行右心导管,以水检压计测定肺动脉压和肺动脉楔压。高     

切除窦神经对慢性缺氧性肺动脉高压的影响

肺动脉高压与颈动脉体化学感受器敏感性降低是高原低氧环境中机体的两个突出变化。过去,我们曾报告过颈动脉体化学感受器可能影响缺氧时肺动脉压的调节,从而与缺氧性肺动脉高压的形成有一定关系。本文对此作了进一步的探讨,报告如下:     

Endogenous nitric oxide as a probable modulator of pulmonary circulation and hypoxic pressor response in vivo

The objective of this study was to investigate the role of endogenous nitric oxide, formed from L-arginine, in the regulation of pulmonary circulation in vivo, with special reference to the hypoxic pressor response. In artificially ventilated open-chest rabbits, pulmonary vascular resistance at normoxic ventilation (F₁₀₂= 21 %) was 78C 16 cmH₂O ml^-l min 1000^-1 (mRU_L). Hypoxic ventilation (F₁₀₂= 10%) increased pulmonary vascular resistance to 117 ± 17 mRU_L. N^w-nitro-L-arginine methylester (L-NAME), an inhibitor of nitric oxide synthase, increased pulmonary vascular resistance at normoxic ventilation to 192 ± 28 mRU_L and during hypoxic ventilation to 462 ± 80 mRU_L. During N^w-nitro-l-arginine methylester infusion there was also an increase in mean arterial blood pressure as well as a decrease in cardiac output that was even more pronounced during hypoxic ventilation. L-arginine reversed the effect of N^w-nitro-l-arginine methylester on pulmonary vascular resistance at normoxic ventilation to 140 ± 26 mRU_L and at hypoxic ventilation to 239 ± 42 mRU_L. In spontaneously breathing closed-chest rabbits, N^w-nitro-L-arginine methylester evoked a marked decrease in arterial P_o2, and increases in respiration frequency and central venous pressure, while blood pH, P_CO2 and base excess remained unchanged. Taken together these findings indicate that endogenous nitric oxide, formed from L-arginine, might be a regulator of ventilation-perfusion matching at normoxic ventilation, and that nitric oxide acts as an endogenous modulator of the hypoxic pressor response.     

Endogenous nitric oxide as a probable modulator of pulmonary circulation and hypoxic pressor response in vivo.

The objective of this study was to investigate the role of endogenous nitric oxide, formed from L-arginine, in the regulation of pulmonary circulation in vivo, with special reference to the hypoxic pressor response. In artificially ventilated open-chest rabbits, pulmonary vascular resistance at normoxic ventilation (FIO2 = 21%) was 78 +/- 16 cmH2O ml-1 min 1000-1 (mRUL). Hypoxic ventilation (FIO2 = 10%) increased pulmonary vascular resistance to 117 +/- 17 mRUL. N omega-nitro-L-arginine methylester (L-NAME), an inhibitor of nitric oxide synthase, increased pulmonary vascular resistance at normoxic ventilation to 192 +/- 28 mRUL and during hypoxic ventilation to 462 +/- 80 mRUL. During N omega-nitro-L-arginine methylester infusion there was also an increase in mean arterial blood pressure as well as a decrease in cardiac output that was even more pronounced during hypoxic ventilation. L-arginine reversed the effect of N omega-nitro-L-arginine methylester on pulmonary vascular resistance at normoxic ventilation to 140 +/- 26 mRUL and at hypoxic ventilation to 239 +/- 42 mRUL. In spontaneously breathing closed-chest rabbits, N omega-nitro-L-arginine methylester evoked a marked decrease in arterial PO2 and increases in respiration frequency and central venous pressure, while blood pH, PCO2 and base excess remained unchanged. Taken together these findings indicate that endogenous nitric oxide, formed from L-arginine, might be a regulator of ventilation-perfusion matching at normoxic ventilation, and that nitric oxide acts as an endogenous modulator of the hypoxic pressor response.     

慢性缺氧对肺动脉增压反应的影响——组胺受体的作用

本实验观察慢性缺氧幼猪(Ch组)和对照组(C组)对急性缺氧的血流动力学反应及组胺H_1、H_2受体阻断剂扑尔敏、甲氰咪呱的作用。急性缺氧可增加肺动脉压(Ppa),Ch组比C组增加明显(前者增加25mmHg、100%;后者增加17mmHg,83.4%)。缺氧时扑尔敏降Ppa的作用亦为Ch组大于C组(Oh组降11mmHg,C组6mmHg)。甲氰咪呱增Ppa的作用两组相近。结果提示:(1)慢性缺氧能增强HPPR;(2)组胺受体参与HPPR调节;(3)慢性缺氧可能使肺动脉H_1受体活性增强,此变化可能与HPPR增强有关。     

Cardiorespiratory and cerebrovascular responses to hyperoxic and hypoxic rebreathing: effects of acclimatization to high altitude

We examined the cardiorespiratory and cerebrovascular responses to hyperoxic and hypoxic rebreathing at low attitude and high altitude. We measured ventilation, middle cerebral artery blood flow velocity (MCAv) and arterial blood pressure in conditions of eucapnia, hypocapnia (voluntary hyperventilation) and during hyperoxic and hypoxic rebreathing firstly at low altitude (1400 m) then again at high altitude (3840 m) in five individuals, following 9 days at altitude >5000 m. High altitude was associated with elevations in the blood pressure response to hyperoxic rebreathing, whilst cerebrovascular reactivity was reduced and ventilatory sensitivity was unchanged. During hypoxic rebreathing, whilst ventilatory and blood pressure reactivity were increased (vs. low altitude and hyperoxic rebreathing), cerebrovascular reactivity was preserved. In conclusion, at high altitude there was an enhancement in peripheral but not central chemosensitivity to CO(2); and during hypoxic rebreathing, marked elevations in blood pressure may restore some of the reduction in cerebrovascular CO(2) reactivity, potentially reflecting a pressure-passive relationship in the brain offsetting sympathetic-induced cerebral vasoconstriction.     

缺氧敏感性不同的大鼠血小板活性的比较研究

HT(Hilltop SD)缺氧敏感大鼠与普通W(Wistar)大鼠,分平原对照组与置模拟5000米高度低压舱10天的慢性缺氧组。慢性缺氧组与对照组肺动脉收缩压的均值(PAP),在HT大鼠分别为51.9±14.2与31.3±3.0mmHg,P<0.001,慢性缺氧组比对照组高65.8%;W大鼠分别为39.7±7.4与28.9±4.7mmHg,P<0.001,慢性缺氧组比对照组高37.4%。对照HT大鼠全血及肺组织5-羟色胺(5-HT)高于对照W大鼠(P<0.05)。慢性缺氧组HT大鼠血小板数增加,与对照组相比,P<0.01;全血及肺5-HT明显减少,与对照组相比,P<0.001及P<0.05;血浆TXB_2增高,与对照组相比,P<0.001;对ADP诱导血小板聚集敏感性降低。慢性缺氧组W大鼠以上指标变化与HT大鼠相似,除血小板聚集外,HT大鼠以上变化比W大鼠更明显。提示对照组两种大鼠血小板功能状态不完全相同,慢性缺氧时,HT大鼠血小板活化程度高于W大鼠,这在HT大鼠肺动脉对缺氧的增压反应敏感中可能起一定作用。     

L-精氨酸和牛磺酸联合抗缺氧损伤及防治缺氧性肺动脉高压的研究

目的研究L-精氨酸、牛磺酸联合应用的抗缺氧损伤以及对缺氧性肺动脉高压(HPH)的防治效果。方法雄性W istar大鼠40只,制作缺氧性HPH模型,随机分为平原对照组(C)、单纯缺氧组(H)、缺氧 L-精氨酸组(Arg)、缺氧 牛磺酸组(Tau)、缺氧 牛磺酸 L-精氨酸组(TA),测定各组的肺动脉压(mPAP)、右心室肥大指数(RVH I)、血浆乳酸脱氢酶(LDH)、脂质过氧化产物丙二醛(MDA)、肺匀浆NO含量的变化。结果H组与C组相比,mPAP高出约25 mmHg(P<0.01),RVH I增加1.56倍(P<0.01),血浆LDH活性增高10.1倍(P<0.01),血浆MDA含量增加1.64(P<0.01),而肺匀浆NO含量降低68%(P<0.01)。各治疗组与H组相比,mPAP均显著降低5 mmHg(P<0.05),RVH I均显著降低20%(P<0.01),血浆LDH活性显著降低(P<0.01),其中TA组与Arg组比较有显著差异(P<0.01),血浆MDA含量显著降低(P<0.01),但各治疗组之间无显著性差异。肺匀浆NO含量在Tau组无显著性变化,在Arg和TA组显著回升(P<0.01)。结论L-精氨酸和牛磺酸具有抗缺氧损伤及防治肺动脉高压的效果,两者联用可进一步增加NO产生,减少乳酸脱氢酶的漏出,加强细胞保护作用。     

前列腺素E_1和花生四烯酸对猪缺氧性肺动脉增压反应的影响

为探讨前列腺素(PG)在缺氧性肺动脉增压反应(HPPR)中的作用,作者在模拟4000米高原将PGE_1和花生四烯酸(AA)经心导管注入猪的腔静脉:PGE_1明显降低了肺动脉平均压(Ppa),肺血管阻力(PVR)、体循环动脉平均压(Psa)和体循环血管阻力(SVR);AA则增强了HPPR,降低了Psa和SVR。上述结果提示:PGE_1对猪的肺循环和体循环具明显的降压效应;注入AA时猪体循环血管可能合成了舒张血管性PG(VDPG),肺血管主要合成了收缩血管性PG(VCPG),破坏了肺血管中VCPG与VDPG的作用平衡,可能为HPPR增强的原因之一。     

The cGMP pathway is not responsible for the blunted hypoxic vasoconstriction in rat lungs after altitude exposure

To examine the contribution of the cyclic guanosine monophosphate (cGMP) pathway in changes in pulmonary vasoconstriction during the initial days of altitude exposure, we tested the effects of LY83583 (an inhibitor of guanylate cyclase activation) and those of N^G-monomethyl-l -arginine (an inhibitor of nitric oxide synthesis) on airway hypoxia- (3% O₂) and angiotensin II- (AII, 0.2 μg) induced vasoconstrictions in lungs from the rats exposed to either moderate altitude (MA, 570 torr) or high altitude (HA, 430 torr). At 2 days' exposure, hypoxic response was significantly blunted compared with the response in low-altitude (LA, 710 torr) lungs in an altitude-dependent manner. At 7 days' exposure, the response was recovered fully in MA lungs but partially in HA lungs. AII response was not significantly blunted at 2 days' exposure, but was significantly augmented in an altitude-dependent manner at 7 days' exposure. LY83583 (10 μmol L^?1) potentiated both responses in LA lungs but did not significantly potentiate either response in any altitude-exposed lungs. N^G-monomethyl-l -arginine (10 μmol L^?1) potentiated both responses in LA lungs but did not significantly potentiate either response in HA lungs at 2 days' and 7 days' exposure. Thus the cGMP pathway is not responsible for either the change in hypoxic vasoconstriction or the change in AII vasoconstriction in rat lungs during the initial 7 days of altitude exposure.     

Hypoxic pulmonary steady-state diffusing capacity for CO and cardiac output in rats born at a simulated altitude of 3500 m

Summary In rats born in the low pressure chamber from sea level parents a higher hypoxic steady-state pulmonary diffusing capacity for CO was found as compared with controls of similar body weight. This difference could be explained by a difference in age or by an increase of blood O₂ capacity. There was no difference in alveolar ventilation and alveolar-arterial O₂ pressure differences, a lower cardiac output, no difference in arterial O₂ tension, no difference in arterial O₂ content but a decreased mixed-venous O₂ content as compared with control rats measured at hypoxia. A shift of the standard blood O₂ dissociation curve to the right was found in the simulated high altitude exposed rats. Calculated mixed-venous O₂ pressure was not altered in these rats; since arterial O₂ pressure was the same no difference in mean tissue capillary O₂ pressure may be presumed as compared with control animals. The results suggest that the first generation of rats exposed to simulated high altitude for their whole life is not only less adapted than animals exposed in their youth (as described in previous work) but that the ability to promote the O₂ transport in time of need in rats born in the low pressure chamber is probably even inferior to that of the controls.