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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。 相似文献
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根据高原缺氧作用特点配制高原Ⅱ(KY-Ⅱ)药物。经动物实验表明:与对照组比较,KY-Ⅱ号药可延长缺氧动物活存时间、活存数(P<0.05)和降低耗氧量(P<0.01)的基础上,选用18~25岁男性青年,分2批于大型低压舱内,减压至模拟海拔4000m高原停留48小时后,再继续减压至模拟5000m高原生活24小时(连续72小时)。将受试者随机分为2组,采取双盲法分别服用KY-Ⅰ(安慰剂)和KY-Ⅱ号药。实验期间,运用阻 相似文献
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The effects of chronic hypoxia on calmodulin levels of lung tissues and small pulmonary ar-terial walls were studied in young pigs, The tissue specimens of hypoxic animals were obtained underhypoxic conditions. The following results were collected:(1) The swine exposed to chronic intermittent hypoxia showed a significant pulmonary pressor re-sponse at a simulated high altitude of 4000 m.(2) A higher level of calmodulin was found in the lung tissues of chronic hypoxic animals. It maybe related to the increased release of some vaosactive substances from pulmonary non-muscularcalls.(3) No significant difference of calmodulin level of small arterial walls was demonstrated between theexperimental animals and the control.The findings suggest that pulmonary vasoconstriction due to hypoxia is not likely to be associatedwith obvious change in calmodulin level in the smooth muscle of blood vessels. 相似文献
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Lung lymph fistula preparation was used to study the effectsof hypoxia and endotoxin on pulmonary pressor response andpulmonary fluid exchange in 9 conscious goats.The results suggestthat 1)the mechanism of pulmonary pressor response induced byhypoxia is somewhat different from that induced by endotxin,2)hypoxia(at a simulated altitude of 4,000 m for 5 hours)exertsno obvious effect on the pulmonary fluid filtration and pulmonaryvascular permeability for protein,and 3)alveolar hypoxia can notenhance the pulmonary injury induced by endotoxin. 相似文献
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作者采用山羊慢性肺淋巴瘘模型,观察缺氧、小剂量的内毒素单独及复合作用,对清醒山羊肺动脉压、肺微血管壁通透性及肺组织问液形成的影响。缺氧(模拟4,000m高原,历时5小时)可使肺动脉压显著升高,但肺淋巴流量、淋巴与血浆蛋白比值及肺淋巴蛋白清除率均无明显改变。在平原注射内毒素后其反应可分为三期:(1)肺动脉高压期;(2)肺微血管损伤期;(3)肺微血管壁通透性增高期。在缺氧与内毒素复合作用时,肺动脉压、肺淋巴流量、淋巴与血浆蛋白比值及肺淋巴蛋白清除率的改变,与内毒素单独作用时基本相同。本实验结果提示:(1)缺氧与内毒素复合作用时肺动脉压增高的幅度,并作二者单独作用时幅度的叠加;(2)缺氧不能加重内毒素引起的肺损伤。 相似文献
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