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首页> 外文期刊>European journal of anaesthesiology >Time course of haemodynamic, respiratory and inflammatory disturbances induced by experimental acute pulmonary polystyrene microembolism.
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Time course of haemodynamic, respiratory and inflammatory disturbances induced by experimental acute pulmonary polystyrene microembolism.

机译:实验性急性肺部聚苯乙烯微栓塞引起的血流动力学,呼吸道和炎性疾病的时程。

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BACKGROUND AND OBJECTIVE: The time course of cardiopulmonary alterations after pulmonary embolism has not been clearly demonstrated and nor has the role of systemic inflammation on the pathogenesis of the disease. This study aimed to evaluate over 12 h the effects of pulmonary embolism caused by polystyrene microspheres on the haemodynamics, lung mechanics and gas exchange and on interleukin-6 production. METHODS: Ten large white pigs (weight 35-42 kg) had arterial and pulmonary catheters inserted and pulmonary embolism was induced in five pigs by injection of polystyrene microspheres (diameter approximately 300 micromol l(-1)) until a value of pulmonary mean arterial pressure of twice the baseline was obtained. Five other animals received only saline. Haemodynamic and respiratory data and pressure-volume curves of the respiratory system were collected. A bronchoscopy was performed before and 12 h after embolism, when the animals were euthanized. RESULTS: The embolism group developed hypoxaemia that was not corrected with high oxygen fractions, as well as higher values of dead space, airway resistance and lower respiratory compliance levels. Acute haemodynamic alterations included pulmonary arterial hypertension with preserved systemic arterial pressure and cardiac index. These derangements persisted until the end of the experiments. The plasma interleukin-6 concentrations were similar in both groups; however, an increase in core temperature and a nonsignificant higher concentration of bronchoalveolar lavage proteins were found in the embolism group. CONCLUSION: Acute pulmonary embolism induced by polystyrene microspheres in pigs produces a 12-h lasting hypoxaemia and a high dead space associated with high airway resistance and low compliance. There were no plasma systemic markers of inflammation, but a higher central temperature and a trend towards higher bronchoalveolar lavage proteins were found.
机译:背景与目的:肺栓塞后心肺功能改变的时程尚未明确证实,全身性炎症对疾病的发病机制也没有作用。这项研究旨在评估聚苯乙烯微球引起的肺栓塞在12小时内对血流动力学,肺力学和气体交换以及白介素6产生的影响。方法:十只大白猪(体重35-42 kg)插入动脉和肺导管,并通过注射聚苯乙烯微球(直径约300 micromol l(-1))诱导五只猪发生肺栓塞,直至肺平均动脉值获得的压力是基线的两倍。另外五只动物仅接受盐水。收集血液动力学和呼吸数据以及呼吸系统的压力-容积曲线。当对动物实施安乐死时,在栓塞术之前和之后12小时进行了支气管镜检查。结果:栓塞组发展为低氧血症,高氧分率,较高的死区值,气道阻力和较低的呼吸顺应性水平无法纠正。急性血液动力学改变包括肺动脉高压,并保留全身动脉压和心脏指数。这些紊乱一直持续到实验结束。两组的血浆白细胞介素6浓度相似。然而,在栓塞组中发现了核心温度的升高和支气管肺泡灌洗蛋白浓度的升高。结论:聚苯乙烯微球在猪中引起的急性肺栓塞产生了持续12小时的低氧血症和高死腔,这与高气道阻力和低顺应性有关。没有血浆全身性炎症标志物,但是发现较高的中心温度和趋向于更高的支气管肺泡灌洗蛋白趋势。

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