高频通气对心血管的影响——可能涉及血栓素

William Durante, Fred A. Sunahara
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引用次数: 5

摘要

最近对高频通气(HFV)的研究表明,HFV引起的平均气道压力升高会导致明显的心血管抑制,尤其是心输出量(CO)。除了机械性事件外,负性肌力因子也可能与前列腺素有关。本研究探讨了血栓素A2 (TXA2)在hfv诱导的心血管恶化中的可能参与。经氯氯醚麻醉的机械通气犬分别接受HFV 4、10和20 mm Hg治疗30分钟。部分动物在接受HFV治疗前还接受咪唑治疗(25 mg/Kg/hr)。动脉中TXB2 (TXA2的稳定代谢物)水平用放射免疫法监测。在HFV期间,气管压力相关的CO和卒中容积(SV)均下降。咪唑治疗显著降低了SV的下降。HFV的应用导致循环TXB2水平的变化。总的来说,HFV的应用并没有导致基线水平的显著变化。此外,CO和SV的变化与动脉TXB2浓度的变化没有相关性。这些结果不支持HFV期间肺部过度扩张导致心脏抑制剂前列腺素释放的假设。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Cardiovascular effects of high frequency ventilation - the possible involvement of thromboxane

Recent studies with high frequency ventilation (HFV) have noted that HFV-induced increases in mean airway pressure leads to a marked cardiovascular depression, especially in cardiac output (CO).Aside from mechanical events a negative inotropic agent possibly prostaglandin in nature may also be involved. This study examined the possible involvement of thromboxane A2 (TXA2) in the HFV-induced cardiovascular deterioration. Chloralose-anesthetized mechanically-ventilated dogs were subjected to HFV 4, 10, and 20 mm Hg for 30 min. Some animals were also treated with imidazole (25 mg/Kg/hr) prior to HFV. Arterial levels of TXB2 (stable metabolite of TXA2) where monitored by radioimmunoassay. During HFV, tracheal pressure-related decreases in both CO and stroke volume (SV) were noted. Imidazole treatment significantly reduced the decrement in SV. Application of HFV resulted in variable changes in circulating TXB2 levels. Overall, application of HFV did not result in a significant change from baseline levels.Furthermore there was no correlation between changes in CO and SV with changes in arterial TXB2 concentration. These results do not support the hypothesis that hyperexpansion of the lungs during HFV causes the release of a cardiodepressant prostanoid.

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