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Inhalative and intravenous stimulation of soluble guanylate cyclase reduces pulmonary vascular resistance and increases cardiac output in experimental septic shock

机译:吸入和静脉内刺激可溶性鸟苷酸环化酶可降低实验性败血性休克中的肺血管阻力并增加心输出量

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摘要

The effects of inhaled and intravenous application of a guanylate cyclase stimulator (BAY 41–8543) on pulmonary vascular resistance (PVR) and cardiac output (CO) were investigated in an experimental model of septic shock. Following induction of septic shock, anaesthetized pigs (n=31) were randomly place into two groups receiving different interventions. Animals in the first group received intravenous BAY 41–8543 (0.6 mg), inhalative BAY 41–8543 (6 mg) or a placebo. In the second group, the dosage of BAY 41–8543 was increased two-fold or combined with inhalation of nitric oxide (iNO). Intravenous and inhaled administration of BAY 41–8543 resulted in a significantly (P<0.05) reduced PVR and increased CO compared with the placebo. Increasing the dosage of BAY 41–8543 or combining it with iNO did not further decrease PVR. The results of the present study indicate that BAY 41–8543 effectively reduces PVR and increases CO in septic shock, through inhaled or intravenous routes of administration.
机译:在败血性休克的实验模型中研究了吸入和静脉内施用鸟苷酸环化酶刺激剂(BAY 41–8543)对肺血管阻力(PVR)和心输出量(CO)的影响。诱导感染性休克后,将麻醉猪(n = 31)随机分为两组,分别接受不同的干预措施。第一组动物接受静脉BAY 41–8543(0.6 mg),吸入性BAY 41–8543(6 mg)或安慰剂。在第二组中,BAY 41–8543的剂量增加了两倍,或者与一氧化氮(iNO)的吸入结合使用。与安慰剂相比,BAY 41–8543的静脉内和吸入给药导致PVR显着降低(P <0.05),CO升高。增加BAY 41–8543的剂量或将其与iNO结合使用并不会进一步降低PVR。本研究的结果表明,BAY 41–8543通过吸入或静脉内给药途径有效降低败血症性休克中的PVR和增加CO。

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