Prowle John R, Bellomo Rinaldo
Adult Critical Care Unit, Department of Renal Medicine and Transplantation, The Royal London Hospital, Barts Health NHS Trust, London, UK; William Harvey Research Institute, Queen Mary University of London, London, UK.
Department of Intensive Care, Austin Hospital, Melbourne, Australia; Australian and New Zealand Intensive Care Research Centre, Department of Epidemiology and Preventive Medicine, Monash University, Melbourne, Australia.
Semin Nephrol. 2015 Jan;35(1):64-74. doi: 10.1016/j.semnephrol.2015.01.007.
Traditionally, renal ischemia has been regarded as central to the pathogenesis of sepsis-associated acute kidney injury (SA-AKI). Accordingly, hemodynamic management of SA-AKI has emphasized restoration of renal perfusion, whereas, experimentally, ischemia reperfusion models have been emphasized. However, in human beings, SA-AKI usually is accompanied by hyperdynamic circulation. Moreover, clinical and experimental evidence now suggests the importance of inflammatory mechanisms in the development of AKI and microcirculatory dysfunction more than systemic alteration in renal perfusion. In this review, we examine systemic, regional, and microcirculatory hemodynamics in SA-AKI, and attempt to rationalize the hemodynamic management of this condition.
传统上,肾缺血一直被视为脓毒症相关性急性肾损伤(SA-AKI)发病机制的核心。因此,SA-AKI的血流动力学管理一直强调恢复肾灌注,而在实验中,则一直强调缺血再灌注模型。然而,在人类中,SA-AKI通常伴有高动力循环。此外,临床和实验证据现在表明,与肾灌注的全身性改变相比,炎症机制在急性肾损伤和微循环功能障碍发展中的重要性更为突出。在这篇综述中,我们研究了SA-AKI中的全身、局部和微循环血流动力学,并试图使这种病症的血流动力学管理合理化。