Pre-Clinical Critical Care Unit, Florey Institute of Neuroscience and Mental Health, University of Melbourne, Melbourne, VIC, Australia.
Cardiovascular Disease Program, Biomedicine Discovery Institute and Department of Physiology, Monash University, Melbourne, VIC, Australia.
Acta Physiol (Oxf). 2021 Apr;231(4):e13596. doi: 10.1111/apha.13596. Epub 2020 Dec 22.
Renal tissue hypoxia during cardiopulmonary bypass could contribute to the pathophysiology of acute kidney injury. We tested whether renal tissue hypoxia can be alleviated during cardiopulmonary bypass by the combined increase in target pump flow and mean arterial pressure.
Cardiopulmonary bypass was established in eight instrumented sheep under isoflurane anaesthesia, at a target continuous pump flow of 80 mL·kg min and mean arterial pressure of 65 mmHg. We then tested the effects of simultaneously increasing target pump flow to 104 mL·kg min and mean arterial pressure to 80 mmHg with metaraminol (total dose 0.25-3.75 mg). We also tested the effects of transitioning from continuous flow to partially pulsatile flow (pulse pressure ~15 mmHg).
Compared with conscious sheep, at the lower target pump flow and mean arterial pressure, cardiopulmonary bypass was accompanied by reduced renal blood flow (6.8 ± 1.2 to 1.95 ± 0.76 mL·min kg) and renal oxygen delivery (0.91 ± 0.18 to 0.24 ± 0.11 mL·O min kg). There were profound reductions in cortical oxygen tension (PO) (33 ± 13 to 6 ± 6 mmHg) and medullary PO (31 ± 12 to 8 ± 8 mmHg). Increasing target pump flow and mean arterial pressure increased renal blood flow (to 2.6 ± 1.0 mL·min kg) and renal oxygen delivery (to 0.32 ± 0.13 mL·O minkg) and returned cortical PO to 58 ± 60 mmHg and medullary PO to 28 ± 16 mmHg; levels similar to those of conscious sheep. Partially pulsatile pump flow had no significant effects on renal perfusion or oxygenation.
Renal hypoxia during experimental CPB can be corrected by increasing target pump flow and mean arterial pressure within a clinically feasible range.
体外循环期间的肾脏组织缺氧可能导致急性肾损伤的病理生理学改变。我们检测在体外循环期间通过同时增加目标泵流量和平均动脉压是否可以减轻肾脏组织缺氧。
在异氟醚麻醉下建立 8 只仪器化绵羊的体外循环，目标连续泵流量为 80mL·kg·min，平均动脉压为 65mmHg。然后，我们用间羟胺（总剂量 0.25-3.75mg）测试同时将目标泵流量增加到 104mL·kg·min 和平均动脉压增加到 80mmHg 的效果。我们还测试了从连续流量过渡到部分脉动流量（脉冲压力约 15mmHg）的效果。
与清醒绵羊相比，在较低的目标泵流量和平均动脉压下，体外循环伴随着肾血流量（6.8±1.2 至 1.95±0.76mL·min·kg）和肾脏氧输送（0.91±0.18 至 0.24±0.11mL·O min·kg）减少。皮质氧张力（PO）（33±13 至 6±6mmHg）和髓质 PO（31±12 至 8±8mmHg）显著降低。增加目标泵流量和平均动脉压增加了肾血流量（至 2.6±1.0mL·min·kg）和肾脏氧输送（至 0.32±0.13mL·O min·kg），使皮质 PO 恢复到 58±60mmHg，髓质 PO 恢复到 28±16mmHg；与清醒绵羊相似。部分脉动泵流量对肾脏灌注或氧合没有显著影响。
在实验性 CPB 期间，通过在临床可行的范围内增加目标泵流量和平均动脉压可以纠正肾脏缺氧。
