Harman P K, Kron I L, McLachlan H D, Freedlender A E, Nolan S P
Ann Surg. 1982 Nov;196(5):594-7. doi: 10.1097/00000658-198211000-00015.
The effect of increased intra-abdominal pressure on cardiac output and renal function was investigated using anesthetized dogs into whom inflatable intraperitoneal bags were placed. Hemodynamic and renal function measurements were made at intra-abdominal pressures of 0, 20, and 40 mmHg. Renal blood flo and glomerular filtration rate decreased to les than 25% of normal when the intra-abdominal pressure was elevated to 20 mmHg. At 40 mmHg intra-abdominal pressure, three dogs became anuric, and the renal blood flow and glomerular filtration rate of the remaining dogs was 7% of normal, while cardiac output was reduced to 37% of normal. Expansion of the blood volume using Dextran-40 easily corrected the deficit in cardiac output, but renal blood flow and glomerular filtration rate remained less than 25% of normal. Renal vascular resistance increased 555% when the intra-abdominal pressure was elevated from 0 to 20 mmHg, an increase fifteen-fold that of systemic vascular resistance. This suggests that the impairment in renal function produced by increased intra-abdominal pressure is a local phenomenon caused by direct renal compression and is not related to cardiac output.
使用放置了可充气腹腔袋的麻醉犬，研究腹内压升高对心输出量和肾功能的影响。在腹内压为0、20和40 mmHg时进行血流动力学和肾功能测量。当腹内压升高到20 mmHg时，肾血流量和肾小球滤过率降至正常的25%以下。在腹内压为40 mmHg时，三只犬出现无尿，其余犬的肾血流量和肾小球滤过率为正常的7%，而心输出量降至正常的37%。使用右旋糖酐40扩充血容量可轻松纠正心输出量不足，但肾血流量和肾小球滤过率仍低于正常的25%。当腹内压从0升高到20 mmHg时，肾血管阻力增加了555%，是全身血管阻力增加的15倍。这表明腹内压升高导致的肾功能损害是由直接肾压迫引起的局部现象，与心输出量无关。
