Hemodynamic differences between alcoholic and nonalcoholic cirrhotics following distal splenorenal shunt--effect on survival?
Hemodynamic differences between alcoholic and nonalcoholic cirrhotics following distal splenorenal shunt--effect on survival?
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远端脾肾分流术后酒精性和非酒精性肝硬化之间的血流动力学差异——对生存的影响？
DOI：
10.1097/00000658-198309000-00009
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发表时间：
1983
影响因子：
9
通讯作者：
W. Warren
中科院分区：
文献类型：
--
作者：
J. Henderson;W. Millikan;L. Wright;M. Kutner;W. Warren
与酒精性肝硬化患者（45%）相比，远端脾肾分流术显著提高了非酒精性肝硬化患者（70%）静脉曲张出血的5年生存率。本研究量化了16名酒精性患者与8名非酒精性患者在DSRS后第一年发生的血流动力学差异。非酒精性患者（8例中的7例）的门静脉血流灌注明显好于酒精性患者（16例中的4例）（p <0.01）。与非酒精组相比，酒精组的平均肝血流量（p <0.07）、流量/单位肝脏体积（p <0.05）和执行特定肝细胞功能所需的流量（p <0.05）均显著增加。酒精性患者的心输出量显著增加（p <0.05），但非酒精性患者无变化。酒精中毒患者分为两个亚组，11例显示流量增加（1082 +/- 260至1496 +/- 388 ml/min），5例未显示流量增加（1246 +/- 269至994 +/- 159 ml/min）。前者的肝细胞功能显著较差（p <0.05），1年时的流量/单位体积和流量/单位功能显著增加（p <0.05），这可能有助于维持肝细胞的完整性。后者，在平行的非酒精性患者，这些参数没有显着变化，并保持了良好的功能性肝细胞质量。这些数据使我们假设：1）酒精性肝损伤导致DSRS后门静脉灌注丧失的风险增加，2）随着肝细胞功能福尔斯下降，酒精性患者的肝动脉血流最初增加，由心输出量增加触发，3）进行性损伤和/或代偿性血流动力学机制失败导致酒精性患者的早期死亡。相比之下，非酒精性肝硬化患者保留了门静脉灌注，并在定量和定性上维持了肝血流，保留了肝细胞功能，提高了生存率。
The distal splenorenal shunt significantly improves 5-year survival from variceal bleeding in nonalcoholic (70%) compared to alcoholic (45%) cirrhosis patients. This study quantitates hemodynamic differences occurring in the first year after DSRS in 16 alcoholic compared to eight nonalcoholic patients. Portal venous perfusion was retained significantly better (p less than .01) by the nonalcoholic (seven of eight) than by the alcoholic (four of sixteen) patients. Mean liver blood flow (p less than 0.07), flow/unit liver volume (p less than .05), and flow required to perform a specific hepatocyte function (p less than 0.05) all increased significantly in the alcoholic compared to nonalcoholic group. Cardiac output increased significantly in the alcoholic patients (p less than 0.05), but was unchanged in the nonalcoholic patients. The alcoholic patients divided into two subsets, 11 who showed increase in flow (1082 +/- 260 to 1496 +/- 388 ml/min) and five who did not (1246 +/- 269 to 994 +/- 159 ml/min). The former had significantly (p less than 0.05) poorer hepatocyte function and had a significant (p less than 0.05) increase in flow/unit volume and flow/unit function at 1 year, which may have helped to maintain hepatocyte integrity. The latter, in parallel with the nonalcoholic patients, showed no significant change in these parameters and maintained a good functional hepatocyte mass. These data lead us to hypothesize that: 1) alcoholic liver injury has an increased risk of leading to loss of portal perfusion after DSRS, 2) as hepatocyte function falls, there is initial increase in hepatic arterial flow in alcoholic patients, triggered by increase in cardiac output, and 3) progressive injury and/or failure of the compensatory hemodynamic mechanism leads to earlier mortality in alcoholic patients. In contrast, the nonalcoholic cirrhosis patients preserve portal perfusion and maintain liver blood flow, both quantitatively and qualitatively, with retained hepatocyte function and improved survival.