ALTERATIONS IN LIVER HEMODYNAMICS IN AN INTACT PORCINE MODEL OF ENDOTOXIN-SHOCK
ALTERATIONS IN LIVER HEMODYNAMICS IN AN INTACT PORCINE MODEL OF ENDOTOXIN-SHOCK
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DOI：
10.1152/ajpheart.1995.268.3.h1106
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发表时间：
1995-03-01
影响因子：
4.8
通讯作者：
ROBOTHAM, JL
中科院分区：
文献类型：
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作者：
AYUSE, T;BRIENZA, N;ROBOTHAM, JL
感染性休克降低前负荷，增加内脏血液淤积和水肿形成，并诱发肝功能障碍。我们假设内毒素休克对门静脉 (PV) 和肝动脉 (HA) 血管床的血流动力学影响促成了这一情况。生成多点压力-流量关系，以评估完整猪内毒素血症模型中每个床的斜率（阻力或电导）和有效背压（P-back）。在内毒素血症期间测定 300 分钟以上的斜率和 P-back (n = 8)，并与假治疗对照研究 (n = 5) 进行比较。在时间 (t) = 60 分钟时，HA 斜率显着下降 (P < 0.05)，而 P-back 没有变化。 HA 缓冲响应 (HABR) 定义为因 PV 流量 (Q(pv)) 减少而产生的 HA 阻力降低，在 t = 90 分钟时被废除。 PV P-back 显着增加，而 PV 斜率没有变化。在 t = 300 分钟时，HA 斜率恢复到基线，并且存在 HABR，同时 PV 斜率和 P-back 增加（P < 0.05）。除了 t = 60 分钟时 HA 分数流量短暂增加外，分数流量（相对于心输出量的流量）保持恒定。组织学研究显示局灶性坏死和出血，但没有血管收缩或血栓形成的证据。总之，内毒素休克导致 Q(pv) 时间依赖性损伤，PV 阻力增加，导致内脏血液汇集增加，随后静脉回流减少。当 HABR 不存在时，HA 床会提前扩张。后来出现了 HABR，但定义为给定 Q(pv) 下 HA 电阻的增加。这些血流动力学稳态的改变有助于解释脓毒症中内脏床的具体参与、肝功能障碍的高发生率，以及如果推广到其他器官床，则有助于解释脓毒症中动脉和静脉室的作用。
Septic shock decreases preload, increases splanchnic blood pooling and edema formation, and induces hepatic dysfunction. We hypothesized that the hemodynamic effects of endotoxemic shock on the portal venous (PV) and hepatic arterial (HA) vascular beds contribute to this picture. Multipoint pressure-flow relationships were generated to evaluate the slope (resistance or conductance) and effective back pressure (P-back) in each bed in an intact porcine model of endotoxemia. Slope and P-back were determined during endotoxemia over 300 min (n = 8) and compared with sham-treated control studies (n = 5). At time (t) = 60 min, HA slope significantly decreased (P < 0.05) without a change in P-back. The HA buffer response (HABR), defined as a decrease in HA resistance produced by reduction in PV flow (Q(pv)), was abolished at t = 90 min. The PV P-back significantly increased without a change in PV slope. At t = 300 min, HA slope returned to baseline, and the HABR was present while PV slope and P-back increased (P < 0.05). Fractional flow (flow relative to cardiac output) was constant except for a transient increase in HA fractional flow at t = 60 min. Histological studies showed focal necrosis and hemorrhage without evidence of vasoconstriction or thrombosis. In conclusion, endotoxic shock leads to time-dependent impairment of Q(pv) with increased PV resistance, causing an increase in splanchnic blood pooling and subsequent decrease in venous return. The HA bed is dilated early with an absent HABR. Later an HABR is present but defined by increased HA resistance for a given Q(pv). These alterations in hemodynamic homeostasis help to account for the specific involvement of the splanchnic bed in septic shock, the high incidence of liver dysfunction, and, if generalized to other organ beds, the roles of arterial and venous compartments in sepsis.