Soini H O, Takala J, Nordin A J, Mäkisalo H J, Höckerstedt K A
Department of Intensive Care, Kuopio University Hospital, Finland.
Crit Care Med. 1992 Sep;20(9):1330-4. doi: 10.1097/00003246-199209000-00022.
Hepatic dysfunction after severe hemorrhagic shock is common and may be a consequence of visceral tissue hypoxia. Peripheral tissue PO2 has been suggested to correlate with the development of visceral hypoxia. To test the hypothesis that changes in peripheral tissue PO2 reflect changes in hepatic PO2, we measured subcutaneous PO2, transcutaneous PO2, transconjunctival PO2, and liver tissue PO2, and their relationship with changes in mean arterial blood pressure (MAP) and systemic oxygen transport (DO2), during progressive bleeding in pigs (n = 23). In addition to the tissue PO2, portal vein PO2 and circulating lactate concentrations were also measured in six of the animals. The animals were anesthetized and bled to an MAP of 50 mm Hg within 1 hr.
After an induced 10% reduction of MAP, only the DO2 decreased significantly (p less than .05). After a 20% reduction of MAP, the DO2 decreased further and was associated with a significant (p less than .05) reduction of all peripheral tissue PO2 values. A significant (p less than .05) reduction of liver tissue PO2 was observed later during bleeding, after induction of a 30% reduction in MAP. In the subgroup with portal venous PO2 and lactate measurements, reductions of all peripheral tissue PO2 and portal venous PO2 values occurred after a 20% reduction (p less than .05) of MAP. An increase (p less than .05) in the portal venous lactate concentration was observed after a 50% reduction of MAP, and a decrease (p less than .05) in liver tissue PO2 was noted after a 60% reduction of MAP.
Reductions of both peripheral and portal venous PO2 values occur early during hemorrhage. The liver tissue PO2, though initially low, appears to be better defended, suggesting either redistribution of splanchnic blood flow or adaptation in hepatic oxygen demand.
严重失血性休克后肝功能障碍很常见，可能是内脏组织缺氧的结果。有研究表明外周组织氧分压与内脏缺氧的发生相关。为验证外周组织氧分压的变化反映肝脏氧分压变化这一假说，我们在猪（n = 23）进行渐进性出血过程中，测量了皮下氧分压、经皮氧分压、经结膜氧分压和肝组织氧分压，以及它们与平均动脉血压（MAP）和全身氧输送（DO2）变化的关系。除了组织氧分压外，还对6只动物测量了门静脉氧分压和循环乳酸浓度。动物麻醉后在1小时内将MAP降至50 mmHg。
MAP诱导降低10%后，仅DO2显著降低（p <.05）。MAP降低20%后，DO2进一步降低，并与所有外周组织氧分压值显著降低（p <.05）相关。在MAP降低30%后，出血后期观察到肝组织氧分压显著降低（p <.05）。在测量门静脉氧分压和乳酸的亚组中，MAP降低20%后，所有外周组织氧分压和门静脉氧分压值均降低（p <.05）。MAP降低50%后，门静脉乳酸浓度升高（p <.05），MAP降低60%后，肝组织氧分压降低（p <.05）。
出血早期外周和门静脉氧分压值均降低。肝组织氧分压虽然最初较低，但似乎得到了更好的维持，提示内脏血流重新分布或肝脏氧需求发生适应。
