Elwyn D H, Parikh H C, Stahr L J, Kim S I, Shoemaker W C
Am J Physiol. 1976 Aug;231(2):377-86. doi: 10.1152/ajplegacy.1976.231.2.377.
Arterial concentrations and net organ metabolism of amino acids (AA), O2, CO2, H+, and glucose (Glc) were measured in two dogs before and during hemorrhage and after blood replacement. Shock caused increased splanchnic and decreased peripheral blood flow and O2 consumption. Po2 decreased more in hepatic venous than in mixed venous blood. pH fell in hemorrhage and increased with retransfusion. Increased liver output and arterial concentration of Glc were observed during hemorrhage. Differences between animals correlated with nutritional status. Blood concentrations of most AA showed little change during hemorrhage but increased after retransfusion. In contrast, arginine concentrations declined sharply. Peripheral output and hepatic uptake of most AA occurred during the control period. During shock, peripheral output and hepatic uptake of total AA and most individual AA declined progressively; after retransfusion peripheral uptake and hepatic output of many AA occurred. By contrast, peripheral output and hepatic uptake increased for alanine, glutamine, serine, phenylalanine, and tyrosine. After retransfusion net transport of some compounds occurred from periphery to liver; others, from liver to periphery. During shock, hepatic protein catabolism increased. and this catabolism, accompanied by decreased hepatic uptake (increased hepatic output), seemed the main cause of increased blood AA concentrations. Protein catabolism in peripheral tissue was not a cause of increased blood concentrations. Pathological changes in pH, Po2, and blood flow, occurred early in hemorrhage. In contrast, changes in AA movements and concentrations were within normal limits until late in shock.
在两只狗身上测量了出血前、出血期间及输血后氨基酸（AA）、氧气（O₂）、二氧化碳（CO₂）、氢离子（H⁺）和葡萄糖（Glc）的动脉浓度及器官净代谢情况。休克导致内脏血流量增加，外周血流量及氧气消耗减少。肝静脉血中Po₂的下降幅度大于混合静脉血。出血时pH下降，输血后pH上升。出血期间观察到肝脏葡萄糖输出及动脉葡萄糖浓度增加。动物之间的差异与营养状况相关。大多数氨基酸的血液浓度在出血期间变化不大，但输血后升高。相比之下，精氨酸浓度急剧下降。在对照期，大多数氨基酸出现外周输出及肝脏摄取。休克期间，总氨基酸及大多数单个氨基酸的外周输出及肝脏摄取逐渐下降；输血后，许多氨基酸出现外周摄取及肝脏输出。相比之下，丙氨酸、谷氨酰胺、丝氨酸、苯丙氨酸和酪氨酸的外周输出及肝脏摄取增加。输血后，一些化合物从外周向肝脏发生净转运；其他化合物则从肝脏向外周转运。休克期间，肝脏蛋白质分解代谢增加，这种分解代谢伴随着肝脏摄取减少（肝脏输出增加），似乎是血液氨基酸浓度升高的主要原因。外周组织中的蛋白质分解代谢并非血液浓度升高的原因。pH、Po₂和血流量的病理变化在出血早期就已出现。相比之下，氨基酸转运和浓度的变化在休克晚期之前都在正常范围内。
