McCoy S, Case S A, Swerlick R A, Bailey A A, Drucker W R
Am Surg. 1977 Dec;43(12):787-93.
Many mechanisms, including alterations in muscle metabolism, cellular damage, decreased blood volume, and hepatic disfunction, are influential in producing the observed progressive rise in the concentration of amino acids in arterial and venous blood during persisting hypovolemic shock. The rapid rise of venous and arterial concentrations of amino acids and the increase in venoarterial concentration difference suggest that hypovolemia causes a net release from muscle of a potential substrate for energy metabolism. The blood flow through peripheral tissues, however, is reduced to such an extent during hypovolemic shock that the net rate of release of amino acids is not greater than preshock release and may be less. Therefore, the homeostatic advantages served by the alteration in protein metabolism during the more chronic stresses of starvation or after injury may not obtain during acute hypovolemia.
许多机制，包括肌肉代谢改变、细胞损伤、血容量减少和肝功能障碍，在持续性低血容量性休克期间动脉血和静脉血中氨基酸浓度持续进行性升高的过程中发挥着作用。静脉血和动脉血中氨基酸浓度的迅速升高以及动静脉浓度差的增加表明，低血容量导致肌肉净释放一种能量代谢的潜在底物。然而，在低血容量性休克期间，流经外周组织的血流量减少到如此程度，以至于氨基酸的净释放率不高于休克前的释放率，甚至可能更低。因此，在饥饿或受伤等更慢性应激期间蛋白质代谢改变所带来的稳态优势，在急性低血容量时可能无法实现。
