Impairment of blood volume restitution after large hemorrhage: a mathematical model.
Impairment of blood volume restitution after large hemorrhage: a mathematical model.
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大出血后血容量恢复受损：数学模型。
DOI：
10.1152/ajpregu.1996.270.5.r1163
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发表时间：
1996
期刊：
影响因子：
--
通讯作者：
Gann,DS
中科院分区：
文献类型：
--
作者：
Carlson,DE;Kligman,MD;Gann,DS
一个数学模型测试了随着血浆渗透压变化的增加，大出血（> 26%）后血容量恢复渐进式失败的可能机制。在出血10%后，模型要求净静水毛细管压力降低，溶质释放到细胞外空间，并从与间质平衡的结合池中释放Na+和K+，以匹配实验数据。溶质和释放的阳离子扩张间质，在3 - 24小时内驱动体积和蛋白质的恢复。30%出血后，细胞膜上的Na(+)-K(+)-腺苷三磷酸酶（ATPase）在0.8 - 3小时内被抑制38.7%，毛细血管压力与血容量之间的比例比10%出血时降低68%，对平均实验反应的预测最好。当30%出血后血浆渗透压变化增加一倍时，atp酶的抑制作用增加到85%，并延长其持续时间至24小时，以符合实验结果。在大出血后可能出现钠转运的相关缺陷，使钠和水进入细胞。这种反应可能反对渗透驱动间质扩张，因此解释了恢复失败。
A mathematical model tests possible mechanisms for the progressive failure of blood volume restitution seen after larger hemorrhages ( > 26%) with increasing changes in plasma osmolality. After 10% hemorrhage, the model requires a decrease in net hydrostatic capillary pressure, the release of solute into the extracellular space, and the release of Na+ and K+ from a bound pool in equilibrium with the interstitium to match the experimental data. The solute and released cations expand the interstitium to drive the restitution of volume and protein from 3 to 24 h. After 30% hemorrhage, the best prediction of the average experimental responses occurs when the Na(+)-K(+)-adenosinetriphosphatase (ATPase) in the cell membrane is inhibited by 38.7% from 0.8 to 3 h, and the proportionality between capillary pressure and blood volume is reduced by 68% from its value for 10% hemorrhage. When the change in plasma osmolality is doubled after 30% hemorrhage, an increase in the inhibition of the ATPase to 85% and extension of its duration to 24 h are necessary to match experimental findings. The associated defect in sodium transport may occur after large hemorrhage so that sodium and water move into cells. This response may oppose osmotically driven expansion of the interstitium and thus account for the failure of restitution.