Physiologic responses to severe hemorrhagic shock and the genesis of cardiovascular collapse: can irreversibility be anticipated?
Physiologic responses to severe hemorrhagic shock and the genesis of cardiovascular collapse: can irreversibility be anticipated?
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DOI：
10.1016/j.jss.2011.12.015
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发表时间：
2012-11
期刊：
影响因子：
--
通讯作者：
Pinsky MR
中科院分区：
文献类型：
--
作者：
Gómez H;Mesquida J;Hermus L;Polanco P;Kim HK;Zenker S;Torres A;Namas R;Vodovotz Y;Clermont G;Puyana JC;Pinsky MR
失血性休克（HS）时发生心血管性虚脱（CC）的原因尚不清楚。我们假设血管张力丧失是CC的特征，动脉脉压/每搏输出量指数比值或血管张力指数（VTI）可以识别CC。将14只Yorkshire-Durock猪流血的至30 mmHg平均动脉压，并通过重复放血保持在该水平，直至无法代偿（CC）或持续90 min（NoCC）。然后将其等份复苏至脱落体积并观察2小时。CC定义为MAP < 30 mmHg持续10 min或< 20 mmHg持续10 sec。在基线（B 0）、出血后30、60、90 min和复苏（R 0）、30和60 min时记录研究变量。猪流血的至总血量的32±9%。与CC猪相比，出血后NoCC中的肾上腺素（Epi）和VTI较低，并且没有变化，CC猪中两者均增加（分别为0.97±0.22至2.57±1.42 mcg/dl和173±181至939±474 mmHg/ml），尽管流血的量没有差异。乳酸增加率（LIR）随出血而增加，CC在R 0时更高，但在NoCC中无变化。VTI在CC之前将CC与NoCC以及幸存者与非幸存者区分开。在CC发生前，LIR的大幅度增加与VTI的减小相一致。在严重HS中，CC之前的血管舒张与LIR增加同时发生，这表明张力丧失是导致CC的机制，能量衰竭是其可能的原因。
The causes of cardiovascular collapse (CC) during hemorrhagic shock (HS) are unknown. We hypothesized that vascular tone loss characterizes CC, and that arterial pulse pressure/stroke volume index ratio or vascular tone index (VTI), would identify CC. 14 Yorkshire-Durock pigs were bled to 30 mmHg mean arterial pressure and held there by repetitive bleeding until rendered unable to compensate (CC) or for 90 min (NoCC). They were then resuscitated in equal parts to shed volume and observed for 2 h. CC was defined as a MAP < 30 mmHg for 10 min or < 20 mmHg for 10 sec. Study variables were recorded at Baseline (B0), 30, 60, 90 min after bleeding and at resuscitation (R0), 30, and 60 min afterward. Swine were bled to 32±9% of total blood volume. Epinephrine (Epi) and VTI were low and did not change in NoCC after bleeding as compared to CC swine, in which both increased (0.97±0.22 to 2.57±1.42 mcg/dl, and 173±181 to 939±474 mmHg/ml, respectively), despite no differences in bled volume. Lactate increase rate (LIR) increased with hemorrhage and was higher at R0 for CC, but did not vary in NoCC. VTI identified CC from NoCC and Survivors from Non-survivors before CC. A large increase in LIR was coincident with VTI decrement before CC occurred. Vasodilatation immediately prior to CC in severe HS occurs at the same time as an increase in LIR, suggesting loss of tone as the mechanism causing CC, and energy failure as its probable cause.
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影响因子：
8.8
作者：
Leverve, Xavier M.
通讯作者：
Leverve, Xavier M.
影响因子：
15.9
作者：
KEUNG, EC;LI, Q
通讯作者：
LI, Q
DOI：
10.1073/pnas.92.23.10688
发表时间：
1995-11-07
影响因子：
11.1
作者：
LAUBACH, VE;SHESELY, EG;SHERMAN, PA
通讯作者：
SHERMAN, PA
影响因子：
20.1
作者：
BERECEK, KH;BOHR, DF
通讯作者：
BOHR, DF
影响因子：
3.8
作者：
Crookes, BA;Cohn, SM;Proctor, KG
通讯作者：
Proctor, KG