Normann N A, Taylor A A, Crawford E S, DeBakey M E, Saleh S A
J Surg Res. 1983 Feb;34(2):97-103. doi: 10.1016/0022-4804(83)90047-1.
During graft replacement of descending thoracic and thoracoabdominal aneurysms, aortic cross clamping without the use of bypass or shunts is accompanied by underperfusion of distal vascular beds. This study, comprising 10 patients, was based on the hypothesis that ischemia of the lower spinal cord and adrenal glands might precipitate release of catecholamines. Arterial blood samples, obtained before (control), during, and after arterial cross clamping, were analyzed for epinephrine (E) and norepinephrine (NE). The E/NE ratio was used as an index of ischemic sympathoadrenal activation. During cross clamping, mean E and E/NE increased by a factor of 4.5 (P = 0.03) and 2.4 (P = 0.001), respectively. The greatest increases were observed in the 5 min postclamp sample: relative to control, mean E increased 22-fold (P = 0.011), NE 3-fold (P = 0.009), and E/NE 8.4-fold (P = 0.013). During the immediate postclamp period, mean E/NE fell exponentially with an average "half-life" of 12.05 +/- 5.83 min (SD). A second-order polynomial related (P = 0.004) log E/NE in first postclamp sample to the ratio between clamp time and mean proximal arterial pressure during clamping (T/AP). Left-ventricular-minute-work-function correlations: (1) positive with log E during clamping (P = 0.043); and (2) none with log E (P = 0.563) or log (E + NE) (P = 0.641) 5 min post-clamp; (3) positive with log (E + NE) 30 min post-clamp (P = 0.016). It is concluded that (1) distal ischemia caused by cross clamping the descending thoracic aorta without bypass or shunts, results in distal regional sympathoadrenal activation, independent of known central reflex mechanisms; (2) this activation leads to marked increases of E/NE and is, in part, dependent upon T/AP during clamping; (3) the activation is probably transitory; (4) by indirect evidence, cardiodepressant factor(s) may transiently be present following declamping; (5) by its magnitude, sympathoadrenal activation is likely to provide compensation for deleterious factors that may affect cardiovascular functions during cross clamping and after declamping; alternatively, it might contribute to postoperative hypertension and cardiac complications such as myocardial ischemia and arrhythmias.
在胸降主动脉和胸腹主动脉瘤的移植物置换过程中，不使用旁路或分流器进行主动脉交叉钳夹会伴随着远端血管床灌注不足。本研究纳入了10例患者，基于以下假设：脊髓下部和肾上腺的缺血可能促使儿茶酚胺释放。采集动脉交叉钳夹前（对照）、钳夹期间和钳夹后的动脉血样本，分析肾上腺素（E）和去甲肾上腺素（NE）。E/NE比值用作缺血性交感肾上腺激活的指标。在交叉钳夹期间，平均E和E/NE分别增加了4.5倍（P = 0.03）和2.4倍（P = 0.001）。在钳夹后5分钟的样本中观察到最大增幅：相对于对照，平均E增加了22倍（P = 0.011），NE增加了3倍（P = 0.009），E/NE增加了8.4倍（P = 0.013）。在钳夹后即刻，平均E/NE呈指数下降，平均“半衰期”为12.05±5.83分钟（标准差）。一个二阶多项式将钳夹后第一个样本中的log E/NE与钳夹时间和钳夹期间平均近端动脉压的比值（T/AP）相关联（P = 0.004）。左心室分钟作功函数相关性：（1）在钳夹期间与log E呈正相关（P = 0.043）；（2）在钳夹后5分钟与log E（P = 0.563）或log（E + NE）（P = 0.641）无相关性；（3）在钳夹后30分钟与log（E + NE）呈正相关（P = 0.016）。得出以下结论：（1）在不使用旁路或分流器的情况下对胸降主动脉进行交叉钳夹所导致的远端缺血，会导致远端区域交感肾上腺激活，独立于已知的中枢反射机制；（2）这种激活导致E/NE显著增加，并且部分取决于钳夹期间的T/AP；（3）这种激活可能是短暂的；（4）通过间接证据表明，松开钳夹后可能短暂存在心脏抑制因子；（5）就其程度而言，交感肾上腺激活可能为在交叉钳夹期间和松开钳夹后可能影响心血管功能的有害因素提供补偿；或者，它可能导致术后高血压和心脏并发症，如心肌缺血和心律失常。
