Catecholamine release during and after cross clamping of descending thoracic aorta.

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.