Biphasic response after brain death induction: Prominent part of catecholamines release in this phenomenon

Background: The physiopathology of hemodynamic instability that occurs afte r brain death remains unknown. The aim of this study was to examine the ini tial response to brain death induction. Methods: After anesthesia and monitoring, 16 pigs were randomized into a co ntrol group (C, n = 8) and a brain death group (BD, n = 8). We inflated a s ubdural catheter balloon to induce brain death. We analyzed hemodynamic and plasmatic biochemical data for 180 minutes after brain death induction. En ergetic compounds were measured. We expressed the results in comparison wit h the C group. Results: The C group remained stable. One minute after brain death, the Gus hing reflex appeared, with a hyperdynamic response to plasma catecholamines levels increasing (norepinephrine and epinephrine, 3.1-fold, p = 0.02, and 3.8-fold, p = 0.07, respectively). After a return to baseline, we recorded a second hyperdynamic profile 120 minutes later. At this time, a second pe ak of catecholamines appeared (6.3-fold, p = 0.04, and 9.1-fold, p = 0.02, concerning norepinephrine and epinephrine). At the same time, we observed b rief myocardial lactate production (+175%, p < 0.01), with a rise of tropon ine I (+64%, p = 0.03). The energetic index was similar in both groups: 0.8 5 (+/-0.02) in the C group vs 0.87 (+/-0.02) in the ED group. Conclusions: In this model, biphasic plasmatic catecholamine release appear s to primarily explain the physiopathology of the hemodynamic response to b rain death induction.