Brain death impairs microcirculation with or without autonomic storm: an intravital microscopy study with thoracic epidural anesthesia in rats
Isaac Azevedo Silva1, Rafael Simas1, Laura Menegat1, Cristiano de Jesus Correia1, Sueli Gomes Ferreira1, Paulina Sannomiya1, Luiz Felipe Pinho Moreira1
1Heart Institute (InCor), University of Sao Paulo Medical School, Sao Paulo, Brazil
Introduction: Brain death (BD) is associated with hemodynamic instability, inflammation and mesenteric hypoperfusion[1]. In a previous study, thoracic epidural anesthesia (TEA) blocked the hypertensive crisis and the hemodynamic instability, without inflammatory response attenuation[2]. The present study aimed to evaluate the influence of sympathetic blockade in mesenteric perfusion in brain dead rats.
Methods: Male Wistar rats were anesthetized with isoflurane (5-2%) and underwent BD by intracranial catheter insufflation immediately after epidural infusion of bupivacaine (Bupi) or saline. Mean arterial pressure (MAP) was monitored over 3h. The mesenteric microcirculation was assessed by intravital microscopy. In the same time point, the expression of mesenteric ICAM-1 was quantified by immunohistochemistry and the serum corticosterone level was determined by ELISA. Sham-operated rats (SH group) was trepanned only. Results are presented as mean±SEM.
Results: The autonomic storm was abolished in Bupi group (p<0.001), however, the percentage of perfused mesenteric microvessels was similar between the study groups and significantly lower than SH (Bupi: 43±6%, saline: 39±7%; SH: 74±6%. p=0.002). The expression of ICAM-1 was similar between the study groups (Bupi: 21±5; Saline: 23±8), but higher than the SH (9±2 mean fluorescence intensity, p<0.001). Serum levels of corticosterone was lower in Bupi and Saline groups compared with SH (p=0.01).
Conclusions: TEA with bupivacaine was effective in abolishing the autonomic storm, however, tissue hypoperfusion, elevated expression of adhesion molecules, and the low serum corticosterone, triggered by BD remained in the animals independently to hemodynamic status. Therefore, inhibition of the hypertensive peak in BD does not improve mesenteric perfusion and does not modulate the endothelial activation.
Finnacial Support: FAPESP.