Does brain death induce a pro‐inflammatory response at the organ level in a porcine model?

Abstract

In this porcine model, brain death induced a severe metabolic response in peripheral blood. At the organ level, however, there was no difference in the cytokine response between the groups.

Paradoxical effects of brain death and associated trauma on rat mesenteric microcirculation: an intravital microscopic study

“…To evaluate the role of BD-associated trauma, matching sham-operated rats were assessed over time. As described previously, BD leads to an increase in the MAP followed by hypotension (6,10), both of which compromise organ perfusion (11). Our study demonstrates that BD-associated trauma did not influence hemodynamic and perfusion parameters, suggesting that all of the observed changes in MAP and mesenteric hypoperfusion were triggered by the BD itself.…”

“…In acute evaluations of human BD, catecholamine levels were above normal values immediately after the BD event and remained higher after several hours, with increased inflammatory responses and apoptosis being observed in different organ samples (1,6,7). In a rodent model of heart transplantation, a longer duration of BD leads to increased leukocyte infiltration and expression of adhesion molecules on the endothelial cells of the transplanted graft, thereby resulting in accelerated acute rejection (8).…”

Standardized experimental brain death model for studies of intracranial dynamics, organ preservation, and organ transplantation in the pig*

“…R ecent advancements in transplantation research have revealed that organs undergo influences by inflammation and catecholamines after brain death (BD) of the donor, and that these effects might affect the outcome of the transplantation (1)(2)(3)(4). To study these issues, there is a need for a clinical relevant BD model.…”

Brain death and its implications for management of the potential organ donor

“…Both the sympathetic storm and the hemodynamic instability following brain death seem to be involved in these processes because they can be attenuated experimentally by a-receptor blockade during brain death avoiding the hypertensive crisis, and by norepinephrine or volume loading after brain death avoiding the subsequent hemodynamic instability. 28,[60][61][62] Both the sympathetic storm and the subsequent hemodynamic instability may lead to hypoperfusion and ischemia in various organs and consequently activate the cytokine system. Several cytokines have been found in brain tissue and cerebrospinal fluid after brain injury and through a defective blood-brain barrier, they may reach the circulation and stimulate target cells in the blood and somatic organs.…”