Initial hepatosplanchnic blood flow distribution and oxygen metabolism in experimental model of hypotensive brain death
Fabio A. De Luca, Ruy J. Cruz Jr., Alejandra del Pilar Gallardo Garrido, Ricardo Prist, Mauricio Rocha-e-Silva
Ann Transplant 2009; 14(1): 38-46
Background: Organs from the so-called marginal donors have been used with a significant higher risk of primary non function than organs retrieved from the optimal donors. We investigated the early metabolic changes and blood flow redistribution in splanchnic territory in an experimental model that mimics marginal brain-dead (BD) donor.
Material/Methods: Ten dogs (21.3±0.9 kg), were subjected to a brain death protocol induced by subdural balloon inflation and observed for 30 min thereafter without any additional interventions. Mean arterial and intracranial pressures, heart rate, cardiac output (CO), portal vein and hepatic artery blood flows (PVBF and HABF, ultrasonic flowprobe), and O[sub]2[/sub]-derived variables were evaluated.
Results: An increase in arterial pressure, CO, PVBF and HABF was observed after BD induction. At the end, an intense hypotension with normalization in CO (3.0±0.2 vs. 2.8±2.8 L/min) and PVBF (687±114 vs. 623±130 ml/min) was observed, whereas HABF (277±33 vs. 134±28 ml/min, p<0.005) remained lower than baseline values.
Conclusions: Despite severe hypotension induced by sudden increase of intracranial pressure, the systemic and splanchnic blood flows were partially preserved without signs of severe hypoperfusion (i.e. hyperlactatemia). Additionally, the HABF was mostly negatively affected in this model of marginal BD donor. Our data suggest that not only the cardiac output, but the intrinsic hepatic microcirculatory mechanism plays a role in the hepatic blood flow control after BD.
Keywords: Brain Death, hemodynamic, Female, metabolic effects, Ischemic Postconditioning