Background: The origin of cardiac impairment during brain death (BD) is controversial. Using a pig experimental model we sought to assess hormonal changes during the first stage of brain death and how these changes contribute to hemodynamic alteration and myocardial dysfunction.
Methods: Twenty-two pigs were randomized into 2 groups: a control (C) group and a BD group. BD was induced by sub-dural inflation of a balloon catheter. Micromanometers and ultrasonic flow probes were placed on the myocardium to measure cardiovascular parameters. Blood samples and hemodynamic parameters were analyzed before and after induction of BD.
Results: A biphasic release of catecholamines was observed, with an initial peak occurring 1 minute after BD induction, followed by a second peak at 60 minutes. Similarly, a biphasic evolution of dP/dt(max) and systolic blood pressure (SBP) was observed at BD, in parallel with catecholamine evolution. In the BD group, both cortisol and aldosterone decreased progressively over time. Circulating triiodothyronine (T3), levothyroxine (T4), prolactin and melatonin concentrations were similar to those of the control group. The difference in arteriovenous (AV) lactate level in arterial and coronary sinus blood was not significantly different between the 2 groups, suggesting an absence of myocardial ischemia. Furthermore, myocardial contractility was not altered during the 3 hours of BD.
Conclusions: During the initial period after induction of brain death, cerebral and thyroid hormones remained stable while cortico- and medullo-surrenal hormones varied significantly. We suggest that suprarenal gland impairment is among the first events occurring during brain death. Paradoxically, hemodynamic parameters and myocardial function were not found to be altered.