Abstract

Objective: Coronary vasospasms might induce multifocal histological damage, seen in hearts after brain death. We investigated the effect of brain death on coronary vasoreactivity towards serotonin, in pathophysiologically relevant concentrations.

Methods: Brain death was induced in dogs by sudden inflation of an intracranial balloon. One hour after brain death or sham operation (n = 2 × 7), coronary segments were harvested and suspended in an organ chamber, connected to a force transducer. Serotonin (10^-7 to 10^-5 mol/l) was added in quiescent rings and rings preconstricted with 2.10^-6 mol/l PGF_2α. To check the potential pathophysiological importance, the serotonin concentration was serially measured in dogs during brain death induction.

Results: In non-preconstricted coronary artery segments of brain dead dogs, serotonin induced a significant vasoconstriction, whereas in control segments only a very slight reaction was seen (fig 1; p < 0.001). After preconstriction, segments from brain dead dogs exhibited significantly less vasodilatation than control segments (fig 2; p < 0.001). This difference disappeared completely after incubation of the segments with the S₂-antagonist ketanserin. Free serotonin in coronary sinus blood increased from 87.9 ± 14.2 to 157.7 ± 10.64 nmol/l 10 min after brain death (p = 0.014), and the serotonin concentration exceeded 10^-7 mol/l in 4 out of 7 experiments.
 

Conclusion: Serotonin, in physiologically relevant concentrations, causes severe coronary vasoconstriction after brain death. This might importantly contribute to the histological damage and myocardial dysfunction seen in potential donor hearts.