BACKGROUND: Brain death results in a rapid decline in left ventricular function, which has clinical relevance for organ transplantation. The aim of the present study was to investigate coronary perfusion changes during brain death and their role in cardiac dysfunction. METHODS: In an in situ isolated canine heart model, brain death was induced by inflation of a subdural balloon catheter. The heart was perfused separately with the animal's own blood by a pressure-controlled roller pump that was coupled to the measured aortic pressure. Myocardial contractility was estimated by the slope of the end-systolic pressure-volume relation. RESULTS: Induction of brain death resulted in a transient hyperdynamic response, followed by a significant decrease in systemic vascular resistance, coronary blood flow, and the end-systolic pressure-volume relation (p<0.05). However, if coronary perfusion pressure was decoupled from aortic pressure and elevated to pre-brain death levels, coronary blood flow and the end-systolic pressure-volume relation were also restored to baseline levels. CONCLUSION: Severe impairment of coronary blood flow may contribute to decreased contractility after brain death that can be reversed by modulation of coronary perfusion pressure.
BACKGROUND:Brain death results in a rapid decline in left ventricular function, which has clinical relevance for organ transplantation. The aim of the present study was to investigate coronary perfusion changes during brain death and their role in cardiac dysfunction. METHODS: In an in situ isolated canine heart model, brain death was induced by inflation of a subdural balloon catheter. The heart was perfused separately with the animal's own blood by a pressure-controlled roller pump that was coupled to the measured aortic pressure. Myocardial contractility was estimated by the slope of the end-systolic pressure-volume relation. RESULTS: Induction of brain death resulted in a transient hyperdynamic response, followed by a significant decrease in systemic vascular resistance, coronary blood flow, and the end-systolic pressure-volume relation (p<0.05). However, if coronary perfusion pressure was decoupled from aortic pressure and elevated to pre-brain death levels, coronary blood flow and the end-systolic pressure-volume relation were also restored to baseline levels. CONCLUSION: Severe impairment of coronary blood flow may contribute to decreased contractility after brain death that can be reversed by modulation of coronary perfusion pressure.
Authors: Vijay Krishnamoorthy; Xenia Borbely; Ali Rowhani-Rahbar; Michael J Souter; Edward Gibbons; Monica S Vavilala Journal: Pediatr Crit Care Med Date: 2015-05 Impact factor: 3.624
Authors: Benjamin B Kenigsberg; Christopher F Barnett; Jeffrey C Mai; Jason J Chang Journal: Curr Neurol Neurosci Rep Date: 2019-11-13 Impact factor: 5.081