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Primary Outcome Assessment in a Pig Model of Acute Myocardial Infarction
Published on: October 14, 2016
Impairment of coronary flow reserve and left ventricular function in the brain-dead canine heart
Yasuhisa Oishi1, Yosuke Nishimura, Ken-ichi Imasaka
1Department of Cardiovascular Surgery, Faculty of Medicine, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan.
Insights
Brain death impairs coronary circulation, reducing coronary flow reserve. This compromised coronary artery function contributes to cardiac dysfunction after brain death, hindering recovery.
Area of Science:
- Cardiovascular Physiology
- Neurocritical Care
Background:
- Cardiac dysfunction is a known complication of brain death.
- The role of coronary circulation in this dysfunction remains unclear, despite theories of massive catecholamine release.
Purpose of the Study:
- To investigate alterations in coronary artery function post-brain death.
- To determine the contribution of coronary circulation changes to overall hemodynamic deterioration in a canine model.
Main Methods:
- Brain death was induced using a subdural balloon catheter in dogs.
- Hemodynamic parameters, left ventricular contractility (pressure-volume relations), and coronary flow reserve were assessed.
- Coronary vasodilation responses to acetylcholine and sodium nitroprusside were measured before and after brain death induction.
Main Results:
- Transient hyperdynamic response followed by decreased cardiac output and coronary blood flow.
- Significant deterioration in left ventricular contractility by 60 minutes post-brain death.
- Reduced coronary flow reserve and increased coronary resistance were observed at 30 and 60 minutes after brain death induction.
Conclusions:
- Brain death leads to impaired coronary flow reserve in canines.
- Compromised coronary circulation is implicated in the development and persistence of cardiac dysfunction following brain death.
Objective:
The mechanisms of cardiac dysfunction after brain death, which are thought to be mainly associated with massive catecholamine release, have not been fully elucidated, especially with respect to the coronary circulation. The aim of this study was to investigate the changes in function of the coronary artery and its contribution to hemodynamic deterioration in a canine brain death model.
Methods:
Brain death was induced by rapid inflation of a subdurally placed balloon catheter. Hemodynamic measurements including assessment of left ventricular contractility using pressure-volume relations and biochemical analyses of blood samples were performed in seven dogs. Coronary flow reserve in the same brain death model was assessed by changes in coronary flow and resistance induced by administering a vasodilator directly into the coronary artery in another eight dogs.
Results:
A hyperdynamic response was transiently observed after induction of brain death, followed by decreases in arterial pressure, cardiac output, and coronary blood flow. Parameters of left ventricular contractility as measured by pressure-volume relations had significantly deteriorated by 60 min after brain death. Percent changes in coronary flow by administration of acetylcholine and sodium nitroprusside were 272 and 209%, respectively, before brain death; these were decreased to 178 and 145% at 30 min after brain death, and to 192 and 153% at 60 min. Coronary resistance ratios were also significantly increased at 30 and 60 min after brain death.
Conclusions:
Impairment of coronary flow reserve was found in the brain-dead canine heart. This impaired coronary circulation may constitute a disadvantage of prevention and recovery of cardiac dysfunction after induction of brain death.
