TY - JOUR
T1 - Impairment of coronary flow reserve and left ventricular function in the brain-dead canine heart
AU - Oishi, Yasuhisa
AU - Nishimura, Yosuke
AU - Imasaka, Ken Ichi
AU - Kajihara, Noriyoshi
AU - Morita, Shigeki
AU - Masuda, Munetaka
AU - Yasui, Hisataka
N1 - Funding Information:
This study was supported by grants-in-aid for Scientific Research (11671331) from the Ministry of Education, Science and Culture of Japan. The authors thank Ms Yoko Kikutake and Ms Aki Takao for technical assistance.
PY - 2003/9/1
Y1 - 2003/9/1
N2 - 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.
AB - 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.
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U2 - 10.1016/S1010-7940(03)00329-4
DO - 10.1016/S1010-7940(03)00329-4
M3 - Article
C2 - 12965312
AN - SCOPUS:0041761115
VL - 24
SP - 404
EP - 410
JO - European Journal of Cardio-thoracic Surgery
JF - European Journal of Cardio-thoracic Surgery
SN - 1010-7940
IS - 3
ER -