High Energy Compound Stability During Experimental Brain Death

R. Ferrera; J. Bopassa; C. Rodriguez; G. Baverel; M. Ovize

doi:10.1016/j.transproceed.2006.06.123

High Energy Compound Stability During Experimental Brain Death

R. Ferrera
, J. Bopassa
, C. Rodriguez
, G. Baverel
, M. Ovize

Research output: Contribution to journal › Article › peer-review

Abstract

The aim of this study was to examine the effect of sudden brain death (BD) on myocardial function and high energy phosphate (HEP) stores. BD was induced by cerebral vessel ligation in six swine (BD group) that were compared to six control swine. At the end of the BD period (3 hours), harvested hearts were stored at 4°C. Myocardial tissue HEP were assessed by: (i) ³¹P-NMR spectroscopy of left ventricle for phosphocreatine (PCr), adenosine triphosphate (ATP), inorganic phosphate (Pi) and intracellular pH (pHi), and by (ii) HPLC for ATP, ADP, and AMP levels in left ventricle biopsies. Brain death resulted in a instantaneous major increase in catecholamines (>50-fold, P < .001) and paradoxically a significant progressive decrease in the regional contractility of the left ventricle. After cardioplegia, no significant differences on HEP compounds (ATP/Pi, PCr/Pi, ATP, energetic index) or in pHi were observed between BD and control groups. These data suggest that early heart injury occuring during BD does not seem to be an ischemic phenomenon.

Original language	English (US)
Pages (from-to)	2285-2286
Number of pages	2
Journal	Transplantation Proceedings
Volume	38
Issue number	7
DOIs	https://doi.org/10.1016/j.transproceed.2006.06.123
State	Published - Sep 2006
Externally published	Yes

ASJC Scopus subject areas

Transplantation
Surgery

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10.1016/j.transproceed.2006.06.123

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title = "High Energy Compound Stability During Experimental Brain Death",

abstract = "The aim of this study was to examine the effect of sudden brain death (BD) on myocardial function and high energy phosphate (HEP) stores. BD was induced by cerebral vessel ligation in six swine (BD group) that were compared to six control swine. At the end of the BD period (3 hours), harvested hearts were stored at 4°C. Myocardial tissue HEP were assessed by: (i) 31P-NMR spectroscopy of left ventricle for phosphocreatine (PCr), adenosine triphosphate (ATP), inorganic phosphate (Pi) and intracellular pH (pHi), and by (ii) HPLC for ATP, ADP, and AMP levels in left ventricle biopsies. Brain death resulted in a instantaneous major increase in catecholamines (>50-fold, P < .001) and paradoxically a significant progressive decrease in the regional contractility of the left ventricle. After cardioplegia, no significant differences on HEP compounds (ATP/Pi, PCr/Pi, ATP, energetic index) or in pHi were observed between BD and control groups. These data suggest that early heart injury occuring during BD does not seem to be an ischemic phenomenon.",

author = "R. Ferrera and J. Bopassa and C. Rodriguez and G. Baverel and M. Ovize",

year = "2006",

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T1 - High Energy Compound Stability During Experimental Brain Death

AU - Ferrera, R.

AU - Bopassa, J.

AU - Rodriguez, C.

AU - Baverel, G.

AU - Ovize, M.

PY - 2006/9

Y1 - 2006/9

N2 - The aim of this study was to examine the effect of sudden brain death (BD) on myocardial function and high energy phosphate (HEP) stores. BD was induced by cerebral vessel ligation in six swine (BD group) that were compared to six control swine. At the end of the BD period (3 hours), harvested hearts were stored at 4°C. Myocardial tissue HEP were assessed by: (i) 31P-NMR spectroscopy of left ventricle for phosphocreatine (PCr), adenosine triphosphate (ATP), inorganic phosphate (Pi) and intracellular pH (pHi), and by (ii) HPLC for ATP, ADP, and AMP levels in left ventricle biopsies. Brain death resulted in a instantaneous major increase in catecholamines (>50-fold, P < .001) and paradoxically a significant progressive decrease in the regional contractility of the left ventricle. After cardioplegia, no significant differences on HEP compounds (ATP/Pi, PCr/Pi, ATP, energetic index) or in pHi were observed between BD and control groups. These data suggest that early heart injury occuring during BD does not seem to be an ischemic phenomenon.

AB - The aim of this study was to examine the effect of sudden brain death (BD) on myocardial function and high energy phosphate (HEP) stores. BD was induced by cerebral vessel ligation in six swine (BD group) that were compared to six control swine. At the end of the BD period (3 hours), harvested hearts were stored at 4°C. Myocardial tissue HEP were assessed by: (i) 31P-NMR spectroscopy of left ventricle for phosphocreatine (PCr), adenosine triphosphate (ATP), inorganic phosphate (Pi) and intracellular pH (pHi), and by (ii) HPLC for ATP, ADP, and AMP levels in left ventricle biopsies. Brain death resulted in a instantaneous major increase in catecholamines (>50-fold, P < .001) and paradoxically a significant progressive decrease in the regional contractility of the left ventricle. After cardioplegia, no significant differences on HEP compounds (ATP/Pi, PCr/Pi, ATP, energetic index) or in pHi were observed between BD and control groups. These data suggest that early heart injury occuring during BD does not seem to be an ischemic phenomenon.

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DO - 10.1016/j.transproceed.2006.06.123

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SN - 0041-1345

VL - 38

SP - 2285

EP - 2286

JO - Transplantation Proceedings

JF - Transplantation Proceedings

IS - 7

ER -

High Energy Compound Stability During Experimental Brain Death

Abstract

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