TY - JOUR
T1 - Electron microscopic and 31-P NMR studies of ischemic injured rat livers during preservation and reflow
AU - Ellermann, J.
AU - Gewiese, B.
AU - David, H.
AU - Stiller, D.
AU - Plötz, M.
AU - Wolf, K. J.
AU - Lüning, M.
N1 - Copyright:
Copyright 2017 Elsevier B.V., All rights reserved.
PY - 1992
Y1 - 1992
N2 - Ischemic injury induced during preservation and reperfusion contributes to post-operative failure in liver transplantation. Hepatic injury and recovery from preservation was studied in an isolated rat liver model reperfused with oxygenated erythrocytes. In order to correlate morphological and functional findings, 31-P nuclear magnetic resonance spectroscopy and electron microscopy were used to investigate metabolic and ultrastructural changes during 6 hours of reperfusion. Following cold preservation, EM's showed a primary sinusoidal cell injury, whereas the hepatocytes were well maintained. During reperfusion, hepatocytes displayed further damage. The simultaneous presence of vacuolarly degenerated mitochondria and mitochondria of increased activity was noted. 31-P NMP spectra demonstrated initially a partial ATP-recovery. The maximum level of 60% of the control ATP-value could not be further increased. EM and 31-P NMR indicate that the progressive injury to the liver is due to microcirculatory malfunction induced by an endothelial cell damage, followed by injured hepatocytes themselves, and the consequent intracellular energy crisis that is produced.
AB - Ischemic injury induced during preservation and reperfusion contributes to post-operative failure in liver transplantation. Hepatic injury and recovery from preservation was studied in an isolated rat liver model reperfused with oxygenated erythrocytes. In order to correlate morphological and functional findings, 31-P nuclear magnetic resonance spectroscopy and electron microscopy were used to investigate metabolic and ultrastructural changes during 6 hours of reperfusion. Following cold preservation, EM's showed a primary sinusoidal cell injury, whereas the hepatocytes were well maintained. During reperfusion, hepatocytes displayed further damage. The simultaneous presence of vacuolarly degenerated mitochondria and mitochondria of increased activity was noted. 31-P NMP spectra demonstrated initially a partial ATP-recovery. The maximum level of 60% of the control ATP-value could not be further increased. EM and 31-P NMR indicate that the progressive injury to the liver is due to microcirculatory malfunction induced by an endothelial cell damage, followed by injured hepatocytes themselves, and the consequent intracellular energy crisis that is produced.
KW - 31-P nuclear magnetic resonance spectroscopy
KW - Endothelial cell damage, liver
KW - Hepatocyte, ischemic injury
KW - Ischemic injury, liver
KW - Liver, endothelial cell damage
KW - Liver, ischemic injury
KW - Liver, microcirculatory malfunction
KW - Liver, post-operative failure
KW - Liver, reperfusion
KW - Liver, sinusoidal cell injury
KW - Microcirculatory malfunction, liver
KW - Reperfusion, Liver
KW - Sinusoidal cell injury, liver
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U2 - 10.1016/S0940-2993(11)80235-6
DO - 10.1016/S0940-2993(11)80235-6
M3 - Article
C2 - 1446161
AN - SCOPUS:0026629777
SN - 0940-2993
VL - 44
SP - 245
EP - 253
JO - Experimental and Toxicologic Pathology
JF - Experimental and Toxicologic Pathology
IS - 5
ER -