TY - JOUR
T1 - Impact of organ temperature on postischemic platelet-endothelial cell interactions in the hepatic microcirculation
AU - Khandoga, A.
AU - Biberthaler, P.
AU - Luchting, B.
AU - Messmer, K.
AU - Krombach, F.
PY - 2001
Y1 - 2001
N2 - In liver transplantation, hypothermie preservation at 4°C is standard to protect the organ from ischemia-reperfusion (I/R) injury. Although the protective mechanisms during cold ischemia remain not fully understood, a critical role of platelet-endothelial cell interactions in the development of 1/R-induced liver injury has been recently demonstrated. The aim of this study was to investigate the influence of ischémie temperature on platelet-endothelial cell interactions in the hepatic microcirculation. A reversible isolated ischemia of the left liver lobe was induced in C57BL/6 mice for 90 min under inhalation anesthesia. The ischémie lobe was placed in a polyethylene well and the organ temperature was adjusted to 37°C (n=3) and 4°C (n=3) by superfusion with warmed/cooled saline solution. Sham-operated animals served as controls (n=3). Platelets were isolated from syngeneic donors and labeled ex vivo using rhodamine-6G. After 20 min of reperfusion, 50x106 labeled platelets were infused i.v. and platelet-endothelial cell interactions were quantitatively analyzed in hepatic microvessels by intravital microscopy. At the end of each experiment, serum AST/ALT activities were measured. In sham-operated animals, only a few adherent platelets were observed in presinusoidal arterioles (17±15/mm 2, postsinusoidal venules (61±19/mm 2), and sinusoids (4.3±3.2/acinus). Ischemia at 37°C caused an increase in the number of adherent platelets (A: 294±149/mm 2, V: 339±110/mm 2, S: 9.7±1.8/acinus), whereas platelet adhesion was attenuated in the hypothermie group (A: 32±35/mm 2, V: 81±56/mm 2, S: 3.1±1.3/acinus). Concomitantly, the postischemic increase in serum ALT/AST activities after ischemia at 37°C (1698±383 IU/L and 3116±728 IU/L) was reduced in the 4°C group (785±108 IU/L and 142±90 IU/L). These in vivo data demonstrate that the protective effect of cold ischemia on hepatic I/R injury is linked to an attenuation of platelet-endothelial cell interactions in the hepatic microcirculation. Future investigations have to clarify the mechanisms responsible for the reduction of postischemic platelet adhesion that is induced by cooling of the organ during ischemia.
AB - In liver transplantation, hypothermie preservation at 4°C is standard to protect the organ from ischemia-reperfusion (I/R) injury. Although the protective mechanisms during cold ischemia remain not fully understood, a critical role of platelet-endothelial cell interactions in the development of 1/R-induced liver injury has been recently demonstrated. The aim of this study was to investigate the influence of ischémie temperature on platelet-endothelial cell interactions in the hepatic microcirculation. A reversible isolated ischemia of the left liver lobe was induced in C57BL/6 mice for 90 min under inhalation anesthesia. The ischémie lobe was placed in a polyethylene well and the organ temperature was adjusted to 37°C (n=3) and 4°C (n=3) by superfusion with warmed/cooled saline solution. Sham-operated animals served as controls (n=3). Platelets were isolated from syngeneic donors and labeled ex vivo using rhodamine-6G. After 20 min of reperfusion, 50x106 labeled platelets were infused i.v. and platelet-endothelial cell interactions were quantitatively analyzed in hepatic microvessels by intravital microscopy. At the end of each experiment, serum AST/ALT activities were measured. In sham-operated animals, only a few adherent platelets were observed in presinusoidal arterioles (17±15/mm 2, postsinusoidal venules (61±19/mm 2), and sinusoids (4.3±3.2/acinus). Ischemia at 37°C caused an increase in the number of adherent platelets (A: 294±149/mm 2, V: 339±110/mm 2, S: 9.7±1.8/acinus), whereas platelet adhesion was attenuated in the hypothermie group (A: 32±35/mm 2, V: 81±56/mm 2, S: 3.1±1.3/acinus). Concomitantly, the postischemic increase in serum ALT/AST activities after ischemia at 37°C (1698±383 IU/L and 3116±728 IU/L) was reduced in the 4°C group (785±108 IU/L and 142±90 IU/L). These in vivo data demonstrate that the protective effect of cold ischemia on hepatic I/R injury is linked to an attenuation of platelet-endothelial cell interactions in the hepatic microcirculation. Future investigations have to clarify the mechanisms responsible for the reduction of postischemic platelet adhesion that is induced by cooling of the organ during ischemia.
UR - http://www.scopus.com/inward/record.url?scp=33746358244&partnerID=8YFLogxK
M3 - Article
AN - SCOPUS:33746358244
SN - 1435-2443
VL - 386
SP - 464
EP - 465
JO - Langenbeck's Archives of Surgery
JF - Langenbeck's Archives of Surgery
IS - 6
ER -