Evolution of the plasma concentration of norepinephrine in cirrhotic patients during liver transplantation

Norepinephrine in Small-For-Size Liver Grafts: An Experimental Study in Pigs

“…Our observations show that only very small-for-size grafts (ratio 1:3) produce norepinephrine increase. A transient increase in plasma norepinephrine in accordance with the anhepatic period has been also observed in patients undergoing orthotopic liver transplantation with intact grafts [9].…”

“…The increase in norepinephrine level is an indicator of stress and evaluates the functioning of the sympa- thetic nervous system [9]. Norepinephrine elevation during the anhepatic phase of liver transplantation can be attributed to an exacerbated response to stress motivated by the considerable surgical aggression and to severe hemodynamic, metabolic, and coagulative alterations that accompany the procedure [9].…”

“…Norepinephrine elevation during the anhepatic phase of liver transplantation can be attributed to an exacerbated response to stress motivated by the considerable surgical aggression and to severe hemodynamic, metabolic, and coagulative alterations that accompany the procedure [9]. Splitgrafts are exposed to higher stress, considering the more time consuming surgical manipulations involved in their preparation and implantation.…”

“…It is known that it produces ␣-adrenoceptor-mediated contraction to hepatic vessels [6,7]. Liver resection and liver transplantation have been found to increase plasma norepinephrine levels [8,9]. However, plasma levels of norepinephrine have not been thoroughly evaluated as a potential causative factor of diminished hepatic artery flow in small-for-size grafts at the early posttransplant period.…”

Doppler Ultrasonographic Findings on Hepatic Arterial Vasospasm Early After Liver Transplantation

“…18 The results of animal and clinical studies suggested that the plasma norepinephrine level was elevated because of surgical stress, occlusion of hepatic inflow, and removal of the donor liver, which might have an appreciable effect on donor agonal arterial spasm. [19][20][21][22] In addition to hepatic vasospasm, older donor age and a prolonged cold ischemic time might be among the contributors. In a clinical study, older donor age (>50 years) and an extended preservation time (410 min) were related to high-resistant hepatic arterial flow during the period immediately after transplantation, although this finding had neither notable clinical repercussions nor prognoses for early and long-term follow-up.…”