Negative impact of systemic catecholamine administration on hepatic blood perfusion after porcine liver transplantation

✍ Scribed by Arianeb Mehrabi; Markus Golling; Arash Kashfi; Tamara Boucsein; Peter Schemmer; Carsten N. Gutt; Jan Schmidt; Markus W. Büchler; Thomas W. Kraus

• Publisher: John Wiley and Sons
• Year: 2005
• Tongue: English
• Weight: 285 KB
• Volume: 11
• Category: Article
• ISSN: 1527-6465
• DOI: 10.1002/lt.20299

✦ Synopsis

Catecholamines are often administered during and after liver transplantation (LTx) to support systemic perfusion and to increase organ oxygen supply. Some vasoactive agents can compromise visceral organ perfusion. We followed the hypothesis that the vasculature of transplanted livers presents with a higher sensitivity, which leads to an increased vulnerability for flow derangement after application of epinephrine (Epi) or norepinephrine (NorEpi).

Hepatic macroperfusion and microperfusion during systemic Epi or

NorEpi infusion were measured by Doppler flow and thermodiffusion probes in porcine native, denervated, and transplanted livers (n ‫؍‬ 16 in each group). Epi or NorEpi were infused (n ‫؍‬ 8 in each subgroup) in predefined dosages (low dose ‫؍‬ 5 g/kg/minute and high dose ‫؍‬ 10 g/kg/minute) over 240 minutes. Systemic cardiocirculatory parameters were monitored continuously. Hepatic perfusion data were compared between all groups at comparable time points and dosages. In all native, denervated, and transplanted liver groups, Epi and NorEpi induced an inconsistent rise of mean arterial pressure and heart rate shortly after onset of infusion in both dosages compared with baseline. No significant differences of cardiovascular parameters at comparable time points were observed. In native livers, Epi and NorEpi induced only temporary alterations of hepatic macrocirculation and microcirculation, which returned to baseline 2 hours after onset of infusion. No significant alterations of hepatic blood flow were detected after isolated surgical denervation of the liver. By contrast, transplanted livers showed a progressive decline of hepatic macrocirculation (33 -75% reduction) and microcirculation (39 -58% reduction) during catecholamine infusions in a dose-dependent fashion. Characteristics of liver blood flow impairment were comparable for both vasoactive agents. In conclusion, pronounced disturbances of hepatic macrocirculation and microcirculation were observed during systemic Epi and NorEpi infusion after LTx compared with native and denervated livers. Microcirculation disturbances after LTx might be explained by impairment of hepatic blood flow regulation caused by an increased sensitivity of hepatic vasculature after ischemia-reperfusion and by lengthening of vasopressor effects caused by reduced hepatocyte metabolism. Clinicians should be aware of this potentially hazardous effect. Therefore, application of catecholamines after clinical LTx should be indicated carefully. (Liver Transpl 2005;11:174-187.)

B ased on current United Network for Organ Shar- ing data, 70% of the patients undergoing liver transplantation (LTx) suffer from cirrhosis. 1 Cirrhosis can be associated with significant cardiovascular impairment caused by hyperdynamic circulation or associated cardiomyopathy. 2,3 Although cardiomyopathy associated with cirrhosis is usually mild or latent, acute left ventricular failure can occur after LTx with an acute need for therapeutic support. 4 LTx induces severe stress on the cardiovascular system, particularly during the anhepatic phase and after graft reperfusion. 5,6 During the anhepatic phase, decreased cardiac preload, left ventricular function impairment, and reduced myocardial contractility are often observed. 5 The so-called postreperfusion syndrome, with an incidence of 20%, can lead to acute systemic hypotension with or without bradycardia and usually occurs during the first minutes after graft reperfusion. 5,7,8 Considering all the problems mentioned previously, cardiovascular complications were encountered in more than 70% of patients after clinical LTx. 9 Severe global left ventricular dysfunction