Understanding the splenic contribution to portal flow: The role of splenic artery ligation as inflow modification in living donor liver transplantation

Splenectomy improves survival by increasing arterial blood supply in a rat model of reduced-size liver

“…Modulation of liver inflow after segmental liver transplantation or massive liver resection was advocated as a way to overcome organ hyperperfusion, including splenic artery ligation and splenectomy or diversion of portal vein blood by means of portocaval and mesocaval shunts [24,[27][28][29]. However, these procedures have been used despite the lack of hemodynamic data [30,31].…”

Elevated Catecholamines and Hepatic Artery Vasospasm in Porcine Small-for-Size Liver Graft

“…The evidence to support this theory is that PVF is significantly increased after reperfusion leading to HA spasm through HABR. This is further confirmed through reduction of PVF using surgical modifications, such as portocaval shunting, which leads to a corresponding increase in HAF [3,6]. Catecholamines increase shortly after reperfusion and peak within the first 6 hours.…”

“…Transplantation of partial liver grafts is envisioned to increase the number of liver transplants and reduce deaths on the waiting list [1][2][3][4], but transplantation of smaller grafts is associated with the small-for-size syndrome (SFSS), which carries significant morbidity and mortality [5][6][7][8]. One of the important pathophysiologic changes associated with SFSS is hepatic artery vasospasm [8],which starts after reperfusion and persists up to post operative day (POD) 14 in smallfor-size-liver (SFS) allografts [3][4][5].…”

“…One of the important pathophysiologic changes associated with SFSS is hepatic artery vasospasm [8],which starts after reperfusion and persists up to post operative day (POD) 14 in smallfor-size-liver (SFS) allografts [3][4][5]. Recent work from our laboratory demonstrated that although the hepatic artery buffer response (HABR) was intact immediately following reperfusion, post-operatively the normal HABR was replaced by sustained hepatic arterial (HA) vasoconstriction, in spite of portal vein (PV) flow rates returning to normal [7].…”

The Role of the A2a Receptor Agonist, Regadenoson, in Modulating Hepatic Artery Flow in the Porcine Small-for-Size Liver Graft

“…It is characterized by cholestasis, coagulopathy, and ascites and, in some cases, gastrointestinal bleeding [2]. This syndrome is initiated by portal hyperperfusion [4][5][6] and perpetuated by sustained hepatic artery (HA) vasospasm, which follows [7]. Work from our laboratory described hepatic artery (HA) vasospasm in the SFS graft for the first time and subsequent work focused on reversing the vasospasm and increasing HAF [8,9].…”