Pathophysiologic Study of the Changes of Blood Flow in Portal Vein and Hepatic Artery and the Role of Administration of Regadenoson in Post-hepatectomy Liver Failure

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Backround Posthepatectomy liver failure syndrome is a well-described complication after extended hepatectomies, which contributes significantly to the perioperative morbidity and mortality of the patient. The major pathophysiological basis of this syndrome is the hepatic arterial buffer response (HABR), which reflects the hemodynamic changes that occur in the liver after a hepatectomy. As the portal vein is unable to adjust blood flow to the diminished hepatic parenchyma, the liver establishes a unique mechanism that leads to a decrease in the flow of hepatic artery via vasoconstriction. There are surgical techniques that are already applied to reverse this phenomenon, but they are still considered risky, as they carry high perioperative mortality. On the other hand, pharmacological modulation of the hepatic vasculature can reverse the HABR phenomenon and contribute to the treatment of post-hepatectomy liver failure (PHLF) syndrome. In our experimental research, we studied the administration of regadenoson, an A2A adenosine agonist, which directly reverses the vasoconstriction of the hepatic artery, showing superior results in the modulation of hepatic vasculature, compared to a portocaval shunt. Methods We designed a prospective experimental cohort study comprising animals that underwent extended left hepatectomy (70%) and portocaval shunt to avoid bowel ischemia after the Pringle maneuver. Regadenoson was administered intra-arterially in the hepatic artery. Variations of liver blood flow were measured with ultrasound Doppler equipment. Results The results of our study have demonstrated that direct administration of regadenoson increased the hepatic artery velocity by reversing the HABR and by creating subsequent vasodilation of the hepatic artery. Additionally, the results of administration of regadenoson in comparison to portocaval (PC) shunt were superior and could potentially reduce the incidence of PHLF. Conclusion Regadenoson significantly enhanced hepatic arterial perfusion and may be associated with a reduced risk of developing PHLF syndrome compared to surgical modulation alone in the porcine model. These results position regadenoson as a promising therapeutic agent for optimizing liver perfusion in cases where portal venous flow is impaired.

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