AIM: To determine the possible existence of a hepato-cardiovascular response and its regulatory mechanism in normal rats. METHODS: Systemic hemodynamic changes following intraportal injection of latex microspheres were studied in two modified rat models of hepatic circulation, in which the extrahepatic splanchnic circulation was excluded by evisceration and the liver was perfused by systemic blood via either the portal vein (model 1) or hepatic artery (model 2) in vivo. RESULTS: In model 1, intraportal injection of two sized microspheres (15-μm and 80-μm) induced a similar decrease in mean arterial pressure, while extrahepatic portal venous occlusion induced an immediate increase in mean arterial pressure. In model 2, microsphere injection again induced a significant reduction in mean arterial pressure, aortic blood flow and aortic resistance. There were no significant differences in these parameters between liver-innervated rats and liver-denervated rats. The degrees of microsphere-induced reduction in mean arterial pressure (-38.1±1.9% in liver-innervated rats and -35.4±2.1% in liver-denervated rats, respectively) were similar to those obtained by withdrawal of 2.0 mL of blood via the jugular vein (-33.3±2.1%) (P>0.05). Injection of 2.0 mL Haemaccel in microsphere-treated rats, to compensate for the reduced effective circulating blood volume, led to a hyperdynamic state which, as compared with basal values and unlike control rats, was characterised by increased aortic blood flow (+21.6±3.3%), decreased aortic resistance (-38.1±3.5%) and reduced mean arterial pressure (-9.7±2.8%). CONCLUSION: A hepato-cardiovascular response exists in normal rats. It acts through a humoral mechanism leading to systemic vasodilatation, and may be involved in the hemodynamic disturbances associated with acute and chronic liver diseases. AIM: To determine the possible existence of a hepato-cardiovascular response and its regulatory mechanism in normal rats. METHODS: Systemic hemodynamic changes following intraportal injection of latex microspheres were studied in two modified rat models of hepatic circulation, in which the extrahepatic splanchnic circulation was excluded by evisceration and the liver was perfused by systemic blood via either the portal vein (model 1) or hepatic artery (model 2) in vivo. RESULTS: In model 1, intraportal injection of two sized microspheres (15-μm and 80-μm ) induced a similar decrease in mean arterial pressure, while extrahepatic portal venous occlusion induced an immediate increase in mean arterial pressure. In model 2, microsphere injection again induced a significant reduction in mean arterial pressure, aortic blood flow and aortic resistance. significant differences in these parameters between liver-innervated rats and liver-denervated rats. The degrees of microsphere- induced reduction in mean arterial pressure (-38.1 ± 1.9% in liver-innervated rats and -35.4 ± 2.1% in liver-denervated rats, respectively) were similar to those obtained from withdrawal of 2.0 mL of blood via the jugular vein (-33.3 ± 2.1%) (P> 0.05). Injection of 2.0 mL Haemaccel in microsphere-treated rats, to compensate for the reduced effective circulating blood volume, led to a hyperdynamic state which, as compared with basal values ​​and unlike control rats, was characterized increased blood flow (+21.6 ± 3.3%), decreased aortic resistance (-38.1 ± 3.5%) and reduced mean arterial pressure (-9.7 ± 2.8%). CONCLUSION: A hepato-cardiovascular response exists in normal rats. It acts through a humoral mechanism leading to systemic vasodilatation, and may be involved in the hemodynamic disturbances associated with acute and chronic liver diseases.