The development of portal hypertension in liver cirrhosis is accompanied by fundamental changes in splanchnic circulation, where the role of the spleen transforms from a passive venous reservoir into an active driver of hemodynamic disturbances. In the present study, based on a comprehensive clinical and instrumental examination of 90 individuals, including 47 patients with liver cirrhosis and established sple- nomegaly (study group) and 43 practically healthy volunteers (control group), Doppler ultrasonography demonstrated the presence of a pronounced hyperdynamic syndrome in the splenic artery basin. Flowmetry results demonstrate a statistically significant increase in linear blood flow velocities in patients with pathology: Peak Systolic Velocity (PSV) reached 150.8 ± 43.6 cm/s, which is 1.8 times higher than in the control group (85.4 ± 26.7 cm/s), and End-Diastolic Velocity (EDV) nearly doubled to 59.9 ± 19.9 cm/s vs 32.3 ± 10.2 cm/s in healthy individuals. Paradoxically, against the background of a multiple increase in volumetric blood flow, the calculated Resistive Index (RI) in the study group remained stable and did not differ from normal values (0.61 ± 0.08 vs 0.60 ± 0.10), indicating profound vascular wall remodeling and the capacity of the vascular bed to accommodate excessive blood volumes without increasing peripheral resistance. As a consequence of arterial hyperperfusion, a significant increase in maximum velocity in the splenic vein was recorded (34.1 ± 15.6 cm/s vs 23.5 ± 6.2 cm/s in controls). The established strong Spearman correlation between the morphometric volume of the spleen and the velocity of arterial inflow (ρ = 0.616; P < 0.001) confirms the formation of a sustained hyperdynamic type of circulation as a potential mecha nism for the development and progression of splenomegaly, and indicates the unconditional predominance of the active splenic component in the pathogenesis of portal hypertension.