Correlation of Systemic Arterial and Portal Venous Pressure in a Healthy Liver Animal Model

Heyansh Kreiselukas^*
*Correspondence: Heyansh Kreiselukas, Department of Medicine, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University, Kaohsiung 833, Taiwan, Email:

Keywords

Systemic arterial pressure • Portal venous pressure • Healthy liver model • Cardiovascular physiology

Introduction

The relationship between Systemic Arterial Pressure (SAP) and Portal Venous Pressure (PVP) plays a pivotal role in maintaining normal liver function and overall cardiovascular homeostasis. In physiological terms, SAP represents the pressure exerted by the blood against the arterial walls during cardiac contraction (systole) and relaxation (diastole), reflecting systemic perfusion and oxygen delivery. On the other hand, PVP reflects the pressure within the portal venous system, influenced by factors such as portal blood flow, hepatic resistance and intrahepatic vascular compliance. In healthy individuals and animal models, SAP and PVP are intricately linked through complex hemodynamic interactions. The liver, acting as a central regulator, receives dual blood supplies-arterial blood from the hepatic artery and venous blood from the portal vein-ensuring metabolic balance and detoxification functions. Understanding the dynamic relationship between SAP and PVP provides insights into cardiovascular adaptations and hepatic perfusion under physiological conditions [1].

Despite their distinct physiological origins, SAP and PVP can influence each other under certain circumstances. Changes in SAP, such as hypertension or hypotension, may affect PVP through alterations in systemic vascular resistance or cardiac output. Conversely, changes in PVP, such as portal hypertension, can impact SAP by altering cardiac preload and afterload, thereby influencing systemic hemodynamics. This study aims to elucidate the close relationship between SAP and PVP in a controlled animal model with a healthy liver. By concurrently measuring SAP and PVP under standardized conditions, we seek to characterize their correlation, assess hemodynamic responses to physiological stimuli and delineate implications for liver function and cardiovascular health. The findings contribute to our understanding of systemic and portal hemodynamics, providing foundational knowledge for studying hepatic diseases and cardiovascular disorders characterized by altered vascular pressures [2].

Literature Review

The relationship between Systemic Arterial Pressure (SAP) and Portal Venous Pressure (PVP) is critical in understanding the hemodynamics of liver function and cardiovascular physiology. In a healthy liver, SAP reflects the pressure within the systemic circulation, influencing organ perfusion and oxygen delivery. Conversely, PVP represents the pressure within the portal venous system, which receives blood from the gastrointestinal tract, spleen and pancreas, supplying the liver with nutrients and metabolic substrates. Studies utilizing animal models have provided valuable insights into the dynamic interactions between SAP and PVP. Some authors demonstrated that under normal physiological conditions, there exists a close correlation between SAP and PVP, with fluctuations in SAP influencing PVP through changes in portal blood flow dynamics and hepatic vascular resistance. These findings underscore the integrated regulation of systemic and portal hemodynamics to maintain hepatic perfusion and function [3].

Furthermore, investigations into hepatic responses to acute and chronic changes in SAP have highlighted adaptive mechanisms that preserve liver homeostasis. For instance, during conditions of increased SAP (e.g., hypertension), the liver may modulate portal vascular tone and flow redistribution to accommodate altered systemic pressures and maintain optimal portal perfusion. Conversely, reductions in SAP (e.g., hypotension) can lead to compensatory changes in hepatic blood flow and vascular resistance to safeguard liver function. Despite these insights, discrepancies in the literature regarding the precise quantitative relationship between SAP and PVP in different animal models and experimental settings necessitate further exploration. Variations in species-specific anatomy, cardiovascular dynamics and experimental methodologies influence the interpretation of SAP-PVP correlations, warranting standardized approaches and comparative analyses across studies [4].

Discussion

The discussion centers on the complexities of interpreting SAP-PVP correlations in animal models with healthy livers. While existing research supports a fundamental relationship between systemic and portal hemodynamics, several factors contribute to variability in SAP-PVP interactions across experimental conditions. Methodological considerations, such as catheter placement accuracy, anesthesia effects and physiological variability among animals, influence the reliability and reproducibility of SAP and PVP measurements [5]. Moreover, the clinical relevance of understanding SAP-PVP correlations lies in its implications for liver disease pathophysiology and cardiovascular management. Dysregulation of SAP-PVP interactions, as observed in conditions like portal hypertension or cirrhosis, underscores the importance of maintaining balanced hemodynamics to prevent hepatic decompensation and cardiovascular complications. Targeted interventions aimed at optimizing SAP-PVP relationships could potentially mitigate risks associated with hepatic and cardiovascular diseases. From a translational perspective, bridging insights from animal models to clinical practice requires robust validation and correlation with human studies. Integrating advanced imaging techniques, computational modeling and non-invasive monitoring approaches may enhance our understanding of SAP-PVP dynamics in patients with liver disease, offering diagnostic and therapeutic opportunities to improve outcomes [6].

Conclusion

In conclusion, the correlation between systemic arterial and portal venous pressures in healthy liver animal models provides foundational insights into hepatic and cardiovascular hemodynamics. Existing literature underscores the interdependent regulation of SAP and PVP to maintain optimal liver perfusion and function under physiological conditions. Variations in experimental methodologies and species-specific responses highlight the need for standardized approaches to enhance comparability and reproducibility across studies. Future research efforts should focus on elucidating the mechanistic pathways underlying SAP-PVP interactions, exploring adaptive responses to acute and chronic hemodynamic changes and translating findings to clinical settings. By advancing our understanding of SAP-PVP correlations, we can optimize diagnostic strategies, refine therapeutic interventions and improve outcomes for patients with liver diseases and associated cardiovascular complications.

Acknowledgment

None.

Conflict of Interest

No conflict of interest.

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