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Hormonal and splanchnic hemodynamic alterations following hepatic resection
Y Wu1, K A Campbell, J V Sitzmann
1Department of Surgery, Johns Hopkins Medical Institutions, Baltimore, Maryland 21287-4665.
The Journal of Surgical Research
|July 1, 1993
Summary
Partial hepatectomy (PH) causes hemodynamic changes, including increased portal pressure and flow. Prostacyclin (PGI2) release appears linked to portosystemic shunting and altered splanchnic blood flow following liver resection.
Area of Science:
- Hepatobiliary Surgery
- Vascular Physiology
- Splanchnic Circulation
Background:
- Partial hepatectomy (PH) induces significant hemodynamic alterations, notably elevated portal blood flow and pressure.
- The underlying mechanisms driving these post-hepatectomy hemodynamic changes remain incompletely understood.
Purpose of the Study:
- To investigate the role of portosystemic shunt (PSS), splanchnic blood flow and resistance (Qspl, Rspl), and key vasoactive substances (prostacyclin [PGI2], glucagon, insulin) in rats following 75% hepatectomy.
Main Methods:
- Rats underwent 75% hepatectomy to induce hemodynamic changes.
- Measurements included portal pressure (Ppv), portal blood flow (Qpv), splanchnic artery blood flow (Qspl) and resistance (Rspl), and levels of PGI2, glucagon, and insulin.
- Portosystemic shunt (PSS) degree was assessed post-resection.
Main Results:
- An immediate threefold increase in portal PGI2 was observed post-PH.
- A hemodynamically significant PSS developed by 48 hours, correlating with increased PGI2, Qpv, Ppv, and decreased Rspl.
- Glucagon levels rose acutely but normalized before PSS and hyperemia resolution; insulin and glucose remained unchanged.
Conclusions:
- The findings suggest a strong relationship between PSS and prostanoid release, influencing splanchnic hemodynamics (Qpv, Qspl, Rspl) after liver resection.
- Partial hepatectomy serves as a model for acute portal hypertension (PHT), with altered splanchnic hemodynamics potentially linked to hepatic regeneration.