Skip to content

Correlation Between Release of Cytokines From Liver Graft and Hemodynamic Instability

Correlation Between Release of Cytokines From Liver Graft and Hemodynamic Stability During Liver Transplantation

Status
Completed
Phases
Unknown
Study type
Observational
Source
ClinicalTrials.gov
Registry ID
NCT01120743
Enrollment
17
Registered
2010-05-11
Start date
2008-08-31
Completion date
2010-04-30
Last updated
2017-11-24

For informational purposes only — not medical advice. Sourced from public registries and may not reflect the latest updates. Terms

Conditions

Liver Transplantation

Keywords

liver failure, cytokines, hemodynamic instability

Brief summary

The primary goal of this project is to identify the source of cytokines that are released into circulation during graft reperfusion. Seventeen patients scheduled to have adult cadaveric liver transplantation at the Milton S. Hershey Medical Center were contacted as prospective participants. Blood samples were obtained from the radial artery, the portal vein, and from the graft irrigation. The level of pro-inflammatory cytokines was verified and compared with the amount of catecholamines used to maintain hemodynamic stability.

Detailed description

Reperfusion of the graft is the most critical part of liver transplantation because of the difficulties in managing the resulting severe hemodynamic instability. The patients who are accepted to be listed for liver transplantation undergo evaluation of their cardiac function and are usually relatively stable with, at most, minimal cardiac problems (a requirement for inclusion in the liver transplantation program). Additionally, we observe completely unpredictable hemodynamic reactions during and after the graft reperfusion, requiring vastly different doses of catecholamine in order to maintain an acceptable level of perfusion pressure. The adverse cardiopulmonary effects are thought to be associated with the preexisting level of various proinflammatory factors, including cytokines (TNF-alpha, IL-6) and proinflammatory phospholipase A2 (sPLA2) produced in the graft as a reaction to the conservation solution and cold temperature (necessary to keep the organ capable for transplantation) and released into the bloodstream during reperfusion. The massive release of cytokines after unclamping of the graft may be responsible for negative inotropy and significant vasodilatation.

Interventions

None listed

Sponsors

Penn State University
Lead SponsorOTHER

Study design

Observational model
COHORT
Time perspective
PROSPECTIVE

Eligibility

Sex/Gender
ALL
Age
18 Years to No maximum
Healthy volunteers
No

Inclusion criteria

* All adult patients scheduled for liver transplantation will be offered the opportunity to participate in this research.

Exclusion criteria

* Patients unable or unwilling to provide adequate informed consent will be excluded.

Design outcomes

Primary

MeasureTime frameDescription
Measurement of cytokine levels (TNF-alpha, IL-1, Il-2, IL-6, IL-8) in the portal vein, radial artery and flush (from irrigation of the liver used to remove preservation solution from the liver graft) blood.A period of 20 minutes, beginning at the start of reperfusion and continuing until 20 minutes after reperfusion.Cytokines released from the liver graft could be a cause for negative inotropy and systemic vasodilatation.

Secondary

MeasureTime frameDescription
Correlation between the level of cytokines and hemodynamic stability during reperfusion.A period of 20 minutes, beginning at the start of reperfusion and continuing until 20 minutes after reperfusion.First 20 minutes after liver graft reperfusion is a time of maximal hemodynamic instability. A correlation between the level of cytokines and hemodynamic instability could be important for understanding of this condition

Countries

United States

Outcome results

None listed

Source: ClinicalTrials.gov · Data processed: Feb 4, 2026