Related Experiment Videos
Early post-operative hyperbaric oxygen therapy modifies neutrophile activation.
1First Department of Surgery, Kagoshima University School of Medicine, Japan.
Hepato-Gastroenterology
|August 3, 1999
Summary
Hyperbaric oxygen therapy (HBOT) reduces neutrophil activation and sinusoidal endothelial cell (SEC) injury after liver surgery. This treatment, particularly when given early, improves patient outcomes and prevents liver damage.
Area of Science:
- Hepatobiliary Surgery
- Hyperbaric Medicine
- Immunology
Background:
- Post-operative liver injury is often caused by activated neutrophils.
- Sinusoidal endothelial cells (SECs) are vulnerable to neutrophil-mediated damage after hepatectomy.
Purpose of the Study:
- To evaluate the impact of acute hyperbaric oxygen therapy (HBOT) on neutrophil-induced SEC damage following liver resection.
- To determine if HBOT can mitigate post-operative liver injury.
Main Methods:
- 12 patients undergoing elective hepatectomy received two courses of HBOT (2.0 atm, 100% oxygen for 60 min) at 3 and 24 hours post-surgery.
- A control group of 12 patients received standard hemodynamic management.
- Markers of neutrophil activation (PMNE, CD18) and endothelial damage (TM) were measured.
Main Results:
- HBOT significantly reduced peak levels and delayed the onset of polymorphonuclear leukocyte elastase (PMNE) and thrombomodulin (TM).
- CD18 expression, a marker of neutrophil activation, was suppressed in the HBOT group compared to controls.
- No patients in the HBOT group experienced post-operative hyperbilirubinemia or hepatic failure, unlike the control group.
Conclusions:
- Acute HBOT, especially when administered 3 hours post-hepatectomy, effectively reduces neutrophil activation.
- HBOT demonstrates a protective effect against SEC injury in the post-operative setting.
- These findings suggest HBOT is a promising therapeutic strategy for preventing liver damage after hepatectomy.