Liver
Transpl. 2005 Dec;11(12):1574-80.
Effects of hyperbaric oxygen exposure on experimental hepatic ischemia reperfusion injury: relationship between its timing and neutrophil sequestration.
Source
Department of
Surgical Oncology and Digestive Surgery, Kagoshima University Graduate School
of Medicine and Dental Sciences, 8-35-1 Sakuragaoka, Kagoshima 890, Japan.
Abstract
Recent
studies have shown that hyperbaric oxygen therapy (HBOT) reduces neutrophil
endothelial adherence in venules and also blocks the progressive arteriolar
vasoconstriction associated with ischemia-reperfusion (I-R) injury in the
extremities and the brain. In order to elucidate the effects of HBOT after I-R
in digestive organs, particularly in the liver, we evaluated the following: 1)
the relationship between timing of HBOT and tissue damage; and 2) HBOT's
effects on neutrophil sequestration. Using a hepatic I-R (45 minute) model in
male rats, survival rate, liver tissue damage, and neutrophil accumulation
within the sinusoids in the HBOT-treated group (Group H) were compared to those
in the nontreated group (Group C). For the HBOT-treated group, HBOT was
administered as 100% oxygen, at 2.5 atm absolute, for 60 minutes. When HBOT was
given 30 minute after I-R, the survival rate was much better in Group H than in
Group C. HBOT performed within 3 hours of I-R markedly suppressed increases in
the malondialdehyde level in tissues of the liver and lessened the congestion
in the sinusoids. In addition, HBOT just after I-R caused decreased number of
cells stained by the naphthol AS-D chloroacetate esterase infiltrating into the
sinusoids. HBOT 3 hours after reperfusion, however, showed no clear effects
upon neutrophil sequestration compared to Group C. These results indicate that
HBOT performed within 3 hours of I-R alleviates hepatic dysfunction and
improves the survival rate after I-R. Herein, we propose 1 possible mechanism
for these beneficial effects: early HBOT given before neutrophil-mediated
injury phase may suppress the accumulation of neutrophils after I-R. In
conclusion, we believe that the present study should lead to an improved
understanding of HBOT's potential role in hepatic surgery.
PMID:
16315298
[PubMed - indexed for MEDLINE]
Acta
Cir Bras. 2011 Dec;26(6):463-9.
Effect of hyperbaric oxygen therapy on the intestinal ischemia reperfusion injury.
Source Department of Surgery and Anatomy, FMRP, USP, Ribeirao Preto, SP, Brazil.
Abstract PURPOSE: Adequate tissue oxygenation is essential for healing. Hyperbaric oxygen therapy (HBOT) has potential clinical applications to treat ischemic pathologies, however the exact nature of any protective effects are unclear at present. We therefore investigated the potential role of HBOT in modulating the ischemia/reperfusion (I/R) injury response in intestinal model of I/R injury.
METHODS: Male Wistar rats were subjected to surgery for the induction of intestinal ischemia followed by reperfusion. HBOT was provided before and/or after intestinal ischemia. Cell viability in the intestinal tissue was assessed using the MTT assay and by measuring serum malondealdehyde (MDA). Microvascular density and apoptosis were evaluated by immunohistochemistry.
RESULTS: The results indicate that HBOT treatment pre- and post-ischemia reduces lesion size to the intestinal tissue. This treatment increases cell viability and reduces the activation of caspase-3, which is associated with increased number of tissue CD34 cells and enhanced VEGF expression.
CONCLUSION: The hyperbaric oxygen therapy can limit tissue damage due to ischemia/reperfusion injury, by inducing reparative signaling pathways.
PMID:
22042109
[PubMed - in process
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