Effects of hyperbaric oxygen exposure on experimental hepatic ischemia reperfusion injury: Relationship between its timing and neutrophil sequestration

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 under- W arm hepatic ischemia-reperfusion (I-R) is characterized by circulatory and metabolic disruptions, liver dysfunction, and tissue damage. Recent advances in the research regarding the basic mechanisms of I-R showed the significance of Kupffer cells and neutrophils. 1 Kupffer cells play a central role as the initial cytotoxic cell type and as a source of many proinflammatory mediators such as tumor necrosis factor-␣ (TNF-␣) and interleukin (IL)-6. 2-6 Subsequently, neutrophils are activated and migrate into the liver. Researchers have pointed out that accumulated neutrophils contribute to the injury several hours after the initiation of reperfusion. 7 In fact, antibodies against adhesion molecules such as Mac-1 (cluster of differentiation molecule 11b/18) or intracellular adhesion molecule-1 (ICAM-1) are still beneficial, ever if administered during the Kupffer cell-mediated injury phase. [7][8][9][10][11][12] Hyperbaric oxygen therapy (HBOT) is a specific type of oxygen administration that aims to improve numerous kinds of hypoxic disorders by increasing the amount of dissolved oxygen within the blood. 13 Recent studies have shown that HBOT reduced neutrophil endothelial adherence in venules and also blocked the progressive arteriolar vasoconstriction associated with repe...

Hyperbaric oxygen therapy aggravates liver reperfusion injury in rats

“…HO decreases endothelial adhesion of neutrophils by reducing the expression of intercellular adhesion molecules on the surface of endothelial cells and may increase the tissue concentration of antioxidant enzymes such as myocardial catalase 10 . The experimental application of HO to liver IRI has been described in two situations: as a preventive method before liver ischemia or reperfusion 11,12 , or as a postoperative therapeutic measure 13 . These studies indicate that the use of HO for short periods of time, causing cell oxidative stress, protects the liver against injuries associated with tissue reperfusion by a biochemical mechanism that is still unknown.…”

Effect of hyperbaric oxygen therapy on liver function during intermittent ischemia

“…Accordingly, the intermittent clamping of the hepatic pedicle proved to be more effective in attenuating ischemia-reperfusion injury compared to the continuous portal triad clamping 7 . In this context, the interest in hyperbaric oxygen therapy (HBO) has grown due to its role in ischemia and reperfusion injury therefore in the liver transplantation field 9,10 . HBO is the inhalation of pure oxygen at hyperbaric conditions which increases the amount of dissolved oxygen in the blood and therefore in body tissues (Henry's Law), promoting a high tissue oxygen tension that demonstrated beneficial biochemical and cellular effects to tissues 11 .…”

Hyperbaric oxygen therapy and ischemia and reperfusion: a valuable association to attenuate ischemic lesion and hepatic reperfusion

“…Although hyperbaric oxygen therapy is widely used in various contexts involving, especially, diseases related to phenomena of hypoxia, ischemia and reperfusion 1,2 there is no scientific consensus on the subject; there are works in favor 3,4 and unfavorable 5 to this association. This phenomenon is due, at least in part, to a lack of studies that explore the biochemical basis of this association 6,7 , precisely the proposal of this work.…”