The effect of hyperbaric oxygen on severe anemia.
ABSTRACT As a respiratory pigment, hemoglobin allows blood to carry unnaturally high levels of nascent, molecular oxygen at one atmosphere of pressure in chemical solution to capillary beds and post-capillary venules supplying parenchymal cells of all organ systems in the body. When hemoglobin drops to critical levels to disallow proper oxygen delivery, hyperbaric oxygen therapy may be used as bridge therapy to emergently supply oxygen. Hyperbaric-administered oxygen allows oxygen to be dissolved in increased concentration in red blood cell-poor plasma or crystalloid/ colloid-diluted intravascular fluids in a volume-resuscitated patient. Additionally in both subacutely and chronically anemic patients, pulsed, intermittently provided normobaric or hyperbaric oxygen induces an increase in red blood cell/hemoglobic mass. Transfusions of separate donor red blood cells are transplantations of tissue not uncomplicated by immunomodulatory reactions. In the long term, autologous blood products may be less problematic than transfused, homologous packed red blood cells to reduce patient oxygen debt in illness or injury. Hyperbaric oxygen can reduce oxygen debt decisively in the polar clinical extremes of exsanguination with cardiopulmonary arrest all the way to resuscitation of the severely anemic patient who cannot be transfused with red blood cells for religious reasons, immunologic reasons, or blood availability problems. A hyperbaric oxygen treatment is equivalent in wholesale cost to a unit of packed red blood cells in the western world. By controversy, but true, hyperbaric oxygen provides a low-technology, cost-competitive means of pharmacologically reducing accumulated oxygen debt in the anemic, injured or critically ill patient with little side effect. To address severe anemia in trauma or illness, the future may well afford the use of hyperbaric oxygen therapy in the military far-forward, in pre-hospital EMS settings, in trauma center emergency departments, in operative and recovery units, and in intensive care units of hospitals.
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ABSTRACT: The aim of this study was to investigate the immunoregulatory effects of hyperbaric oxygen (HBO) via promoting the apoptosis of peripheral blood lymphocytes (PBLs) to attenuate the severity of early stage acute pancreatitis (AP) in rats. Additionally, the persistence of the HBO treatment effects was evaluated. One hundred and twenty male Wistar rats were randomized into four groups: sham, AP, AP + normobaric oxygen (NBO), and AP + HBO. Each group consisted of 30 rats. Four hours after the induction of AP, the 30 rats in the AP + NBO group were given normobaric oxygen treatment with 100 % oxygen at 1 atm for 90 min. The 30 rats in the AP + HBO group received 100 % oxygen at 2.5 atm for 90 min, with a compression/decompression time of 15 min. The 30 rats in the AP group remained untreated. At 6, 12, and 24 h after the induction of AP, surviving rats from each group were sacrificed, and the blood and tissue samples were collected for the following measurements: the partial pressure of oxygen (PaO2) and oxygen saturation (SaO2) of the arterial blood, the levels of serum amylase, lipase, interleukin-2 (IL-2), interferon-γ (IFN-γ), interleukin-10 (IL-10), hepatocyte growth factor (HGF), and reactive oxygen species (ROS), and the mitochondrial membrane potential (∆Ψm) of the PBLs. The expression levels of procaspase-3, caspase-3, procaspase-9, and caspase-9 were also evaluated in the PBLs. Additionally, the apoptosis of PBLs was assessed, and the pancreatic tissues were subjected to a histopathological analysis by pathological grading and scoring. The histopathology of the lung, liver, kidney, duodenum, and heart was also analyzed at 12 h after the induction of AP. Significant differences were found at 6 and 12 h after AP induction. The HBO treatment significantly elevated the PaO2 and SaO2 levels, and the ROS levels in the PBLs. Additionally, HBO downregulated the levels of amylase and lipase. The HBO treatment also reduced the ∆Ψm levels, upregulated the expression of caspase-3 and caspase-9, and increased the apoptosis rate of the PBLs. Moreover, the HBO treatment decreased the serum concentrations of IL-2, IFN-γ and HGF, and reduced the pathological scores of the pancreatic tissue. The histopathological changes of the lung, liver, kidney, duodenum, and heart were also improved. A significant elevation of IL-10 occurred only at the 12-h time point. However, no obvious differences were found at the 24-h time point. This study demonstrated that the HBO treatment can promote the apoptosis of PBLs via a mitochondrial-dependent pathway and inhibit the inflammatory response. These immunoregulatory effects may play an important therapeutic role in attenuating the severity of early stage AP. The repeated administration of HBO or the use of HBO in combination with other approaches may further improve outcomes.Apoptosis 10/2013; DOI:10.1007/s10495-013-0911-x · 3.61 Impact Factor