Hyperbaric oxygen HBO

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4.2.1 HBO and leukocyte adhesion

Several studies in brain and muscles or flaps demonstrate the decrease of

leukocyte adhesion when hyperbaric oxygen is administered , - , by

temporarily (or not , ) inhibiting neutrophil beta2-integrin function - , via endothelial intercellular adhesion molecule-1 (ICAM-1) modulation15,30,35,36 and from peroxynitrite-related inhibition of P-selectin expression37 on the endothelial cells.

4.2.2 HBO and lipid peroxidation

Increased oxygen tensions in ischemia-reperfusion syndromes have been associated with an increase38, no increase39 or a reduction in lipid peroxidation, the latter particularly when HBO is used33, 40 41. Hyperbaric oxygen appears to play a crucial role in protecting against neuronal death induced by brain ischemia42, 43.

4.2.3 HBO and ischemia-reperfusion in CNS models

Ischemic neurological diseases are an important cause of death and a leading cause of long-term disability.44 In experimental and clinical settings hyperbaric oxygen has been demonstrated to have ameliorating and protective effects45, within a narrow time frame46,47 and at certain pressures48'49; with an ensuing reduction in neuronal apoptosis following ischemic damage of the brain and spinal cord 14,50-56. This might seem paradoxical given the nature of hyperoxic vasoconstriction (see chapter 1.5) and indeed the literature is divided on this mechanism48,57-59. However, changes in NO levels may explain the differential and sometimes variably detrimental or positive effects of HBO58, 60.

The clinical efficacy of HBO for the treatment of stroke remains controversial31 and is still in need of being validated61,62. Experimentally, ischemic tolerance can be induced using hyperbaric oxygen pretreatment in ischemia-reperfusion models63,64. It also appears as though hyperbaric oxygen is able to regulate brain metabolites that explain its protective effects in a rat microdialysis middle cerebral artery occlusion model.65 Hyperbaric oxygen certainly demonstrates a superior protective effect than normobaric oxygen.66

Acute carbon monoxide intoxication gives rise to hypoxemic, ischemic and histotoxic hypoxia and shares many pathological similarities with ischemia-reperfusion syndrome. Different oxygen pressures seem to have different effects on lipid peroxidation33 and as this is related to increased free radical production, it may be paradoxically counteracted by HBO.

4.2.4 HBO and ischemia-reperfusion in myocardial models

Ischemia-reperfusion is a common element of coronary bypass surgery, thrombolysis, PTCA, and transplant surgery. Even with a successful reperfusion procedure, myocardial dysfunction is often observed. HBO has been shown to exert (or not67,68) favorable effects on the myocardium and myocardial functions in these conditions8,69,70. Routinely treating patients with acute myocardial infarction in hyperbaric chambers seems impractical and difficult71, therefore aqueous oxygen in solution with a high oxygen concentration has been tested72. In a porcine model of myocardial infarction, intracoronary reperfusion with aqueous oxygen revealed significant improvement in left ventricular ejection fraction, mean infarct size, postmortem hemorrhage score and myocardial myeloperoxidase levels.73 Similar results were obtained by infusion of a hyperbaric oxygen solution into the anterior interventricular vein at reperfusion, giving rise to a reduction the infarct size in swine.74 Ischemic tolerance against ischemia-reperfusion appears to be related to catalase induction in an ischemic myocardium model in rat75.

4.2.5 HBO and ischemia-reperfusion in intestinal models

The intestine is one of the most susceptible organs to ischemia. Intestinal cells but also hepatocytes, have the highest concentration of xanthine dehydrogenase of all tissues. Ischemia-reperfusion injury to the gut causes enterocyte apoptosis that may contribute to intestinal barrier failure76. In the rat model, evidence suggests that HBO before ischemia may ameliorate the ischemia-reperfusion injury of the liver77'78. Hyperbaric oxygen inhibits TNF-alpha production during intestinal ischemia-reperfusion which may be related to the beneficial effects of HBO79-81. Hyperbaric oxygen in circulatory shock induced by splanchnic artery occlusion and reperfusion in rats exhibited a significantly higher survival rate 82. HBO also demonstrated a favourable effect on experimental colitis in rats83.

4.2.6 HBO and ischemia-reperfusion in reconstructive surgery and urology

Skeletal muscles demonstrate an important resistance to ischemia. Hyperbaric oxygen has been shown to reduce (or not84) ischemia-induced skeletal muscle injury55,85-88, skin grafts and flaps36, 89-91 as demonstrated with videomicroscopy and laser Doppler studies. A rat testicular model suggests a potential benefit of HBO treatment in clinical situations of testicular torsion92. Hyperbaric oxygen even might increase the beneficial effect of fibrinolysis93.

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