Capillary hemorheological status HBO

Kerrigan16 proposed a capillary model including three phases (post-hypoxic vasodilation, hemoconcentration and a vasoconstriction induced suboptimal flow) to explain the pathophysiological changes in flap microcirculation.

Rheologic properties of blood at the microvasculature level have a predominant role in the pathogenesis of compromised flaps and skin grafts as partial or total arterial occlusion may occur.

Zamboni6 reports that especially in free tissue transfer, where the accepted thrombosis rate is at least 5-10 %, there is a secondary ischemia prior to the one of revision anastomosis, resulting in desperate situation.

After the tissue detachment, microcirculation is acutely interrupted and hemo-rheological disturbances appear like local vasoconstriction, vasodilation, alterations of fibrinolysis and blood viscosity as a result of hypoxia.

Augmented plasma exudation in compromised microcirculation is followed by hemoconcentration in parallel with the existing endothelial edema favoring capillary occlusion.

The fibrinolytic system possesses a strategic role in the pathogenesis of thrombi. Endothelial cells produce plasminogen activator (t-PA) to allow fibrinolysis to occur and plasminogen activator (inhibitor type one PAI-1) as antagonist. PAI-1 antagonises t-PA, regulating fibrinolytic activity.

HBO was shown clinically42 to enhance t-PA activity favoring fibrinolysis and decrease of PAI-I. Another study43 using cultured human endothelial cells following anoxia demonstrated HBO to affect the fibrinolytic response preventing thrombosis or microembolization.

Platelet aggregation is enhanced by thromboxane A2 coming from the cell membrane released arachidonic acid as a result of hypoxic insult.

An animal study44 showed that the maximal rate of ADP and collagen-induced platelet aggregation decreased after hyperbaric exposure.

In hypoxia free radicals have a direct effect upon red blood cells, like the peroxidation of membranes lipids resulting in structural changes of red cell membrane. This results in red cellular deformability which promotes furthermore the rheological disturbance of blood flow enhancing tissue subperfusion. The grade of this deformability may be evaluated through the erythrocyte filtration index.

In an experimental controlled animal study45 exposure to hyperbaric oxygen demonstrated a decrease in RBC deformability confirmed with electron microscope and a significant increase of the filtration index. The authors suggested that rheological alteration of red cells might affect their flow through small-caliber blood vessels.

Mathieu et al.46 also demonstrated the improvement of red cells filtration index after HBO treatment. Dise et al.47 proposed that HBO inhibits erythrocyte phospholipid fatty acid turn over.

HBO has been shown clinically48 to increase prostacyclin (PGI2) products (6-Keto-PG F) and in parallel to decrease thromboxane (TxA2) sub-products, (TxB2) thus promoting vessel dilation.

In summary, although the evidence is mostly from experimental studies HBO seems to favor the decrease of thrombotic occlusion in capillary or microcirculatory level.

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