Vasospasm oedema HBO action

Vasospasm is one of the main causes for the genesis of compromised cutaneous and musculocutaneous flaps due to diminished blood flow. Although the mechanism is unclear, it seems that it is induced through a myogenic irritation by trauma or strech.

Microcirculatory events take place similar to those in R. I. which are: vasodilation followed by vasoconstriction, low flow, increased vascular endothelial permeability and edema formation.

The adjunct application of HBO usually promotes vascular constriction explained as a defense mechanism against hyperoxia, thus diminishing the arterial flow by 20-30% as demonstrated experimentally and clinically37, 38.

The "hypoperfused" tissues are compensated from the increased amount of carried oxygen through the hyperoxygenated plasma. However this unique event flow reduction - more oxygen delivery known as "HBO paradox" is applied only to normal vasculature without any influence on the problematic microcirculation39.

Acquired therapeutic experience with HBO proposes that the induced vasospasm is a collateral effect of major importance in treating injuries complicated with presence of edema.

Zamboni et al.20 using intravital microscopy showed that in hypoxic tissue treated with HBO arteriolar diameter had no significant change.

In another study the same author using Laser Doppler flowmetry demonstrated that HBO improved distal microvascular perfusion in rat ischemic flaps27.

Hammarlund et al.40 showed that blood supply on microcirculation of acute derma wound was increased through HBO instead of being suppressed or maintained.

The vasoconstriction of intact skin vasculature under the HBO stimulus results in redistribution of arterial content in favor of the problematic areas and counteracts the hypoxia from impaired local blood flow39, 40.

High-pressure arterial oxygen is indispensable for oxygen to diffuse and overpass interstitial liquids in order to reach the distal ends of hypoxic and hypovascular tissues as the oxygenation of nearby tissue volume depends on the capillary integrity. This may explain the too often observed complication in distal flap necrosis.

Under HBO, plasma oxygen content increases directly as a function of its inspired partial pressure. Oxygen gradient in arterioles represents the driving force for tissular supplementation and normal cellular metabolic balance. In clinically applied HBO treatment arterial PO2 may be elevated up to 1500 mmHg or more, increasing the transfer of oxygen into tissues by 20 fold, corresponding in 300 mmHg or more of tissue partial pressure41.

Hypoxia enhances the installed vasodilation of occluded venous microcirculation, the inflammatory metabolite secretion and the free radical production, promoting furthermore the endothelium cellular injury leading to increased permeability and edema formation. The presence of edema acts like a mechanical diffusion barrier in oxygen movement from arterioles to cellular components.

HBO through induced vasospasm reduces the arterial-arteriole flow thus leading to diminished venous stasis and better draining, permitting the reduction of pressure in the free flap compartment and restoring a low arterial inflow.

The less edema is present the more enhanced is the diffusion range of oxygen.

The "antiedematic" effect of HBO may jeopardize the vicious circle of ischaemia, hypoxia and edema and restore or even improve the capillary flow.

The combined therapeutic action of HBO on vasospasm and swelling reduction in hypoxic tissues is of major importance in compromised tissue transfers in order to improve normal capillary function.

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