Relation between the onset of vasoconstriction and pressures of oxygen in the tissues

The occurrence of hyperoxic vasoconstriction has often been an argument against the use of HBO in ischemic situations. A decrease in blood flow could induce a further decrease in peripheral DO2 causing hypoxia in the tissues83,84. Furthermore, hyperoxic vasoconstriction of arteries supplying already ischemic areas would also aggravate the hypoxia72.

However, although this theoretical concern has often been mentioned, no study has reported evidence of an occurrence of tissue hypoxia due to hyperoxia. In fact a number of authors have shown that despite a decrease in blood flow caused by vasoconstriction, the hyperoxygenation of the arterial blood causes an increase in PO2 in the tissues85,86.

This is because hyperoxic vasoconstriction is a local vascular response to an increase in PO2. Although we cannot describe the detailed mechanism, it appears to be the increase in PO2 at the level of the terminal arterioles or the periarteriolar space that triggers vasoconstriction. So this is a very precise regulation of blood flow to adjust for the requirements of the perfused tissue unit. The hypothesis can thus be made that as long as in a given area, oxygen pressure has not increased beyond a certain threshold, the vasoconstrictive effect does not occur. In support of this hypothesis, we carried out a study on cutaneous microcirculation due to its accessibility and sensitivity to hyperoxic vasoconstriction42.

Ten patients treated for localized ischemia with HBO 2.5 ata underwent a study in which transcutaneous pressures of oxygen (TcPO2) were measured and microcirculatory blood flow was measured. Using transcutaneous oximetry and Doppler laser flowmetry respectively, the ischemic and controlateral (control) areas were evaluated in 3 different conditions: atmospheric air, NBO and HBO 2.5 ata. Our results showed that cutaneous blood flow decreased in the areas where pressures of oxygen increased beyond normal levels but that this decrease did not take place in areas where the values of pressures of oxygen remained subnormal (Table 1.5-1 - Figure 1.5-1).

Area

Ischemic

Contralateral

Area

Ischemic

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