[Measurement of arterial O 2 pressure with and without O 2 inhalation after lung damage by smoke. Bioenergetic switch of the microcirculation in the whole body with various effects on the lung and moreover in the tissue. Decrease of venous mixed pO 2 as further basic effect of the O 2 multistep regeneration process].

During an (involuntary) self-test with pulmonary impairment by smoke exposure the following physiological basic principles were disclosed in the blood capillary system (and lung alveoli): 1. The normal arterial response of the lung to pO2 changes can be paralysed by severe smoke exposure to such an extent that the Oxygen Multistep Regeneration Process is not or hardly able to elevate the arterial pO2 resting level above the age-matched expected value. As a cause of this failure a very large volume of functionally shunted blood of 15-20% was detected using a method according to Thews. Very intensive and long-lasting exercise training acts as an antidote. 2. Severe stress influences lead to such changes in the tissue capillary system that the oxygen utilization deteriorates markedly and, hence, both the peripheral (pO2-ven) and mixed venous pO2-ven increase noticeably, followed by a surprisingly diminished oxygen transport to tissue (see eta nomogram). 3. Both the peripheral venous pO2-ven and the mixed venous pO2-ven are permanently decreased by the Oxygen Multistep Regeneration Process. It follows that by this process the utilization eta of oxygen-binding capacity of blood is much more improved than hitherto supposed (see measurement given in the text: decrease of pO2-ven from 40 mm Hg (5.3 kPa) to 27 mm Hg (3.6 kPa). This corresponds to an increase of eta from 20 to 44% [!] ). Considering these recent findings, it is inadmissible to conclude only from the lack of permanently increased arterial pO2 to the failure of the Oxygen Multistep Regeneration Process. According to our suggestions these three basic principles are jointly founded on an bioenergetic switch (or trigger) mechanism of microcirculation exerting different influences on the lung (change of arterial pO2) and on the peripheral tissue (change of pO2-ven). The trigger mechanism mentioned above is discussed in more detail in this paper. In case of pulmonary impairment by smoke exposure appropriate therapeutic measures have to aim at re-opening of the capillary network in the best possible way and at restoring optimum gassing of alveoli, i.e., reducing micro-atelectases.