DIAPHRAGM MICROVASCULAR PLASMA PO2 MEASURED IN-VIVO

Phosphorescence quenching techniques measure microvascular PO2 without direct surgical manipulation of the tissue. At a given arterial Pot, microvascular got reflects the local O-2 uptake-to-O-2 delivery ratio, i.e., V overdot O-2/Q overdot O-2. We evaluated the potential of phos phorescence quenching to determine microvascular PO2 in the rat costal diaphragm (Pdia(O2)). Pdia(O2) and arterial blood gases were monitore d across transient changes of inspired O-2 among 21, 10, and 100% and also during hypotensive states evoked by progressive phlebotomy. After a transit delay, Pdia(O2) responded rapidly to alterations of inspire d and thus arterial PO2, with half times of the response averaging 5-7 s for switches to a lower inspired O-2 (i.e., from 21 to 10%, from 10 0 to 21%, and from 100 to 10%) and also from 10 to 21%. By comparison, half times of the 10 to 100% and 21 to 100% switches were longer [11 s (P = 0.085) and 21 s (P < 0.05), respectively]. Below a mean arteria l blood pressure (BP) of 120-130 mmHg, Pdia(O2) decreased as a linear function of BP, with these variables being significantly correlated in each instance (n = 5, r = 0.851-0.937, P < 0.01 for all animals). Fro m these results, it appears feasible to measure Pdia(O2) in the sponta neously breathing rat in vivo under steady-state and transient conditi ons. Also, during progressive hypotension, the fall in Pdia(O2) is sig nificantly related to falling BP, likely as a consequence of an increa sed metabolic demand (increased ventilation and diaphragm V overdot O- 2) concomitant with decreased blood flow. We conclude that phosphoresc ence quenching techniques offer a powerful tool for assessing diaphrag m physiology and pathophysiology.