Diaphragm microvascular plasma po measured in vivo.
Poole, David C., Peter D. Wagner, and David F. Wilson.
Departments of Kinesiology and Anatomy/Physiology, Kansas State
University, Manhattan, KS. 66506-5602. Department of Medicine,
University of California, San Diego, 9500 Gilman Drive, La Jolla, CA.
92093-0623 and Department of Biochemistry and Biophysics, Medical
School, University of Pennsylvania, Philadelphia, PA. 19104
APStracts 2:0306A, 1995.
Phosphorescence quenching techniques measure microvascular PO2 without
direct surgical manipulation of the tissue. At a given arterial PO2,
microvascular PO2 reflects the local O2 uptake to O2 delivery ratio
i.e., O2/O2. We evaluated the potential of phosphorescence quenching
to determine microvascular PO2 in the rat costal diaphragm (PO2dia).
PO2dia and arterial blood gases were monitored across transient
changes of inspired O2 among 21, 10 and 100% and also during
hypotensive states evoked by progressive phlebotomy. Following a
transit delay, PO2dia responded rapidly to alterations of inspired
and thus arterial PO2 with half-times of the response averaging 5-7 s
for switches to a lower inspired O2 (i.e., 21-10, 100-21, 100-10%)
and also 10-21%. By comparison, half-times of the 10-100 and 21-100%
switches were longer (11 s [P=0.085] and 21 s [P&LT0.05],
respectively). Below a mean arterial blood pressure (BP) of 120-130
mmHg, PO2dia decreased as a linear function of BP with these
variables being significantly correlated in each instance (n=5, range
for r=0.851-0.937, p&LT0.01 for all animals). From these results,
it appears feasible to measure PO2dia in the spontaneously breathing
rat in vivo under steady-state and transient conditions. Also, during
progressive hypotension, the PO2dia fall is significantly related to
falling BP, likely as a consequence of an increased metabolic demand
(increased ventilation and diaphragm O2) concommitant with decreased
blood flow. We conclude that phosphorescence quenching techniques
offer a powerful tool for assessing diaphragm physiology and
pathophysiology.
Received 22 December 1994; accepted in final form 6 July 1995.
APS Manuscript Number A1299-4.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 18 July 1995.