Me. Ward et al., SYSTEMIC AND DIAPHRAGMATIC OXYGEN DELIVERY-CONSUMPTION RELATIONSHIPS DURING HEMORRHAGE, Journal of applied physiology, 77(2), 1994, pp. 653-659
When tissue O-2 delivery falls below a critical threshold, tissue O-2
uptake (Vo(2)) becomes limited. We compared critical O-2 delivery and
critical and maximum O-2 extraction ratios of the resting and contract
ing left hemidiaphragm with those of nondiaphragmatic tissues in seven
dogs. The left hemidiaphragm was perfused through the left inferior p
hrenic artery with blood from the left femoral artery. Phrenic venous
blood was sampled through a catheter in the inferior phrenic vein. Sys
temic O-2 delivery was reduced in stages by controlled hemorrhage. Lef
t diaphragmatic Vo(2) during rest and during 3 min of continuous stimu
lation (3 Hz) of the left phrenic nerve and Vo(2) of the remaining non
left hemidiaphragmatic tissues were measured at each stage. Critical d
iaphragmatic O-2 delivery for the resting diaphragm averaged 0.8 +/- 0
.16 ml.min(-1).100 g(-1) with a critical O-2 extraction ratio of 65.5
+/- 6%. In the contracting diaphragm, they averaged 5.1 +/- 0.9 ml.min
(-1).100 g(-1) and 81 +/- 5%, respectively. Whole body O-2 delivery at
which resting diaphragmatic Vo(2) became supply limited was similar t
o that for nondiaphragmatic tissues. By comparison, supply limitation
of Vo(2) occurred at a higher systemic O-2 delivery in the contracting
diaphragm than in the rest of the body despite the increase in critic
al diaphragmatic extraction ratio. Thus, oxygenation of the isolated d
iaphragm does not appear to be preferentially preserved during general
ized reductions in O-2 delivery. These results suggest that, in diseas
es associated with increased work of breathing and decreased O-2 deliv
ery, the diaphragm may become metabolically impaired before limitation
of Vo(2) is observed systemically.