Vol. 276, Issue 5, H1616-H1624, May 1999
Dynamics of tissue oxygenation in isolated rabbit heart as
measured with near-infrared spectroscopy
Bas
de Groot,
Coert J.
Zuurbier, and
Johannes H. G. M.
van Beek
Laboratory for Physiology, Institute for Cardiovascular
Research, Vrije Universiteit, 1081 BT Amsterdam, The Netherlands
We investigated the role of myoglobin (Mb) in
supplying O2 to mitochondria
during transitions in cardiac workload. Isovolumic rabbit hearts
(n = 7) were perfused retrogradely
with hemoglobin-free Tyrode solution at 37°C. Coronary venous
O2 tension was measured polarographically, and tissue oxygenation was measured with
two-wavelength near-infrared spectroscopy (NIRS), both at a time
resolution of ~2 s. During transitions to anoxia, 68 ± 2% (SE)
of the NIRS signal was due to Mb and the rest to cytochrome oxidase.
For heart rate steps from 120 to 190 or 220 beats/min, the NIRS signal
decreased significantly by 6.9 ± 1.3 or 11.1 ± 2.1% of the
full scale, respectively, with response times of 11.0 ± 0.8 or 9.1 ± 0.5 s, respectively. The response time of end-capillary
O2 concentration
([O2]), estimated from
the venous [O2], was
8.6 ± 0.8 s for 190 beats/min (P < 0.05 vs. NIRS time) or 8.5 ± 0.9 s for 220 beats/min
(P > 0.05). The mean response times
of mitochondrial O2 consumption
(
O2) were 3.7 ± 0.7 and
3.6 ± 0.6 s, respectively. The deoxygenation of oxymyoglobin
(MbO2) accounted for only
12-13% of the total decrease in tissue
O2, with the rest being physically
dissolved O2. During 11%
reductions in perfusion flow at 220 beats/min, Mb was 1.5 ± 0.4%
deoxygenated (P < 0.05), despite the
high venous PO2 of 377 ± 17 mmHg,
indicating metabolism-perfusion mismatch. We conclude that the
contribution of MbO2 to the
increase of O2 during heart
rate steps in saline-perfused hearts was small and slow compared with
that of physically dissolved
O2.
myoglobin; mitochondrial oxygen consumption; Gregg
phenomenon
