Jm. Lash et Hg. Bohlen, EXCESS OXYGEN DELIVERY DURING MUSCLE CONTRACTIONS IN SPONTANEOUSLY HYPERTENSIVE RATS, Journal of applied physiology, 78(1), 1995, pp. 101-111
These experiments determined whether a deficit in oxygen supply relati
ve to demand could account for the sustained decrease in tissue Po-2 o
bserved during contractions of the spinotrapezius muscle in spontaneou
sly hypertensive rats (SHR). Relative changes in blood flow were deter
mined from measurements of vessel diameter and red blood cell velocity
. Venular hemoglobin oxygen saturation measurements were performed by
using in vivo spectrophotometric techniques. The relative dilation [ti
mes control (XCT)] of arteriolar vessels during contractions was as la
rge or greater in SHR than in normotensive rats (Wistar-Kyoto), as wer
e the increases in blood flow (2 Hz, 3.50 +/- 0.69 vs. 3.00 +/- 1.05XC
T; 4 Hz, 10.20 +/- 3.06 vs. 9.00 +/- 1.48XCT; 8 Hz, 16.40 +/- 3.95 vs.
10.70 +/- 2.48XCT). Venular hemoglobin oxygen saturation was lower in
the resting muscle of SHR than of Wistar-Kyoto rats (31.0 +/- 3.0 vs.
43.0 +/- 1.9%) but was higher in SHR after 4- and 8-Hz contractions (
4 Hz, 52.0 +/- 4.8 vs. 43.0 +/- 3.6%; 8 Hz, 51.0 +/- 4.6 vs. 41.0 +/-
3.6%). Therefore, an excess in oxygen delivery occurs relative to oxyg
en use during muscle contractions in SHR. The previous and current res
ults can be reconciled by considering the possibility that oxygen exch
ange is limited in SHR by a decrease in anatomic or perfused capillary
density, arteriovenular shunting of blood, or decreased transit time
of red blood cells through exchange vessels.