EXCESS OXYGEN DELIVERY DURING MUSCLE CONTRACTIONS IN SPONTANEOUSLY HYPERTENSIVE RATS

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.