Lash J M
Department of Physiology and Biophysics, Indiana University School of Medicine, Indianapolis 46202.
J Appl Physiol (1985). 1995 Jan;78(1):93-100. doi: 10.1152/jappl.1995.78.1.93.
During contractions of the spinotrapezius muscle in spontaneously hypertensive rats (SHR), arteriolar dilation is of normal magnitude but tissue PO2 is significantly depressed relative to normotensive [Wistar-Kyoto (WKY)] rats. This study examined the possibility that this low PO2 results from suppressed dilation of the upstream arterial feed vessels and a limitation of muscle blood flow. Contraction-induced changes in vascular resistances (R) and conductances (G) were calculated for upstream (Rup, Gup), microvascular (Rst, Gst), and downstream (Rdown, Gdown) vascular segments from measurements of pressure and flow in the rostral feed artery and vein. Feed arteries were smaller in SHR than in WKY rats at rest and after contractions (rest, 63.0 +/- 2.6 vs. 86.0 +/- 4.8 microns; 2 Hz 84.0 +/- 4.5 vs. 111.0 +/- 7.3 microns; 8 Hz, 130.0 +/- 5.9 vs. 144.0 +/- 7.1 microns). However, relative increases [times control (xCT)] in diameter and flow were greater in SHR (8 Hz diam, 2.080 +/- 0.072 vs. 1.690 +/- 0.042 xCT; 8 Hz flow, 15.700 +/- 2.057 vs. 8.170 +/- 0.752 xCT). In both groups, Rup and Rst decreased 60-70 and 85-90% after 2- and 8-Hz contractions, respectively. However, segmental vascular conductances increased more in SHR than in WKY rats (8 Hz: Gup, 18.50 +/- 3.76 vs. 8.00 +/- 1.26 xCT; Gst, 19.90 +/- 3.73 vs. 10.10 +/- 0.96 xCT; Gdown, 8.80 +/- 1.70 vs. 5.50 +/- 0.88 xCT). Therefore, upstream arterial dilation is not suppressed during muscle contractions in SHR, and deficits in muscle blood flow and oxygen delivery cannot account for the abnormally low tissue PO2 observed during muscle contractions in SHR.
在自发性高血压大鼠（SHR）斜方肌收缩期间，小动脉扩张幅度正常，但相对于正常血压的[Wistar-Kyoto（WKY）]大鼠，组织氧分压显著降低。本研究探讨了这种低氧分压是否源于上游动脉供血血管扩张受抑制以及肌肉血流受限。通过测量吻侧供血动脉和静脉的压力和流量，计算上游（Rup，Gup）、微血管（Rst，Gst）和下游（Rdown，Gdown）血管段收缩诱导的血管阻力（R）和电导（G）变化。在静息和收缩后，SHR的供血动脉均小于WKY大鼠（静息时，63.0±2.6对86.0±4.8微米；2赫兹时，84.0±4.5对111.0±7.3微米；8赫兹时，130.0±5.9对144.0±7.1微米）。然而，SHR的直径和流量相对增加倍数[相对于对照（xCT）]更大（8赫兹直径，2.080±0.072对1.690±0.042 xCT；8赫兹流量，15.700±2.057对8.170±0.752 xCT）。在两组中，2赫兹和8赫兹收缩后，Rup和Rst分别降低60 - 70%和85 - 90%。然而，SHR的节段性血管电导增加幅度大于WKY大鼠（8赫兹：Gup，18.50±3.76对8.00±1.26 xCT；Gst，19.90±3.73对10.10±0.96 xCT；Gdown，8.80±1.70对5.50±0.88 xCT）。因此，SHR肌肉收缩期间上游动脉扩张未受抑制，肌肉血流和氧输送不足不能解释SHR肌肉收缩期间观察到的异常低组织氧分压。
