Bohlen H G
Circ Res. 1983 Jun;52(6):677-82. doi: 10.1161/01.res.52.6.677.
Chronic diabetes mellitus induced in rats by streptozotocin or of genetic origin in Db/Db mice is associated with a loss of capillaries, arteriolar constriction, and a decrease in resting and maximum blood flow. As a result of these vascular changes, as well as glycolysation of hemoglobin, it is possible that tissue Po2 is reduced at rest and cannot be substantially increased during dilatation. Tissue Po2 in the intestinal muscle layer was measured at rest and during maximal dilation. In addition, the spacing between capillaries with active flow and the velocity of red blood cell flow in capillaries were measured at rest and at maximum dilation. These measurements were made in normal and diabetic rats (streptozotocin) at age 26-30 weeks; the diabetic animals had been hyperglycemic (greater than 350 mg/100 ml) for 12-15 weeks. Tissue Po2 at a distance of about 15 microns from the arterial, mid-point, and venous end of capillaries in normal rats was 24.8 +/- 1.1 (SE), 23.1 +/- 1.2, and 22.4 +/- 0.9 mm Hg, respectively, compared with 25.8 +/- 0.9, 24.1 +/- 1.2, and 22.4 +/- 1.1 mm Hg, respectively, in diabetic rats. The maximum mid-capillary tissue Po2 during dilation was 27.7 +/- 1.3 mm Hg in normal rats and 29.7 +/- 1.5 mm Hg in diabetic rats. The average distance between capillaries was 37.6 +/- 2.0 microns in normal rats and 46.8 +/- 2.9 microns in diabetic animals; vasodilation did not change the capillary spacing in either group of animals. Capillary red cell velocity in normal rats increased from 0.98 +/- 0.11 mm/sec at rest to 2.1 +/- 0.4 mm/sec during dilatation. For comparable conditions in diabetic rats, the velocities were 0.41 +/- 0.07 and 1.06 +/- 0.19 mm/sec. The data presented indicate that the diabetic animals have tissue Po2 equivalent to those in normal rats, both at rest and during maximum vasodilation. The loss of capillaries and decreased resting and maximum capillary red cell velocity in diabetic rats would decrease the delivery of oxygen, but, apparently, a decrease in oxygen consumption occurred that allowed the intestinal tissue to have a normal Po2.
链脲佐菌素诱导大鼠产生的慢性糖尿病或基因源性的 Db/Db 小鼠糖尿病，与毛细血管丧失、小动脉收缩以及静息和最大血流量减少有关。由于这些血管变化以及血红蛋白糖基化，有可能静息时组织氧分压降低，且在血管扩张时不能大幅升高。在静息和最大扩张时测量了肠肌层的组织氧分压。此外，还测量了有血流的毛细血管之间的间距以及静息和最大扩张时毛细血管中红细胞的流速。这些测量是在 26 - 30 周龄的正常和糖尿病大鼠（链脲佐菌素诱导）中进行的；糖尿病动物已高血糖（大于 350 mg/100 ml）12 - 15 周。正常大鼠中，距毛细血管动脉端、中点和静脉端约 15 微米处的组织氧分压分别为 24.8±1.1（标准误）、23.1±1.2 和 22.4±0.9 mmHg，而糖尿病大鼠分别为 25.8±0.9、24.1±1.2 和 22.4±1.1 mmHg。扩张时毛细血管中点处的最大组织氧分压在正常大鼠中为 27.7±1.3 mmHg，在糖尿病大鼠中为 29.7±1.5 mmHg。正常大鼠中毛细血管的平均间距为 37.6±2.0 微米，糖尿病动物中为 46.8±2.9 微米；血管扩张未改变两组动物的毛细血管间距。正常大鼠毛细血管中红细胞速度从静息时的 0.98±0.11 mm/秒增加到扩张时的 2.1±0.4 mm/秒。在糖尿病大鼠的类似条件下，速度分别为 0.41±0.07 和 1.06±0.19 mm/秒。所呈现的数据表明，糖尿病动物在静息和最大血管扩张时的组织氧分压与正常大鼠相当。糖尿病大鼠毛细血管丧失以及静息和最大毛细血管红细胞速度降低会减少氧气输送，但显然，耗氧量的降低使肠组织具有正常的氧分压。
