Lieberthal W, Thompson A, Valeri C R
Evans Memorial Department of Clinical Research, Boston University Medical Center, Mass., USA.
Kidney Blood Press Res. 1996;19(6):340-6. doi: 10.1159/000174097.
The systemic and renal hemodynamic responses to nitric oxide (NO) inhibition with L-Name were compared in both normotensive, normovolemic rats and in rats following acute hemorrhagic hypotension. The mean arterial blood pressure increased in normovolemic as well as in hemorrhaged, hypotensive rats. The systemic vascular resistance also increased in both groups, but the increase was greater in normotensive rats (104 +/- 11%) than in hypotensive rats (64 +/- 14%). The renal vascular resistance also increased more in normotensive rats (189 +/- 20%) than in hypotensive rats (102 +/- 19%; p < 0.05). The glomerular filtration rate was markedly reduced by L-Name in normovolemic rats (from 3.0 +/- 0.1 to 2.1 +/- 0.1 ml/min/300 g), but increased in hemorrhaged rats following L-Name (from 1.8 +/- 0.2 to 2.5 +/- 0.2 ml/min/300 g). In summary, the L-Name-induced increase in vascular resistance is markedly reduced following hemorrhage, suggesting that NO production or availability is reduced. However, the NO production continues in the hemorrhaged rat and contributes substantially to the hypotension and functional renal insufficiency associated with acute severe volume depletion.
在正常血压、血容量正常的大鼠以及急性失血性低血压大鼠中，比较了L-精氨酸甲酯（L-Name）抑制一氧化氮（NO）后全身和肾脏的血流动力学反应。正常血容量以及出血性低血压大鼠的平均动脉血压均升高。两组的全身血管阻力也均增加，但正常血压大鼠的增加幅度更大（104±11%），高于低血压大鼠（64±14%）。正常血压大鼠的肾血管阻力增加幅度也大于低血压大鼠（189±20% 对比102±19%；p<0.05）。L-精氨酸甲酯使正常血容量大鼠的肾小球滤过率显著降低（从3.0±0.1降至2.1±0.1 ml/min/300 g），但使出血大鼠在使用L-精氨酸甲酯后的肾小球滤过率增加（从1.8±0.2升至2.5±0.2 ml/min/300 g）。总之，出血后L-精氨酸甲酯诱导的血管阻力增加明显降低，提示NO生成或可用性降低。然而，出血大鼠中NO生成仍在继续，并在很大程度上导致了与急性严重容量耗竭相关的低血压和功能性肾功能不全。
