Hayward R, Lefer A M
Department of Physiology, Jefferson Medical College, Thomas Jefferson University, Philadelphia, PA 19107, USA.
Endothelium. 1998;6(1):71-9. doi: 10.3109/10623329809053406.
We investigated the effects of L-arginine administration in a rat model of traumatic shock. Pentobarbital-anesthetized rats subjected to drum trauma developed a severe shock condition characterized by marked hypotension to 55-70 mmHg, a survival time of only 90 +/- 21 min, and significant increases in ileal myeloperoxidase (MPO) activity (P < 0.01). In addition, superior mesenteric artery (SMA) rings isolated from rats subjected to traumatic shock relaxed to the endothelium-dependent vasodilator acetylcholine significantly less than rings isolated from control rats (p < 0.01). Administration of L-arginine (30 mg/kg bolus + 10 mg/kg/hr, i.v.) 10 min following trauma prolonged survival time to 213 +/- 33 min (p < 0.05) and attenuated ileal MPO activity (p < 0.01) indicative of reduced neutrophil infiltration. Furthermore, SMA endothelial function was significantly (p < 0.01) preserved in L-arginine treated traumatic shock rats. These results indicate that L-arginine plays a key role in the endothelial dysfunction associated with traumatic shock and affords significant protective effects which may be manifested by an inhibition of leukocyte-endothelial cell interactions.
我们研究了给予L-精氨酸对创伤性休克大鼠模型的影响。戊巴比妥麻醉的大鼠遭受鼓面创伤后出现严重休克状态，其特征为显著低血压至55 - 70 mmHg，存活时间仅90±21分钟，回肠髓过氧化物酶（MPO）活性显著增加（P<0.01）。此外，从遭受创伤性休克的大鼠分离的肠系膜上动脉（SMA）环对内皮依赖性血管舒张剂乙酰胆碱的舒张反应明显低于从对照大鼠分离的环（p<0.01）。创伤后10分钟静脉注射L-精氨酸（30 mg/kg推注+10 mg/kg/小时）可将存活时间延长至213±33分钟（p<0.05），并减弱回肠MPO活性（p<0.01），表明中性粒细胞浸润减少。此外，L-精氨酸治疗的创伤性休克大鼠的SMA内皮功能得到显著保留（p<0.01）。这些结果表明，L-精氨酸在与创伤性休克相关的内皮功能障碍中起关键作用，并提供显著的保护作用，这可能通过抑制白细胞与内皮细胞的相互作用来体现。
