| Abstract: | Several studiesindicate that immune responses are markedly depressed early after onsetof hemorrhage. Decreased organ blood flow has been implicated in thepathophysiology of altered immune responses after trauma-hemorrhage. Inthis regard, administration ofL-arginine has been shown torestore depressed intestinal and hepatic blood flow aftertrauma-hemorrhage, probably due to provision of substrate forconstitutive nitric oxide synthase (cNOS). It remains unknown, however,whether administration ofL-arginine also amelioratesdepressed splenic blood flow and whether this agent has any salutaryeffects on depressed splenocyte functions after trauma-hemorrhage. Malerats underwent sham operation or laparotomy and were bled to andmaintained at a mean arterial blood pressure of 40 mmHg until 40% ofmaximum shed blood volume (MBV) was returned as Ringer lactate (RL).Hemorrhaged rats were then resuscitated with RL (4 times MBV over 1 h).During resuscitation, rats received 300 mg/kgL-arginine or saline (vehicle)intravenously; 4 h later, splenic blood flow, splenocyte proliferation,and splenocyte interleukin (IL)-2 and IL-3 were determined.Administration of L-arginineimproved depressed splenic blood flow and restored depressed splenocytefunctions after trauma-hemorrhage. Therefore, provision ofL-arginine during resuscitationafter trauma-hemorrhage should be considered a novel and safe approachfor improving splenic organ blood flow and depressed splenocytefunctions under such conditions. |
