Greenberg R S, Helfaer M A, Kirsch J R, Moore L E, Traystman R J
Department of Anesthesiology and Critical Care Medicine, Johns Hopkins Medical Institutions, Baltimore, MD.
Crit Care Med. 1994 Mar;22(3):384-92. doi: 10.1097/00003246-199403000-00006.
We tested the hypothesis that, in piglets, the intravenous administration of the reversible inhibitor of nitric oxide synthase, NG-mono-methyl-L-arginine, decreases cerebral blood flow via a mechanism unrelated to cerebral oxygen consumption.
Prospective, randomized, controlled animal study.
Animal laboratory at a university.
Pentobarbital-anesthetized piglets (1 to 2 wks of age; 2.6 to 4.0 kg).
Piglets were treated with either 50 mg of NG-mono-methyl-L-arginine, 100 mg of NG-mono-methyl-L-arginine, or an equal volume of saline by intravenous infusion over 10 mins.
Mean arterial pressure increased after NG-mono-methyl-L-arginine (50 mg dose: 84 +/- 6 to 100 +/- 7 mmHg; 100 mg dose: 82 +/- 4 to 107 +/- 4 mmHg; p < .001). Forebrain blood flow (microspheres) decreased (37 +/- 2 to 30 +/- 2 mL/min/100 g; p < .05) and cerebrovascular resistance increased (2.1 +/- 0.2 to 3.5 +/- 0.3 mmHg/mL/min/100 g; p < .05) only after 100 mg of NG-mono-methyl-L-arginine. Neurohypophysis blood flow decreased to 56 +/- 9% of the control value, while forebrain blood flow decreased only to 81 +/- 4% of the control value after 100 mg of NG-mono-methyl-L-arginine administration. Blood flow returned to control values by 30 mins after infusion. NG-mono-methyl-L-arginine administration had no effect on cerebral oxygen consumption at either dose. Intravenous administration of L-arginine (300 mg) immediately after the infusion of 100 mg of NG-mono-methyl-L-arginine was associated with prompt (by 3 mins) recovery of blood flow to all brain regions that were affected by NG-mono-methyl-L-arginine.
These data suggest that nitric oxide and/or a nitric oxide-containing substance is an important mediator of cerebrovascular tone in piglets, acting via a mechanism unrelated to altering cerebral oxygen consumption.
我们检验了如下假设，即对于仔猪，静脉注射一氧化氮合酶可逆抑制剂NG-单甲基-L-精氨酸会通过一种与脑氧消耗无关的机制降低脑血流量。
前瞻性、随机、对照动物研究。
一所大学的动物实验室。
戊巴比妥麻醉的仔猪（1至2周龄；体重2.6至4.0千克）。
仔猪通过静脉输注在10分钟内分别接受50毫克NG-单甲基-L-精氨酸、100毫克NG-单甲基-L-精氨酸或等体积的生理盐水治疗。
注射NG-单甲基-L-精氨酸后平均动脉压升高（50毫克剂量组：从84±6毫米汞柱升至100±7毫米汞柱；100毫克剂量组：从82±4毫米汞柱升至107±4毫米汞柱；p<0.001）。仅在注射100毫克NG-单甲基-L-精氨酸后，前脑血流量（微球法）降低（从37±2降至30±2毫升/分钟/100克；p<0.05），脑血管阻力增加（从2.1±0.2升至3.5±0.3毫米汞柱/毫升/分钟/100克；p<0.05）。注射100毫克NG-单甲基-L-精氨酸后，神经垂体血流量降至对照值的56±9%，而前脑血流量仅降至对照值的81±4%。输注后30分钟血流量恢复至对照值。两种剂量的NG-单甲基-L-精氨酸对脑氧消耗均无影响。在输注100毫克NG-单甲基-L-精氨酸后立即静脉注射L-精氨酸（300毫克），可使受NG-单甲基-L-精氨酸影响的所有脑区的血流量迅速（3分钟内）恢复。
这些数据表明，一氧化氮和/或含一氧化氮的物质是仔猪脑血管张力的重要调节因子，其作用机制与改变脑氧消耗无关。
