Lorente J A, Landín L, De Pablo R, Renes E, Liste D
Unidades de Cuidados Intensivos, Hospital Ramón y Cajal, Madrid, Spain.
Crit Care Med. 1993 Sep;21(9):1287-95. doi: 10.1097/00003246-199309000-00010.
To investigate the role of nitric oxide in the regulation of vascular tone in patients with the sepsis syndrome.
Prospective, intervention study.
Tertiary care hospital.
Fifteen patients admitted to our medical intensive care unit with the diagnosis of sepsis syndrome by defined criteria.
Eight patients received N omega-nitro-L-arginine (20 mg/kg, iv bolus) followed by L-arginine (200 mg/kg, iv bolus). Seven patients received L-arginine alone (200 mg/kg).
In the first group, hemodynamic and oxygen transport variables were recorded at baseline, during 45 mins after the injection of N omega-nitro-L-arginine, and during 45 mins after the administration of L-arginine. In the second group, hemodynamic parameters were recorded at baseline and during 15 mins after the administration of L-arginine. Data are mean +/- SEM. The administration of N omega-nitro-L-arginine was followed by hypertension (mean blood pressure increased from 89 +/- 8 to a maximum of 140 +/- 12 mm Hg) accompanied by a decrease in cardiac index (from 3.51 +/- 0.39 to a minimum of 2.65 +/- 0.21 L/min/m2) and an increase in right atrial and pulmonary artery occlusion pressure. Systemic vascular resistance index increased from 1871.1 +/- 302.3 to 3825.6 +/- 244.4 dyne.sec/cm5.m2, and pulmonary vascular resistance increased from 533.2 +/- 125.8 to 816.0 +/- 117.3 dyne.sec/cm5.m2. These changes induced by N omega-nitro-L-arginine were reversed by the administration of L-arginine. The administration of L-arginine to another group of patients caused transient hypotension (from 103 +/- 6 to 81 +/- 10 mm Hg) and an increase in cardiac index (from 3.57 +/- 0.15 to 4.74 +/- 0.54 L/min/m2). Both systemic and pulmonary vascular resistance indices decreased (from 1987.6 +/- 163.9 to 1251.4 +/- 231.5 dyne.sec/cm5.m2, and from 486.1 +/- 65.2 to 380.5 +/- 70.3 dyne.sec/cm5.m2). Parallel to the increase in oxygen transport due to the increase in cardiac output, oxygen consumption index increased significantly 1 min after L-arginine (from 127.0 +/- 19.0 to 182.5 +/- 37.3 mL/min/m2). All mentioned changes were statistically significant (p < .05).
A continuous basal release of nitric oxide plays a role in the regulation of systemic and pulmonary vascular tone in patients with sepsis syndrome. L-arginine has systemic and pulmonary vasodilatory actions.
研究一氧化氮在脓毒症综合征患者血管张力调节中的作用。
前瞻性干预研究。
三级医疗中心。
15例因脓毒症综合征确诊收入我院重症监护病房的患者。
8例患者先静脉推注Nω-硝基-L-精氨酸（20mg/kg），随后静脉推注L-精氨酸（200mg/kg）。7例患者仅静脉推注L-精氨酸（200mg/kg）。
第一组在基线、注射Nω-硝基-L-精氨酸后45分钟以及给予L-精氨酸后45分钟记录血流动力学和氧运输变量。第二组在基线以及给予L-精氨酸后15分钟记录血流动力学参数。数据以均值±标准误表示。给予Nω-硝基-L-精氨酸后出现高血压（平均血压从89±8mmHg升高至最高140±12mmHg），同时心脏指数降低（从3.51±0.39降至最低2.65±0.21L/min/m²），右心房和肺动脉闭塞压升高。全身血管阻力指数从1871.1±302.3升至3825.6±244.4达因·秒/厘米⁵·平方米，肺血管阻力从533.2±125.8升至816.0±117.3达因·秒/厘米⁵·平方米。Nω-硝基-L-精氨酸引起的这些变化在给予L-精氨酸后逆转。另一组患者给予L-精氨酸后出现短暂性低血压（从103±6mmHg降至81±10mmHg），心脏指数升高（从3.57±0.15升至4.74±0.54L/min/m²）。全身和肺血管阻力指数均降低（分别从1987.6±163.9降至1251.4±231.5达因·秒/厘米⁵·平方米，从486.1±65.2降至380.5±70.3达因·秒/厘米⁵·平方米）。与心输出量增加导致的氧运输增加并行，给予L-精氨酸后1分钟氧消耗指数显著升高（从127.0±19.0升至182.5±37.3mL/min/m²）。所有上述变化均具有统计学意义（p<0.05）。
一氧化氮的持续基础释放对脓毒症综合征患者的全身和肺血管张力调节起作用。L-精氨酸具有全身和肺血管舒张作用。
