Miles D, Hurst T S, Saxena A, Mayers I, Johnson D H
Department of Surgery, University of Saskatchewan, Saskatoon, Canada.
Can J Anaesth. 1999 Feb;46(2):142-7. doi: 10.1007/BF03012548.
To study the effects of a systemic thermal injury on the pulmonary vasculature with and without inhibitors of lipid peroxidation (U74389G).
In a prospective, placebo control, randomized, and blinded multi-group study, burn shock was induced by scalding thermal injury (65C) to 35% body surface area in rabbits (n = 28). Hemodynamics and gas exchange were followed for 240 min post burn in four groups: No Burn, Burn-Control, Burn-U74 (10 mg.Kg-1 U74389G), No Burn-U74 (10 mg.Kg-1 U74389G).
Scald resulted in early pulmonary injury as measured by increased pulmonary vascular resistance in the pooled Burn group compared with the No Burn groups (942 +/- 358 vs 605 +/- 255 dynes.sec-1.cm-5 respectively, P < 0.05). These pulmonary changes were associated with alveolar sequestration of leukocytes (4.8 +/- 2.9 vs 17.7 +/- 6.0 cells x 10(9).L-1, P < 0.05) in the No Burn and Burn groups respectively. Histological evidence of decreased neutrophil sequestration after scald injury was present in U74 treated animals (3+ vs 2+, P < 0.05 in the Burn and No Burn groups respectively and 2+ vs 2+, P > 0.05 in the Burn-U74 and No Burn-U74 groups respectively) although bronchial alveolar lavage still demonstrated neutrophil sequestration (5.3 +/- 2.5 vs 12.2 +/- 3.3 cell 10(9).L-1, P < 0.05 in No Burn-U74 and Burn-U74 groups respectively). Similarly, circulating white blood cells were increased in the Burn group but not Burn-U74 group four hours post burn. The increase in pulmonary vascular resistance after burn was not altered by administration of U74.
Systemic burn results in early pulmonary vascular changes associated with leukocyte sequestration. After scald injury administration of lazaroids (U744389G) did not lessen pulmonary vascular resistance changes but did reduce neutrophil sequestration.
研究全身性热损伤对肺血管系统的影响，以及脂质过氧化抑制剂（U74389G）在其中的作用。
在一项前瞻性、安慰剂对照、随机双盲多组研究中，通过将兔体表面积35%烫伤（65℃）诱导烧伤休克（n = 28）。四组动物在烧伤后240分钟内监测血流动力学和气体交换情况，分组如下：未烧伤组、烧伤对照组、烧伤-U74组（10 mg·Kg-1 U74389G）、未烧伤-U74组（10 mg·Kg-1 U74389G）。
与未烧伤组相比，烫伤导致合并的烧伤组早期肺损伤，表现为肺血管阻力增加（分别为942±358与605±255达因·秒-1·厘米-5，P < 0.05）。这些肺部变化分别与未烧伤组和烧伤组肺泡内白细胞滞留有关（分别为4.8±2.9与17.7±6.0细胞×10(9)/L，P < 0.05）。U74处理的动物烫伤后中性粒细胞滞留减少有组织学证据（烧伤组和未烧伤组分别为3+比2+，P < 0.05；烧伤-U74组和未烧伤-U74组分别为2+比2+，P > 0.05），尽管支气管肺泡灌洗仍显示有中性粒细胞滞留（未烧伤-U74组和烧伤-U74组分别为5.3±2.5与12.2±3.3细胞×10(9)/L，P < 0.05）。同样，烧伤后4小时烧伤组循环白细胞增加，但烧伤-U74组未增加。给予U74并未改变烧伤后肺血管阻力的增加。
全身性烧伤导致早期肺血管变化并伴有白细胞滞留。烫伤后给予拉扎罗类药物（U744389G）并未减轻肺血管阻力变化，但确实减少了中性粒细胞滞留。
