Genco C M, Connolly R J, Peterson M B, Bernstein E A, Ramberg K, Zhang X, Cleveland R J, Diehl J T
Department of Cardiothoracic Surgery and Pediatric Critical Care, Tufts University School of Medicine, Boston, Massachusetts.
Ann Thorac Surg. 1992 Feb;53(2):217-26. doi: 10.1016/0003-4975(92)91322-z.
We investigated the role of pulmonary granulocyte sequestration in the development of early failure of the autoperfused working heart-lung preparation. A significant decline in the total circulating leukocyte count in 21 preparations at 60 minutes of perfusion (5.0 to 1.4 x 10(3)/microL; 28% of baseline; p less than 0.001) was observed. Differential cell counts in 14 of these preparations revealed a predominant decrease in granulocyte count (8.7% of baseline) and a moderate decline in lymphocyte count (46% of baseline). In study I, indium 111-labeled autologous granulocytes were injected intravenously into 10 adult New Zealand White rabbits. In group I (n = 5), an autoperfused working heart-lung preparation was harvested and perfused for 60 minutes. In group II (controls, n = 5), the heart-lung block was harvested following 60 minutes of in situ perfusion. Organ blocks were imaged before and after saline flush. There was a significant decline in granulocyte counts at 60 minutes of perfusion in group I versus no change in group II (I, 2.3 +/- 0.4 to 0.3 +/- 0.1; p less than 0.01; II, 1.7 +/- 0.2 to 2.3 +/- 0.5; not significant; x 10(3)/microL +/- standard error of the mean). Postflush lung activity was significantly increased in group I versus group II (I, 3,751 +/- 566; II, 1,867 +/- 532; p less than 0.05; counts +/- standard error of the mean). In study II, 15 autoperfused preparations were divided into two groups. Group I (n = 10) preparations were controls. Group II (n = 5) animals were depleted of leukocytes by pretreating with nitrogen mustard. Group I (controls) produced a bimodal survival distribution (Ia, 8.2 +/- 1.0; Ib, 26.4 +/- 2.0; hours +/- standard error of the mean). Group II survival was significantly longer than that of group Ia and similar to that of group Ib (II, 25.3 +/- 2.2; p less than 0.01 versus group Ia, not significant versus group Ib; hours +/- standard error of the mean). Hemodynamic profiles for group II closely paralleled those of group Ib. In conclusion, pulmonary sequestration of granulocytes occurs early in the autoperfused working heart-lung preparation (within 60 minutes of autoperfusion), and preoperative leukocyte depletion prolongs survival of the autoperfused working heart-lung preparation by eliminating the subset group Ia (short survivors) seen in untreated preparations.
我们研究了肺粒细胞隔离在自体灌注工作心肺制备早期功能衰竭发展过程中的作用。观察到21个制备物在灌注60分钟时循环白细胞总数显著下降(从5.0降至1.4×10³/μL;为基线的28%;p<0.001)。其中14个制备物的细胞分类计数显示粒细胞计数显著减少(为基线的8.7%),淋巴细胞计数中度下降(为基线的46%)。在研究I中,将铟111标记的自体粒细胞静脉注射到10只成年新西兰白兔体内。在I组(n = 5)中,获取自体灌注工作心肺制备物并灌注60分钟。在II组(对照组,n = 5)中,原位灌注60分钟后获取心肺组织块。在盐水冲洗前后对器官组织块进行成像。I组在灌注60分钟时粒细胞计数显著下降,而II组无变化(I组,2.3±0.4降至0.3±0.1;p<0.01;II组,1.7±0.2至2.3±0.5;无显著差异;×10³/μL±平均标准误差)。I组冲洗后肺活性显著高于II组(I组,3751±566;II组,1867±532;p<0.05;计数±平均标准误差)。在研究II中,15个自体灌注制备物分为两组。I组(n = 10)制备物为对照组。II组(n = 5)动物通过用氮芥预处理使白细胞减少。I组(对照组)呈现双峰生存分布(Ia组,8.2±1.0;Ib组,26.4±2.0;小时±平均标准误差)。II组的生存期显著长于Ia组,与Ib组相似(II组,25.3±2.2;与Ia组相比p<0.01,与Ib组相比无显著差异;小时±平均标准误差)。II组的血流动力学曲线与Ib组密切平行。总之,在自体灌注工作心肺制备中(自体灌注60分钟内)早期会发生粒细胞的肺隔离,术前白细胞减少通过消除未处理制备物中出现的Ia亚组(短期存活者)来延长自体灌注工作心肺制备物的生存期。