Horton J W
Department of Surgery, University of Texas Southwestern Medical Center, Dallas 75235-9031, USA.
Am J Physiol. 1996 Dec;271(6 Pt 2):H2615-21. doi: 10.1152/ajpheart.1996.271.6.H2615.
We have shown that cutaneous burn injury impairs cardiac contractile performance; however, the mechanisms remain unclear. In this study, New Zealand White rabbits were anesthetized with isoflurane, given a full-thickness scald burn over 30% of total body surface area, and resuscitated with lactated Ringer solution (4 ml.kg-1.%burn-1 for 24 h); rabbits handled in an identical fashion were given a sham burn. Serum obtained from burned and control (sham-burned) rabbits was aliquoted and frozen at -70 degrees C until assay. Polymorphonuclear neutrophils (PMN) were isolated 24 h postburn from both sham and burned rabbits to yield preparations with > 95% PMN with > 95% viability. Cardiac myocytes were isolated by retrograde perfusion of hearts with Ca(2+)-free collagenase-Tyrode buffer, suspended in Krebs-Henseleit buffer containing 10% fetal bovine serum and 1.8 mM Ca2+, and incubated (1 x 10(5) cells/well) in a CO2 incubator under several experimental conditions, including buffer alone, buffer plus 10% burn serum, buffer plus 10% sham serum, or buffer plus either burn or sham PMN (25 x 10(5) cells/well). Myocyte viability (%) and creatine kinase (CK; units.ml-1.10(5) cells-1) were unchanged after incubation with sham plasma or sham PMN. Incubation of sham myocytes with burn plasma caused viability to fall (from 79 +/- 3 to 54 +/- 4%, P < 0.002), whereas CK rose (from 1,639 +/- 115 to 2,803 +/- 132 units.ml-1.10(5) cells-1, P < 0.01). Similarly, incubation of sham myocytes with burn PMN reduced viability (from 83 +/- 2 to 50 +/- 3%, P < 0.01), whereas CK remained unchanged (1,880 +/- 168 units.ml-1.10(5) cells-1). Our data indicate that circulating myocardial depressant factors after burn injury contribute to cardiac myocyte injury.
我们已经表明，皮肤烧伤会损害心脏收缩功能；然而，其机制仍不清楚。在本研究中，用异氟烷麻醉新西兰白兔，对其30%的体表面积进行全层烫伤，并用乳酸林格氏液（4 ml·kg-1·%烧伤-1，持续24小时）进行复苏；以相同方式处理的兔子进行假烧伤。从烧伤和对照（假烧伤）兔子获得的血清进行分装，并在-70℃下冷冻直至检测。在烧伤后24小时从假烧伤和烧伤兔子中分离多形核中性粒细胞（PMN），以获得PMN含量>95%且活力>95%的制剂。通过用无钙胶原酶-台氏缓冲液逆行灌注心脏来分离心肌细胞，将其悬浮于含有10%胎牛血清和1.8 mM Ca2+的Krebs-Henseleit缓冲液中，并在几种实验条件下于二氧化碳培养箱中孵育（1×10(5)个细胞/孔），这些条件包括单独的缓冲液、缓冲液加10%烧伤血清、缓冲液加10%假烧伤血清，或缓冲液加烧伤或假烧伤PMN（25×10(5)个细胞/孔）。与假血浆或假PMN孵育后，心肌细胞活力（%）和肌酸激酶（CK；单位·ml-1·10(5)个细胞-1）没有变化。用烧伤血浆孵育假心肌细胞导致活力下降（从79±3降至54±4%，P<0.002），而CK升高（从1,639±115升至2,803±132单位·ml-1·10(5)个细胞-1，P<0.01）。同样，用烧伤PMN孵育假心肌细胞降低了活力（从83±2降至50±3%，P<0.01），而CK保持不变（1,880±168单位·ml-1·10(5)个细胞-1）。我们的数据表明，烧伤后循环中的心肌抑制因子会导致心肌细胞损伤。
