Nishikawa Y, Lew W Y
Department of Medicine, Department of Veterans Affairs Medical Center, San Diego, California 92161, USA.
Am J Physiol. 1995 Sep;269(3 Pt 2):H1098-105. doi: 10.1152/ajpheart.1995.269.3.H1098.
We examined endotoxin-induced myocardial depression in 31 anesthetized rabbits using left ventricular end-systolic and end-diastolic pressure-volume relationships (sonomicrometers). In the control group, endotoxin (100 micrograms/kg iv) induced systolic depression (> 10% increase in end-systolic volume at matched end-systolic pressure) in 9 of 16 and diastolic dilation (> 10% increase in end-diastolic volume at matched end-diastolic pressure) in 8 of 16 rabbits within 7 h, unrelated to hypotension, acidosis, or hypoxia. Seven rabbits were pretreated with nitrogen mustard (1-2 mg/kg iv 4 and 2 days before) to decrease circulating neutrophils and monocytes by 98%. Endotoxin did not induce systolic depression in any rabbit (P = 0.01 compared with control), and diastolic dilation developed in one rabbit (P = 0.12). In eight rabbits pretreated with dimethylthiourea (DMTU; 500 mg/kg iv 30 min before), an intracellular free radical scavenger, systolic depression developed in one (P = 0.05) and diastolic dilation in five (P = 0.44). We conclude that cells inhibited by nitrogen mustard (e.g., neutrophils, monocytes, or macrophages) mediate endotoxin-induced left ventricular systolic depression. DMTU inhibited endotoxin-induced systolic but not diastolic dysfunction.
我们使用左心室收缩末期和舒张末期压力-容积关系（超声心动图），在31只麻醉兔中研究了内毒素诱导的心肌抑制。在对照组中，16只兔子中有9只在7小时内出现收缩期抑制（在匹配的收缩末期压力下，收缩末期容积增加>10%），16只兔子中有8只出现舒张期扩张（在匹配的舒张末期压力下，舒张末期容积增加>10%），这与低血压、酸中毒或缺氧无关。7只兔子预先用氮芥（在4天和2天前静脉注射1-2mg/kg）处理，以使循环中的中性粒细胞和单核细胞减少98%。内毒素在任何兔子中均未诱导收缩期抑制（与对照组相比，P = 0.01），仅1只兔子出现舒张期扩张（P = 0.12）。在8只预先用细胞内自由基清除剂二甲基硫脲（DMTU；在30分钟前静脉注射500mg/kg）处理的兔子中，1只出现收缩期抑制（P = 0.05），5只出现舒张期扩张（P = 0.44）。我们得出结论，受氮芥抑制的细胞（如中性粒细胞、单核细胞或巨噬细胞）介导内毒素诱导的左心室收缩期抑制。DMTU抑制内毒素诱导的收缩期功能障碍，但不抑制舒张期功能障碍。
