Niemann James T, Garner Daniel, Lewis Roger J
Department of Emergency Medicine, Research and Education Institute at Harbor-UCLA Medical Center, 1000 West Carson Street, Torrance, CA 90509, USA.
Crit Care Med. 2004 Aug;32(8):1753-8. doi: 10.1097/01.ccm.0000132899.15242.d3.
Left ventricular dysfunction after successful cardiopulmonary resuscitation contributes to early death following resuscitation. The stress-induced proinflammatory cytokines, particularly tumor necrosis factor-alpha and interleukin-1beta, are known to depress myocardial function. We hypothesized that tumor necrosis factor-alpha and interleukin-1beta, synthesized and released in response to the stress of global ischemia accompanying cardiac arrest, play a role in development of postresuscitation left ventricular dysfunction.
Hemodynamic variables, tumor necrosis factor-alpha , interleukin-1beta, interleukin-6 (enzyme-linked immunosorbent assay method), and ionized calcium were measured in ten anesthetized swine before and after 7 mins of cardiac arrest and during the early postresuscitation period (60-90 mins).
Tumor necrosis factor-alpha increased three-fold within 15 mins of restoration of circulation and remained elevated throughout the observation period. A significant negative correlation was observed between tumor necrosis factor-alpha and left ventricular systolic change in pressure over time (r = -.54, p <.001). Interleukin-1beta was undetectable before and after resuscitation, and interleukin-6 was detectable in only two animals after resuscitation. Although a significant decline in ionized calcium was observed and correlated with left ventricular systolic change in pressure over time, an independent role for ionized calcium in postresuscitation left ventricular dysfunction was not demonstrated.
Tumor necrosis factor-alpha increases during the early postresuscitation period and may play a role in postresuscitation myocardial dysfunction.
心肺复苏成功后的左心室功能障碍会导致复苏后早期死亡。已知应激诱导的促炎细胞因子，特别是肿瘤坏死因子-α和白细胞介素-1β，会抑制心肌功能。我们推测，在心脏骤停伴随的全身缺血应激反应中合成并释放的肿瘤坏死因子-α和白细胞介素-1β，在复苏后左心室功能障碍的发生中起作用。
在十只麻醉猪心脏骤停7分钟前后及复苏后早期（60 - 90分钟），测量血流动力学变量、肿瘤坏死因子-α、白细胞介素-1β、白细胞介素-6（酶联免疫吸附测定法）和离子钙。
循环恢复后15分钟内，肿瘤坏死因子-α增加了三倍，且在整个观察期内一直升高。肿瘤坏死因子-α与左心室收缩压随时间的变化之间存在显著负相关（r = -0.54，p < 0.001）。复苏前后均未检测到白细胞介素-1β，复苏后仅在两只动物中检测到白细胞介素-6。尽管观察到离子钙显著下降且与左心室收缩压随时间的变化相关，但未证明离子钙在复苏后左心室功能障碍中起独立作用。
肿瘤坏死因子-α在复苏后早期升高，可能在复苏后心肌功能障碍中起作用。
