Department of Anesthesiology and Reanimatology, Gunma University School of Medicine, 3-39-22 Showa-machi, Maebashi, 371, Gunma, Japan.
J Anesth. 1996 Mar;10(1):49-54. doi: 10.1007/BF02482068.
In this study to investigate whether β-adrenergic receptor systems in the heart are impaired during endotoxemia, we examined two models of septic shock in rats, each of which has a different time course for the shock state. Male Wistar rats were divided into two groups: (1) the LPS (lipopolysaccharide) iv group (Escherichia coli endotoxin 1.0 mg·kg(-1) iv bolus administration), and (2) the CLP (cecal ligation and puncture model) group. As a control group for each model, a 0.9% saline injection group and a sham-operated group were also prepared. At 3, 12, and 24 h after treatment, the rats were killed and their hearts were removed as rapidly as possible. In the LPS iv and CLP groups, an increase in the plasma epinephrine (E) and norepinephrine (NE) levels compared with the control and sham-operated groups was observed at both 3 and 12h after treatment (P<0.05). There was a decrease in myocardial tissue NE concentration at 3, 12 and 24h in the CLP group. This decrease was especially marked at 24h. In the LPS iv group, a decrease in β-receptor density was observed at 3 h (control, 87.07±4.59 fmol·mg(-1) protein; LPS iv, 60.73±3.51 fmol·mg(-1) protein), but was not observed at 24h. In contrast, a decrease in β-receptor density in the CLP group was observed at 24h (sham-operated, 80.9±3.65 fmol·mg(-1) protein; CLP, 66.1±4.08 fmol·mg(-1) protein), but was not observed at 3h. The β-receptor density in the hearts of LPS iv rats and the altered hemodynamics recovered in line with the decrease in plasma catecholamines (CA). However, in the CLP group the alteration in hemodynamics was not in line with plasma CA. The alteration in hemodynamics of septic-shock rats observed in this study was linked to the change in heart β-receptor density rather than the change in plasma CA. These observations suggested that the alterations which occur in the β-receptor system during endotoxemia depend upon the model of animal sepsis that is employed, and the time course of the septic-shock state. These alterations in the β-adrenergic system are thought to cause myocardial dysfunction during endotoxemia.
在这项研究中，我们研究了在败血症休克期间心脏β-肾上腺素能受体系统是否受损，为此我们检查了两种败血症休克的大鼠模型，每种模型的休克状态的发生时间都不同。雄性 Wistar 大鼠分为两组：（1）LPS（脂多糖）iv 组（大肠杆菌内毒素 1.0mg·kg(-1)iv 推注给药），（2）CLP（盲肠结扎和穿刺模型）组。每组模型的对照组还包括生理盐水注射组和假手术组。治疗后 3、12 和 24 小时，大鼠被迅速处死并取出心脏。与对照组和假手术组相比，LPS iv 和 CLP 组在治疗后 3 和 12 小时时血浆肾上腺素（E）和去甲肾上腺素（NE）水平升高（P<0.05）。CLP 组在 3、12 和 24 小时时心肌组织 NE 浓度降低。这种降低在 24 小时时尤为明显。在 LPS iv 组，在 3 小时时观察到β-受体密度降低（对照组，87.07±4.59 fmol·mg(-1)蛋白；LPS iv，60.73±3.51 fmol·mg(-1)蛋白），但在 24 小时时未观察到。相反，CLP 组在 24 小时时观察到β-受体密度降低（假手术组，80.9±3.65 fmol·mg(-1)蛋白；CLP，66.1±4.08 fmol·mg(-1)蛋白），但在 3 小时时未观察到。LPS iv 大鼠心脏中的β-受体密度和改变的血液动力学与血浆儿茶酚胺（CA）的减少一致恢复。然而，在 CLP 组中，血液动力学的改变与血浆 CA 不一致。在这项研究中观察到的败血症休克大鼠的血液动力学改变与心脏β-受体密度的变化有关，而与血浆 CA 的变化无关。这些观察结果表明，内毒素血症期间β-受体系统发生的改变取决于所使用的动物败血症模型以及败血症休克状态的发生时间。内毒素血症期间β-肾上腺素能系统的这些改变被认为会导致心肌功能障碍。
