Romano F D, Jones S B
Circ Shock. 1985;17(3):243-52.
Sympathetic nervous system activity and myocardial response to adrenergic stimulation were studied in the rat during endotoxicosis. Plasma glucose concentration, adrenal norepinephrine (NE) and epinephrine (E) content, spleen NE content, and myocardial NE and cAMP content were analyzed in fed rats given saline or endotoxin (ETOX, 16.7 mg/kg). Values were determined at various times during a 6-hour period or at the agonal stage of shock. Myocardial cAMP content was reduced by 1 hour, recovered at 4 hours, and was again depressed at the agonal stage. In addition, isoproterenol-stimulated cAMP production in ventricular slices from ETOX rats was attenuated by 3 hours after administration. These data suggest that myocardial beta-adrenergic receptor mechanisms are altered during endotoxicosis, which may account for reports of decreased functional responsiveness to catecholamines under similar conditions. At 1 hour after ETOX, adrenal NE did not change, but E was depleted and remained low throughout the period. By 2 hours, spleen NE was also found depleted. Myocardial NE did not change until the agonal stage, when it was severely depressed. This implies that there may be nonuniform activation (duration and/or intensity) of sympathetic pathways during endotoxicosis.
在内毒素血症期间，对大鼠的交感神经系统活动及心肌对肾上腺素能刺激的反应进行了研究。分析了给予生理盐水或内毒素（ETOX，16.7mg/kg）的喂食大鼠的血浆葡萄糖浓度、肾上腺去甲肾上腺素（NE）和肾上腺素（E）含量、脾脏NE含量以及心肌NE和cAMP含量。在6小时期间的不同时间或休克濒死期测定各项数值。心肌cAMP含量在1小时时降低，4小时时恢复，在濒死期再次降低。此外，ETOX大鼠心室切片中异丙肾上腺素刺激的cAMP生成在给药后3小时减弱。这些数据表明，在内毒素血症期间心肌β-肾上腺素能受体机制发生改变，这可能解释了在类似情况下对儿茶酚胺功能反应性降低的报道。ETOX后1小时，肾上腺NE未改变，但E耗竭且在此期间一直维持在低水平。到2小时时，脾脏NE也被发现耗竭。心肌NE直到濒死期才发生改变，此时严重降低。这意味着在内毒素血症期间交感神经通路可能存在非均匀激活（持续时间和/或强度）。
