Silverman H J, Penaranda R, Orens J B, Lee N H
Department of Medicine, Pulmonary and Critical Care Division, University of Maryland School of Medicine, Baltimore.
Crit Care Med. 1993 Jan;21(1):31-9. doi: 10.1097/00003246-199301000-00010.
To determine whether myocardial hyporesponsiveness to administered catecholamines occurs in human sepsis and whether this phenomenon is associated with impaired beta-adrenergic receptor stimulation of cyclic adenosine monophosphate.
Prospective study.
Medical ICU in a university hospital.
Normal human volunteers (n = 7), critically ill patients who were not septic (n = 9), septic patients not in shock (n = 16), and septic patients in shock (n = 17).
Pulmonary artery catheter-derived hemodynamic data were obtained in patients with sepsis and septic shock. Isoproterenol and sodium fluoride-stimulated cyclic adenosine monophosphate accumulations were measured in circulating lymphocytes. The hemodynamic response to sequential infusions of dobutamine, 5 and 10 micrograms/kg/min, was obtained in septic and septic shock patients. Baseline hemodynamic values for mean arterial pressure, cardiac index, left ventricular stroke work index, and oxygen delivery index at approximately 2 days after the onset of sepsis were significantly lower in septic shock patients compared with septic (nonshock) patients (p < .01 p < .05, p < .001, p < .01, respectively). Isoproterenol- and sodium fluoride-stimulated cyclic adenosine monophosphate accumulations were significantly reduced in septic shock patients compared with those accumulations observed in septic patients (p < .01 and p < .001, respectively). The heart rate response to 10 micrograms/kg/min of dobutamine was significantly (p < .01) lower in septic shock patients compared with septic patients.
In patients with septic shock, impaired beta-adrenergic receptor stimulation of cyclic adenosine monophosphate is associated with myocardial hyporesponsiveness to catecholamines, suggesting that beta-adrenergic receptor dysfunction may contribute to the reduced myocardial performance observed in this shock state.
确定人类脓毒症患者是否存在心肌对给予的儿茶酚胺反应性降低的情况，以及这种现象是否与环磷酸腺苷的β-肾上腺素能受体刺激受损有关。
前瞻性研究。
大学医院的医学重症监护病房。
正常人类志愿者（n = 7）、非脓毒症的重症患者（n = 9）、未发生休克的脓毒症患者（n = 16）和发生休克的脓毒症患者（n = 17）。
获取脓毒症和脓毒性休克患者通过肺动脉导管测得的血流动力学数据。测量循环淋巴细胞中异丙肾上腺素和氟化钠刺激后的环磷酸腺苷积累量。在脓毒症和脓毒性休克患者中，依次输注多巴酚丁胺（5和10微克/千克/分钟）后获得血流动力学反应。脓毒性休克患者在脓毒症发作后约2天的平均动脉压、心脏指数、左心室每搏功指数和氧输送指数的基线血流动力学值显著低于脓毒症（非休克）患者（分别为p <.01、p <.05、p <.001、p <.01）。与脓毒症患者相比，脓毒性休克患者中异丙肾上腺素和氟化钠刺激后的环磷酸腺苷积累量显著降低（分别为p <.01和p <.001）。与脓毒症患者相比，脓毒性休克患者对10微克/千克/分钟多巴酚丁胺的心率反应显著降低（p <.01）。
在脓毒性休克患者中，环磷酸腺苷的β-肾上腺素能受体刺激受损与心肌对儿茶酚胺反应性降低有关，提示β-肾上腺素能受体功能障碍可能导致在这种休克状态下观察到的心肌功能降低。
