Li X, Eschun G, Bose D, Jacobs H, Yang J J, Light R B, Mink S N
Department of Medicine, University of Manitoba, Winnipeg, Manitoba, Canada R3E OZ3.
J Appl Physiol (1985). 1998 Nov;85(5):1693-701. doi: 10.1152/jappl.1998.85.5.1693.
In the heart, histamine (H3) receptors may function as inhibitory presynaptic receptors that decrease adrenergic norepinephrine release in conditions of enhanced sympathetic neural activity. We hypothesized that H3-receptor blockade might improve cardiovascular function in sepsis. In a canine model of Escherichia coli sepsis, we found that H3-receptor blockade increased cardiac output (3.6 to 5.3 l/min, P < 0.05), systemic blood pressure (mean 76 to 96 mmHg, P < 0.05), and left ventricular contractility compared with pretreatment values. Plasma histamine concentrations increased modestly in the H3-blocker-sepsis group compared with values obtained in a nonsepsis-time-control group. In an in vitro preparation, histamine H3 activation could be identified under conditions of septic plasma. We conclude that activation of H3 receptors may contribute to cardiovascular collapse in sepsis.
在心脏中，组胺（H3）受体可能作为抑制性突触前受体发挥作用，在交感神经活动增强的情况下减少肾上腺素能去甲肾上腺素的释放。我们推测H3受体阻断可能改善脓毒症时的心血管功能。在大肠杆菌脓毒症犬模型中，我们发现与预处理值相比，H3受体阻断可增加心输出量（从3.6升至5.3升/分钟，P<0.05）、全身血压（平均从76毫米汞柱升至96毫米汞柱，P<0.05）以及左心室收缩力。与非脓毒症时间对照组相比，H3受体阻断剂 - 脓毒症组的血浆组胺浓度略有升高。在体外制剂中，在脓毒症血浆条件下可识别组胺H3的激活。我们得出结论，H3受体的激活可能导致脓毒症时的心血管衰竭。
