Li Z, Chapleau M W
Department of Internal Medicine, University of Iowa College of Medicine, USA.
J Auton Nerv Syst. 1995 Jan 20;51(1):59-65. doi: 10.1016/0165-1838(95)80007-w.
We have demonstrated recently that platelets aggregating in the carotid sinus decrease baroreceptor sensitivity. The goals of the present study were to determine whether platelet-induced suppression of baroreceptor activity is mediated by a diffusible, transferable factor and, if true, whether the factor is short-lived or stable. Baroreceptor activity was recorded from the isolated carotid sinus during slow ramp increases in nonpulsatile pressure in rabbits anesthetized with sodium pentobarbital. Intraluminal exposure of the carotid sinus to washed rabbit platelets resuspended in Krebs buffer (3-5 x 10(8) cells/ml) and activated by thrombin decreased baroreceptor activity significantly (n = 7, P < 0.05). Maximum baroreceptor activity recorded at a pressure of 140 mmHg was reduced to 81 +/- 7% of the control maximum. Injection of cell-free supernatant obtained from filtered thrombin-activated platelets also suppressed baroreceptor activity to a similar extent after 10 min (n = 7) and after 2 h (n = 5) of incubation when maximum baroreceptor activity was reduced to 84 +/- 5 and 82 +/- 5% of the control maximum, respectively. The inhibitory influence of activated platelets and platelet supernatant on baroreceptor activity was still apparent after 10-60 min of heating (95 degrees C) (n = 5) and was reversible upon removal of platelets and supernatant from the sinus. The results indicate that activated platelets release a stable diffusible factor that suppresses baroreceptor activity. We speculate that this 'inhibitory factor' may contribute to impairment of the baroreceptor reflex and neurally-mediated increases in arterial pressure in atherosclerotic and thrombotic states.
我们最近证实，在颈动脉窦聚集的血小板会降低压力感受器的敏感性。本研究的目的是确定血小板诱导的压力感受器活性抑制是否由一种可扩散、可转移的因子介导，如果是，该因子是短期存在还是稳定的。在用戊巴比妥钠麻醉的家兔中，在非搏动性压力缓慢斜坡增加期间，从分离的颈动脉窦记录压力感受器活性。将颈动脉窦腔内暴露于重悬于 Krebs 缓冲液（3 - 5×10⁸ 个细胞/ml）中并经凝血酶激活的洗涤兔血小板，可显著降低压力感受器活性（n = 7，P < 0.05）。在 140 mmHg 压力下记录的最大压力感受器活性降至对照最大值的 81±7%。注射从经滤过的凝血酶激活血小板获得的无细胞上清液，在孵育 10 分钟（n = 7）和 2 小时（n = 5）后，也能将压力感受器活性抑制到相似程度，此时最大压力感受器活性分别降至对照最大值的 84±5%和 82±5%。激活的血小板和血小板上清液对压力感受器活性的抑制作用在加热（95℃）10 - 60 分钟后仍然明显（n = 5），并且在从窦中去除血小板和上清液后是可逆的。结果表明，激活的血小板释放一种稳定的可扩散因子，该因子抑制压力感受器活性。我们推测这种“抑制因子”可能导致动脉粥样硬化和血栓形成状态下压力感受器反射受损以及神经介导的动脉血压升高。
