Longhurst J C, Ordway G A
Adv Exp Med Biol. 1983;156:639-50.
To determine whether bradykinin, an algesic substance produced in certain inflammatory states, can stimulate gallbladder receptors to cause significant cardiovascular reflexes, we applied this agent to the serosal surface of the gallbladder in cats anesthetized with methoxyflurane. As a control, bradykinin was also applied to the serosal surface of the liver surrounding the gallbladder. Significant cardiovascular reflexes were obtained from the gallbladder in an increasing, dose related fashion over a range of concentrations from 50 pg/ml to 100 micrograms/ml of bradykinin. The cardiovascular responses occurred after a latency of 13 +/- 0.92 seconds (mean +/- SE) and included increases in mean arterial pressure, systemic vascular resistance, heart rate and myocardial contractility (dP/dt at 40 mmHg developed pressure). There was also a small but significant increase in left ventricular end-diastolic pressure, but no change in aortic flow. Application of bradykinin to the liver did not evoke any cardiovascular responses. Bilateral vagus nerve transection just above the diaphragm did not alter the cardiovascular responses to application of bradykinin on the gallbladder. However, the hemodynamic responses were partially diminished by right splanchnic nerve transection and were completely eliminated by bilateral splanchnic nerve transection. We conclude that bradykinin, a substance that is formed within the gastrointestinal tract and possibly in bile, can stimulate gallbladder receptors to induce significant reflex activation of the cardiovascular system.
为了确定缓激肽（一种在某些炎症状态下产生的致痛物质）是否能刺激胆囊受体引发显著的心血管反射，我们将该物质应用于用甲氧氟烷麻醉的猫的胆囊浆膜表面。作为对照，缓激肽也被应用于胆囊周围肝脏的浆膜表面。在缓激肽浓度范围为50皮克/毫升至100微克/毫升时，从胆囊获得了以剂量相关方式增加的显著心血管反射。心血管反应在13±0.92秒（平均值±标准误）的潜伏期后出现，包括平均动脉压、全身血管阻力、心率和心肌收缩力（在40毫米汞柱发展压力下的dP/dt）增加。左心室舒张末期压力也有小幅但显著的增加，但主动脉血流量没有变化。将缓激肽应用于肝脏未引发任何心血管反应。在横膈膜上方双侧切断迷走神经并未改变对胆囊应用缓激肽时的心血管反应。然而，右内脏神经切断术使血流动力学反应部分减弱，双侧内脏神经切断术则使其完全消除。我们得出结论，缓激肽这种在胃肠道内且可能在胆汁中形成的物质，能刺激胆囊受体诱导心血管系统的显著反射激活。
