Veelken R, Sawin L L, DiBona G F
Department of Internal Medicine, University of Iowa College of Medicine, Iowa City.
Am J Physiol. 1990 Feb;258(2 Pt 2):H466-72. doi: 10.1152/ajpheart.1990.258.2.H466.
To investigate cardiac chemoreceptors in rats a catheter was chronically implanted into the pericardial sac via the thymus. Intrapericardial (ipc) injection of 200 microliters isotonic saline vehicle did not alter arterial blood pressure, heart rate, right atrial pressure, or respiratory rate. Phenyl biguanide (PBG) and nicotine (NIC) were injected into the pericardial sac. In intact rats anesthetized with methohexital sodium, 90 micrograms PBG ipc decreased blood pressure (BP), heart rate (HR), and renal nerve activity (RNA), whereas 300 micrograms NIC ipc increased BP and decreased HR and RNA. Sinoaortic baroreceptor denervation (SAD) did not affect the responses to PBG and abolished only the HR response to NIC. When vagotomy was added to SAD, all responses to intrapericardial PBG were abolished, but the increase in BP and decrease in RNA resulting from intrapericardial NIC persisted. In SAD rats anesthetized with methohexital, PBG produced dose-dependent decreases in BP and RNA, whereas NIC produced dose-dependent increases in BP and decreases in RNA; the serotonin (5-HT3) antagonist MDL 72222 (80 micrograms ipc) abolished the responses to PBG but not to NIC. MDL 72222 inhibited BP and RNA responses to PBG to a similar extent in conscious and anesthetized SAD rats. Anesthesia attenuated the magnitude and time course of BP and RNA responses to PBG compared with the conscious state. In conclusion, 1) sympathoinhibitory responses to intrapericardial PBG and NIC are mediated by epicardial receptors with different afferent neural pathways, PBG by cardiac vagal afferents and NIC by nonvagal, possibly cardiac sympathetic afferents; 2) PBG exerts its effects via epicardial 5-HT3 receptors; 3) anesthesia attenuates the responses to PBG.
为了研究大鼠的心脏化学感受器，通过胸腺将导管长期植入心包腔。心包腔内（ipc）注射200微升等渗盐水载体不会改变动脉血压、心率、右心房压力或呼吸频率。将苯双胍（PBG）和尼古丁（NIC）注入心包腔。在用美索比妥钠麻醉的完整大鼠中，心包腔内注射90微克PBG可降低血压（BP）、心率（HR）和肾神经活动（RNA），而心包腔内注射300微克NIC可升高血压并降低心率和RNA。去窦主动脉压力感受器（SAD）并不影响对PBG的反应，且仅消除了对NIC的心率反应。当在SAD基础上增加迷走神经切断术时，对心包腔内PBG的所有反应均被消除，但心包腔内NIC引起的血压升高和RNA降低仍然存在。在用美索比妥钠麻醉的SAD大鼠中，PBG产生剂量依赖性的血压和RNA降低，而NIC产生剂量依赖性的血压升高和RNA降低；5-羟色胺（5-HT3）拮抗剂MDL 72222（心包腔内注射80微克）消除了对PBG的反应，但未消除对NIC的反应。在清醒和麻醉的SAD大鼠中，MDL 72222对PBG引起的血压和RNA反应的抑制程度相似。与清醒状态相比，麻醉减弱了血压和RNA对PBG反应的幅度和时间进程。总之，1）对心包腔内PBG和NIC的交感抑制反应由具有不同传入神经通路的心外膜受体介导，PBG通过心脏迷走传入神经，NIC通过非迷走神经，可能是心脏交感传入神经；2）PBG通过心外膜5-HT3受体发挥作用；3）麻醉减弱了对PBG的反应。
