Sun Lingling, Tanida Mamoru, Wang Mofei, Kuda Yuhichi, Kurata Yasutaka, Shibamoto Toshishige
Department of Physiology II, Kanazawa Medical University, Uchinada, Ishikawa, Japan; Department of Hematology, the Fourth Affiliated Hospital of China Medical University, Shenyang, China.
Department of Physiology II, Kanazawa Medical University, Uchinada, Ishikawa, Japan.
PLoS One. 2014 Nov 25;9(11):e113945. doi: 10.1371/journal.pone.0113945. eCollection 2014.
The autonomic nervous system plays an important role in rat anaphylactic hypotension. It is well known that sympathetic nerve activity and cardiovascular function are affected by anesthetics. However, the effects of different types of anesthesia on the efferent renal sympathetic nerve activity (RSNA) during anaphylactic hypotension remain unknown. Therefore, we determined the renal sympathetic responses to anaphylactic hypotension in anesthetized and conscious rats and the roles of baroreceptors in these responses. Sprague-Dawley rats were randomly allocated to anesthetic groups that were given pentobarbital, urethane, or ketamine-xylazine and to a conscious group. The rats were sensitized using subcutaneously injected ovalbumin. The systemic arterial pressure (SAP), RSNA and heart rate (HR) were measured. The effects of sinoaortic baroreceptor denervation on RSNA during anaphylaxis were determined in pentobarbital-anesthetized and conscious rats. In all of the sensitized rats, the RSNA increased and SAP decreased after antigen injection. At the early phase within 35 min of the antigen injection, the antigen-induced sympathoexcitation in the conscious rats was significantly greater than that in the anesthetized rats. Anaphylactic hypotension was attenuated in the conscious rats compared to the anesthetized rats. The anesthetic-induced suppression of SAP and RSNA was greater in the order ketamine-xylazine >urethane = pentobarbital. Indeed, in the rats treated with ketamine-xylazine, RSNA did not increase until 40 min, and SAP remained at low levels after the antigen injection. The baroreceptor reflex, as evaluated by increases in RSNA and HR in response to the decrease in SAP induced by sodium nitroprusside (SNP), was suppressed in the anesthetized rats compared with the conscious rats. Consistent with this finding, baroreceptor denervation attenuated the excitatory responses of RSNA to anaphylaxis in the conscious rats but not in the pentobarbital-anesthetized rats. RSNA was increased markedly in conscious rats during anaphylactic hypotension. Anesthetics attenuated this antigen-induced renal sympathoexcitation through the suppression of baroreceptor function.
自主神经系统在大鼠过敏性低血压中起重要作用。众所周知，交感神经活动和心血管功能受麻醉剂影响。然而，不同类型麻醉对过敏性低血压期间肾交感神经传出活动（RSNA）的影响尚不清楚。因此，我们确定了麻醉和清醒大鼠对过敏性低血压的肾交感神经反应以及压力感受器在这些反应中的作用。将Sprague-Dawley大鼠随机分为接受戊巴比妥、乌拉坦或氯胺酮-赛拉嗪的麻醉组和清醒组。大鼠通过皮下注射卵清蛋白致敏。测量全身动脉压（SAP）、RSNA和心率（HR）。在戊巴比妥麻醉和清醒的大鼠中，确定了去窦主动脉压力感受器对过敏反应期间RSNA的影响。在所有致敏大鼠中，注射抗原后RSNA增加而SAP降低。在抗原注射后35分钟内的早期阶段，清醒大鼠中抗原诱导的交感兴奋明显大于麻醉大鼠。与麻醉大鼠相比，清醒大鼠的过敏性低血压有所减轻。麻醉剂对SAP和RSNA的抑制作用按氯胺酮-赛拉嗪>乌拉坦=戊巴比妥的顺序更大。事实上，在用氯胺酮-赛拉嗪治疗的大鼠中，直到40分钟RSNA才增加，抗原注射后SAP保持在低水平。与清醒大鼠相比，麻醉大鼠中由硝普钠（SNP）诱导的SAP降低所引起的RSNA和HR增加所评估的压力感受器反射受到抑制。与此发现一致，去压力感受器减弱了清醒大鼠而非戊巴比妥麻醉大鼠中RSNA对过敏反应的兴奋反应。在过敏性低血压期间，清醒大鼠的RSNA明显增加。麻醉剂通过抑制压力感受器功能减弱了这种抗原诱导的肾交感兴奋。
