Differential cardiovascular responses elicited by point‐specific acupuncture during phenylbiguanide‐induced reflex stimulation (686.4)

Abstract

Stimulation of cardiopulmonary receptors with phenylbiguanide (PBG) consequent to vagal activation decreases blood pressure (BP) and heart rate (HR) mediated by the nucleus ambiguus (NA) and nucleus tractus solitarii (NTS). EA at P5‐6 reverses PBG‐induced reflex bradycardia through modulatory actions in the NA. The current study examined effects of EA at P5‐6 (median nerves), ST36‐37 (deep peroneal nerve), LI4‐L7 (branches of median and superficial radial nerves) and G37‐39 (superficial peroneal nerve) acupoints on the PBG reflexes in the NTS. We hypothesized that point specific EA modulation of PBG‐induced vasodepression and bradycardia is related to differential levels of EA‐related somatic and cutaneous afferent evoked activity in cardiovascular and EA‐sensitive NTS neurons. NTS activity and HR and BP responses were recorded every 10 min during either repeated stimulation of the cervical vagus or iv PBG in cats. After two consistent responses, 30 min EA was applied bilaterally at P5‐6, ST36‐37, LI4‐L7 or G37‐39. NTS neurons displayed cardiac rhythmicity, convergence from vagal and baroreceptor afferents, and nerves located under acupoints. Kainic acid into the medial NTS decreased bradycardia from ‐40±10 to ‐18±2 b/m and depressor from ‐32±6 to ‐20±2 mmHg. EA at P5‐6 reduced for over 60 min the depressor by 67% and bradycardia by 60%. Unlike LI4‐L7 and G37‐39, EA at ST36‐37 reduced the depressor by 56% and the bradycardia by 60%. Brief activation of median and deep peroneal nerves showed much greater NTS evoked activity, compared to cutaneous nerves. Unlike LI4‐L7 and G37‐39, EA at P5‐6 and ST 36‐37 reduced vagal evoked NTS activity from 12±2.0 to 2±0.8 and 11.5±1.3 to 2±1.2 spikes/30stim, respectively. Thus at the different acupoints, brief stimulation differentially activates cardiovascular NTS neurons and following 30 min EA elicits point specific responses to PBG stimulation. These data support point specific EA responses that reverse cardiovascular inhibitory reflex responses.Grant Funding Source: HL‐72125, HL‐63313