Published online Jul 28, 2013. doi: 10.5320/wjr.v3.i2.11
Revised: May 31, 2013
Accepted: June 18, 2013
Published online: July 28, 2013
Processing time: 148 Days and 10.6 Hours
AIM: To test whether high-frequency electrical stimulation (HES) of the bilateral cervical vagus nerves reduces the airway responses to methacholine (MCh).
METHODS: Guinea pigs were pretreated with saline (Sal, n = 9) or ovalbumin (Ova, n = 10) aerosol for two weeks (5 min/d, 5 d/wk) and subsequently anesthetized, paralyzed, tracheotomized and artificially ventilated. Both total lung resistance (RL) and dynamic pulmonary compliance (Cdyn) were recorded. In addition, the effects of vagal low-frequency electrical stimulation (LES, monophasic, 50 Hz) and HES (monophasic and biphasic, 1 and 2.5 kHz) for about 10 s or 2 min on the responses of RL and Cdyn to MCh aerosol-induced bronchoconstriction were compared in both groups of guinea pigs. In a few guinea pigs, the impact of bivagotomy on the RL responses to MCh was assessed.
RESULTS: Before MCh challenge, LES, but not HES, significantly increased RL by about 30% (P < 0.01) and decreased Cdyn by about 20% (P < 0.01) similarly in both groups. MCh aerosol for 2 min elevated RL and diminished Cdyn more in Ova- than Sal-treated animals (RL: 313% ± 52% vs 113% ± 17%, P < 0.01; Cdyn: -56% ± 7% vs -21% ± 3%, P < 0.01). During MCh-induced airway constriction, LES further enhanced, but HES decreased RL and this decrease was greater in Ova- (about 45%) than Sal-treated animals (about 34%, P < 0.01) with little change in cardiovascular activity. On the other hand, LES further reduced whereas HES increased Cdyn more in Ova- (about 20%) than Sal-treated animals (about 13%, P < 0.01). In addition, bivagotomy almost eliminated the RL and Cdyn responses to MCh.
CONCLUSION: We conclude that vagal HES is able to alleviate the bronchoconstriction induced by MCh in anesthetized guinea pigs, likely via reversible inhibition/blockade of vagal conduction.
Core tip: In summary, our study revealed that vagal high-frequency electrical stimulation (HES) significantly suppressed the airway response to methacholine (MCh) more greatly in the ovalbumin- than saline-treated animals, while vagal low-frequency electrical stimulation always increased airway resistance. Importantly, the HES-evoked bronchodilation during MCh challenge is concomitant with the on-and-off electrical stimulation and with no effect on cardiovascular activity. These, along with the greatly blunted airway resistance response to MCh after bivagotomy, suggest that vagal HES may be a potentially useful approach in alleviating asthmatic bronchoconstriction (likely via reversible inhibition or blockade of the vagal nerve conduction).