The effects of vagal stimulation on laryngeal vascular resistance and intraluminal pressure in the dog

Abstract

In anaesthetized dogs (sodium pentobarbitone 30 mg/kg, i.v.) laryngeal vascular resistance was measured by unilateral perfusion at constant flow of the branch of the cranial superior thyroid artery that supplies the larynx. Arterial perfusion was at constant flow and inflow pressure was divided by flow to give laryngeal vascular resistance (R-LV). Intraluminal laryngeal pressure (P-L) and systemic arterial blood pressure (BP) were also measured. Stimulation (20 V, 20 Hz, 0.2 milliseconds) of the central end of cervical vagus caused an increase in R-LV (+22.9+/-6.1%) and a decrease in P-L (-12.1+/-4.4%). Stimulation (10 V, 10 Hz, 0.2 milliseconds) of the central end of the recurrent laryngeal nerve (RLN) reduced R-LV (-3.4+/-0.8%) and P-L (-7.5+/-4.1%). Stimulation of the peripheral end of the RLN decreased RLV (-7.1+/-1.9%) and increased P-L (+21.6+/-7.7%). Stimulation of the central end of the superior laryngeal nerve (SLN) increased R-LV (+17.9+/-3.2%) and P-L (+59.8+/-2.7%), whereas stimulation of the peripheral end of the SLN decreased R-LV (-4.8+/-1.6%) and P-L (-4.1+/-2.4%). After treatment with alpha-adrenoreceptor antagonist phentolamine (0.5 mg/kg, Lv.), stimulation of the central end of cervical vagus nerve reduced R-LV by 25% and decreased BP. Phentolamine caused a decrease in BP and reduced the magnitude of increase in R-LV in response to stimulation of central end of SLN. After atropine sulphate (0.5-2.0 mg/kg, i.v.), the stimulation of both central and peripheral ends of RLN reduced RLV. The decrease in R-LV during stimulation of peripheral end of SLN was reduced by atropine. Thereafter, pancuronium bromide (0.06-0.1 mg/kg, i.v.) was given and dogs were artifically ventilated. After paralyzed, stimulation of the central end of the SLN decreased R-LV (+26.0+/-4.5%) but produced no change in P-L. It is concluded that parasympathetic motor fibers in the RLN and SLN are effective for the laryngeal vascularity and non-adrenergic system may be responsible for laryngeal vasoconstriction.