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

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

Central and peripheral effects of the non-neural substances on respiration before and after vagotomy

The central effects of capsaicin, veratrine, histamine and bradykinin were studied by injecting them directly into the cerebrospinal fluid and their peripheral effects were examined by injecting into femoral vein. Our experiments were performed in Na-pentobarbital-anaesthetized dogs. Tidal volume (V-T), respiratory frequency (f/min), systemic arterial pressure (BP) were recorded. A significant increase in f, and an initial apnea or hypoventilation followed by a significant increase in V-T were observed with central and peripheral capsaicin. Vagotomy removed the peripheral V-T response, but not the central one. While central capsaicin administration increased BP, peripheral administration decreased. After vagotomy, a significant increase was observed in BP for both administrations. Respiratory responses to central and peripheral administrations of veratrine mere similar to those of capsaicin. Significant increases were observed in f and V-T of the intact group in response to central and peripheral administration of histamine. Response to peripheral administration disappeared after vagotomy. While central and peripheral bradykinin increased V-T significantly, there was no significant change in f. Vagotomy only removed the increase in V-T in response to peripheral administration. In conclusion, respiratory responses to central administration of capsaicin and veratrine are due to direct effects of these substances on respiratory neurons. In peripheral administration, disappearance of the responses after vagotomy indicate that the responses are brought about by stimulation of the lung receptors. (C) 1997 Tohoku University Medical Press

Hypoxic initiation of pulmonary hypertension is mediated by serotonin secretion from neuroepithelial bodies in chemodenervated dogs

The purpose of this study was to investigate the stimulatory effect of hypoxia on the secretion of serotonin by neuroepithelial bodies (NEB) as well as to determine the relation between its level and changes in pulmonary arterial pressure (PAP) and also to determinate the effect of serotonin antagonists (pizotifen and methysergide) on the responses of pulmonary and systemic arterial pressures. The experiments were carried out in peripheral chemoreceptor-denervated dogs anesthetized with Na penthabarbital (30 mg/kg i.v.). On the breathing of normoxic and hypoxic (7% O-2-93% N-2) gas mixtures and on the injection of KCN (80 mug/kg i.v.), PAP, systemic arterial blood pressure (BP), tidal volume (V-T), respiratory frequency (f/min), ventilation minute volume (V-E) were determined. Also PAP and BP were recorded before and after the injection of pizotifen (0.5 mg/kg i.v.) and methysergide (1 mg/kg i.v.) during normoxic or hypoxic gas mixture breathing. At the end of each experimantal phase, serotonin level, PaO2, PaCO2 and pH(a) values in blood samples obtained from left ventricle and femoral artery were determined. On the breathing of the hypoxic gas mixture of the chemodenervated dogs, VT, VE and BP significantly decreased (P<0.001, P<0.001, P<0.01). The mean value of PAP and serotonin levels (ventricular and femoral) were found significantly increased when compared with the corresponding normoxic values (P<0.001, P<0.05). On the other hand, injection of KCN produced no significant changes in PAP, serotonin levels, BP and respiratory parameters. After the injection of pizotifen, PAP was significantly increased in hypoxia (P<0.01). After the injection of methysergide, the response of PAP was completely abolished during the breathing of hypoxic gas mixture. The finding of the abolition of response of PAP to hypoxia after the injection of methysergide indicates that serotonin release from NEB may be responsible for the elevation of PAP in hypoxic hypoxia