Search PubMed⌕ Search

Biomedical subjects

J Machida

Publications and source records attributed to J Machida.

48 records · Page 3Linked to original sources
PubMed1976

The motor nerve supply of the velopharyngeal muscles.

The present study attempted to clarify the motor nerve supply of the velopharyngeal muscles. Experiments were carried out on 20 anesthetized rhesus monkeys. Evoked EMG responses of the levator veli palatini, uvula, and superior constrictor pharyngeus muscles, which seem to contribute to velopharyngeal closure, were analyzed by stimulating the cranial nerves within the skull. Results were as follows: 1. Muscle action potentials (M-waves) from the selected muscles could be recognized on stimulating the facial, glossopharyngeal, and vagus nerves at the petrosal area of the temporal bone but were not noted upon accessory nerve stimulation. 2. At maximal stimulation, the vagus gave a greater increase in muscle amplitude than the other nerves studied. This was followed by the glossopharyngeal with the facial nerve producing the least increase in amplitude. 3. Also at maximal stimulation, latencies in the response of the levator veli palatini and uvula muscles were reduced to the greatest degree by stimulation of the vagus, to a lesser extent for the glossopharyngeal, and least for the facial nerve. 4. On stimulating the facial nerve below the stylomastoid foramen, M-waves could not be recognized. From the present study, it was concluded that the levator veli palatini, uvula, and superior constrictor pharyngeus muscles are double innervated by the facial nerve and branches of the pharyngeal plexus derived from the glossopharyngeal and vagus nerves and that the facial nerve plays an important role as one of the motor nerves in movements responsible for velopharyngeal closure.

Accessory Nerve↗
PubMedDate not supplied

Comparison of the effects of various anticholinergic drugs on human isolated urinary bladder.

We investigated the effects of various anticholinergic drugs (atropine, oxybutynin, terodiline and propiverine) on the contractions induced by acetylcholine, KCl, CaCl2, and electrical field stimulation, in human isolated urinary bladder smooth muscles using the muscle bath technique. Urinary bladders were obtained from 20 patients who underwent total cystectomy due to malignant bladder tumor. The detrusor preparations were taken from the intact part of the dome of the bladder. Acetylcholine caused a concentration-dependent contraction in human detrusor preparations. Atropine (10(-9)-10(-6) M), oxybutynin (10(-8)-10(-5) M), terodiline (10(-7)-10(-5) M) and propiverine (10(-7)-10(-5) M) caused parallel shifts to the right of the concentration-response curves to acetylcholine. The rank order of pA2 values was: atropine > oxybutynin > terodiline = propiverine. Atropine did not suppress the maximum contraction to acetylcholine, while the other drugs significantly suppressed the maximum contractions at the higher concentrations. Each drug caused a concentration-dependent inhibition of the KCl (80 mM)- and CaCl2 (5 mM)-induced contractions; the maximum inhibitions of terodiline and propiverine were significantly greater than those of oxybutynin and atropine. Each drug caused a concentration-dependent inhibition of the contraction induced by electrical field stimulation; the maximum inhibitions of terodiline and propiverine were significantly greater than those of oxybutynin and atropine. The results suggest that the drugs have both anticholinergic and calcium antagonistic effects. Furthermore, it also appears that part of the human bladder contraction, which was significantly inhibited by terodiline and propiverine, is an atropine-resistant component.

Acetylcholine↗