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B Nail

Publications and source records attributed to B Nail.

6 recordsLinked to original sources
PubMed1996

Tachykinin receptors and non-cholinergic bronchoconstriction in the anaesthetized guinea-pig.

1. Bronchoconstriction can be evoked by electrical stimulation of the vagus nerves in the presence of atropine. We have used novel, highly selective tachykinin receptor antagonists, together with a procedure for on-line, breath-by-breath analysis of total lung resistance (R(L), subtractor method) and dynamic lung compliance (C(dyn)), to investigate the role of tachykinins in this response in anaesthetized, paralysed guinea-pigs. 2. In the presence of 1 mg/kg phosphoramidon (a neutral endopeptidase inhibitor), CP 96345 (the non-peptide NK1 selective antagonist) at 200 nmol/kg had no effect on the increase in R(L) caused by vagal stimulation, but significantly inhibited the associated decrease in C(dyn). 3. The NK2 selective antagonist, MDL 29913 (1 mu mol/kg), significantly antagonized the changes in both R(L) and C(dyn). In the absence of phosphoramidon, MDL 29913 again significantly inhibited the changes in R(L) and C(dyn) although CP 96345 no longer had any effect. 4. The non-peptide NK2 selective antagonist, SR 48968 (100 nmol/kg), also effectively inhibited the responses to vagal stimulation and was more potent than MDL 29913. 5. These results emphasize the importance of the NK2 receptor system in mediating non-cholinergic bronchoconstriction evoked by vagal stimulation in the guinea-pig.

Animals↗
PubMed1987

Laryngeal afferents activated by phenyldiguanide and their response to cold air or helium-oxygen.

In anesthetized cats, sensory neurons in the superior laryngeal nerves (SLN) were identified with respect to their response to (1) phenyldiguanide (PDG) i.v., (2) mechanical stimulation and (3) lowering temperature in an isolated tracheolaryngeal segment. The activity originating from 107 SLN afferent units activated by PDG was recorded using glass microelectrodes advanced in the nodose ganglion. All tested afferent units increased their discharge rate during direct touching of the airway mucosa. None showed flow or pressure related activity during abrupt changes in constant laryngeal flow or transmural pressure in the isolated segment. Fifteen units were inhibited by cold air. Sixty-two units significantly increased their firing rate when the temperature approached 18 degrees C, reached a peak discharge near 15 degrees C, then their activity decreased or stopped. The response to cold air was compared to cold heliox (79% He-21% O2), which enhanced the respiratory heat loss by conduction. The peak firing rate was significantly higher with heliox (+356% compared to +246% with air), the temperature threshold higher (25 degrees C +/- 1.0 degree C) and the temperature range broader (25-11.5 degrees C). Present results show that a large proportion (58%) of afferent SLN fibres activated by PDG are likely non-proprioceptive units, which are stimulated by cooling the inspired gas. Thermosensitive units in the upper airways may act as sensors of the thermal flux through the airway wall more than as detectors of the absolute value of temperature in the airway lumen.

Action Potentials↗
PubMed1987

Phrenic and external intercostal motoneuron activity during progressive asphyxia.

Phrenic and external intercostal motoneuron activities were compared during progressive asphyxia induced by the interruption of artificial ventilation in the pentobarbital-urethan-anesthetized, gallamine-paralysed rabbit. The relative augmentation of inspiratory activity of the T1-T4 external intercostal nerves was significantly greater than that of the phrenic nerve during asphyxic hyperpnea. This was associated with a greater recruitment of intercostal than of phrenic motoneurons, particularly late in the hyperpneic phase immediately before the period of asphyxic apnea. However, peak and average discharge frequencies developed by intercostal motoneurons (n = 20) were only approximately 60% of those of the phrenic motoneurons (n = 28). Gasping respiration terminated the apneic period and was associated with a further intense recruitment of intercostal though not of phrenic motoneurons, but discharge frequencies developed by the intercostal motoneurons remained approximately 60% of those of the phrenic motoneurons. The instantaneous frequency profiles generated by the motoneurons often exhibited progressive changes during the terminal stages of hyperpnea (reduction in inspiratory duration and duty cycle and increases in inspiratory slope and discharge frequencies) such that much of the character of gasping respiration became evident before the apnea. Such smooth transitional sequences do not obviate the existence of an "independent gasping center" but do require that such a proposed center at least possess the capacity for interaction with those sites responsible for the generation of eupneic and hyperpneic respiration.

Action Potentials↗
PubMed1986

Inspiratory augmentation during asphyxic hyperpnoea and gasping: proprioceptive influences.

The relative inspiratory augmentations of sternomastoid, scalene, external intercostal, interchondral and diaphragmatic electromyographic activities were examined during the progressive asphyxia induced by rebreathing in pentobarbitone/urethane anaesthetized rabbits. Diaphragmatic activity augmented significantly less than that of the scalene, intercostal and interchondral muscles in response to the asphyxic increase in inspiratory drive (hyperpnoea). Cervical vagotomy significantly increased the levels of inspiratory activity during the asphyxic hyperpnoea but did not abolish these relations. Dorsal rhizotomy at levels appropriate for the respective recording sites significantly limited the intercostal and interchondral augmentations, and depressed diaphragmatic activity to a less pronounced extent, but did not affect scalene activity. The asphyxic apnoea succeeding the hyperpnoea was terminated by gasping respiration. Excepting the interchondrals each muscle exhibited significantly greater electromyographic amplitudes during gasping than during the terminal hyperpnoeic efforts. Only during gasping were the sternomastoid muscles recruited. The intercostal and scalene gasps were significantly greater than those exhibited by either the interchondrals or the diaphragm. Such disproportionate responses were not affected by vagotomy or dorsal rhizotomy. The disparate inspiratory contributions during progressive asphyxia can therefore only be partially accounted for by differences in proprioceptive control.

Animals↗