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Biomedical subjects

H Don

Publications and source records attributed to H Don.

11 recordsLinked to original sources

Reversal of the relation between respiratory drive and airway tone in cats.

To examine the relationship between respiratory drive and airway tone in the exercise pressor reflex in the cat, we recorded tension in a tracheal segment and activity in the phrenic nerve, before and after injecting capsaicin in various doses (0.3-20 micrograms/kg) into the femoral artery. Injection of all doses of capsaicin relaxed the tracheal segment. However, high doses of capsaicin evoked neural apnea followed by increased phrenic nerve activity whereas low doses evoked only increased phrenic nerve activity. All responses were abolished by cutting hindleg nerves. We were certain that relaxation was due to decreases of parasympathetic bronchoconstrictor activity and not to increases in activity of other inhibitory pathways, because we found no change in capsaicin-evoked relaxation after beta-adrenergic blockade with propranolol and no capsaicin-evoked relaxation after muscarinic blockade with atropine and restoration of tone with 5-hydroxytryptamine. These results provide good evidence that injecting capsaicin into the femoral artery reverses the direct relation between respiratory drive and airway tone and does so by decreasing parasympathetic bronchoconstrictor activity.

Animals↗

Absence of nonadrenergic noncholinergic relaxation in the cat cervical trachea.

Published in vivo experiments have not supported in vitro reports of the presence of nonadrenergic noncholinergic (NANC) inhibitory pathways in the cat trachea. We therefore examined these pathways, measuring tension in an innervated tracheal segment, flow resistance in more distal airways, and dynamic compliance, in 10 anesthetized mechanically ventilated cats. Initially, cervical vagal stimulation evoked contraction followed by relaxation of smooth muscle of trachea and lower airways; sympathetic stimulation evoked relaxation only. After muscarinic blockade and restoration of smooth muscle tone with 5-hydroxytryptamine (5-HT) applied topically to the tracheal mucosa, vagal stimulation did not affect tracheal segment tension, whereas sympathetic-evoked relaxation was preserved. Similar results were found when tone was restored with intravenous 5-HT, with vagal stimulation also decreasing resistance and increasing compliance. We conclude that NANC pathways are present in lower airways but not in the cervical trachea of the cat. We hypothesize that parasympathetic constriction of cat airway smooth muscle can occur without simultaneous NANC activation, whereas NANC activity occurs only in tandem with parasympathetic stimulation.

Airway Resistance↗

Catecholamines abolish vagal but not acetylcholine tone in the intact cat trachea.

To obtain evidence in the airways that catecholamines inhibit cholinergic neurotransmission, we recorded transverse tension in the posterior wall of an upper tracheal segment in anesthetized cats and compared the inhibitory effect of stimulating cervical sympathetic nerves when segment contraction was evoked by endogenous acetylcholine (vagal tone) with the effect when contraction was evoked by exogenous acetylcholine applied directly to the mucosal surface of the tracheal segment (ACh tone). We found that sympathetic stimulation abolished all contraction evoked by vagal tone but reduced ACh tone by only one-half. In a second group of cats we compared the inhibitory effects of sympathetic stimulation and intravenous isoproterenol during vagal and ACh tone and also during tone evoked by exogenous 5-hydroxytryptamine (5-HT tone). Sympathetic stimulation or isoproterenol injection abolished all vagal and 5-HT tone but again reduced ACh tone by only one-half. Our results suggest that catecholamines released from sympathetic nerves or injected into the circulation completely inhibit vagal tone. This inhibition may be partially responsible for inducing relaxation in airway smooth muscle.

Acetylcholine↗

The mechanical properties of the respiratory system during anesthesia.

1. Static compliance of the total respiratory system is decreased during anesthesia, 2. The fall in total static compliance is probably caused by a fall in lung compliance. 3. It seems unlikely that the fall in lung compliance is the primary event. The change in pleural pressures at FRC before and during anesthesia would answer this question, but the data are conflicting. 4. It is more likely that the position of the chest wall pressure-volume curve shifts to the right as a consequence of anesthesia, so that the position of equilibrium for the lung and chest wall at FRC is at a lower volume. The alteration in the chest wall is possibly because of loss of respiratory muscle tone. 5. FRC is reduced. Gas trapping occurs as a secondary event if FRC falls to below CC. 6. Lung compliance falls as a consequence of the fall in FRC, but only if FRC drops below CC, and closure occurs. No data of the correlation of change in lung compliance to the relationship of FRC to CC have been published. 7. A-aDo2 increases because of an increase in the amount of lung where ventilation is reduced compared to perfusion. Areas of zero ventilation (shunt) will also be produced. 8. The changes in lung compliance, FRC, and A-aDo2 appear to have similar characteristics. They are not influenced by depth or type of general anesthesia or the presence of neuromuscular blockade. They appear as soon as anesthesia is induced and are not progressive with time during anesthesia. They are less in the sitting position and in taller, thinner subjects. They appear to be only transiently affected by hyperinflations. 9. The fall in total respiratory system compliance may contribute to the apparent depression of the ventilatory response to carbon dioxide.

Anesthesia, General↗