Key points are not available for this paper at this time.
Answers are grounded in this paper and cite their sources.
Lung inflation reflexes in dogs should not alter practice; leaves open their role in human cardio-respiratory coupling.
In dogs, inflating the lungs to pressures of 9 cm H2O or less reflexly increases heart rate, whereas inflating the lungs to pressures of 10-30 cm H2O reflexly decreases heart rate. The afferent fibers responsible for the cardioacceleration travel in the vagus nerves and are believed to be pulmonary stretch receptors, whereas the afferent responsible for the deceleration also travel in the vagus nerves, but are believed to be lung C-fibers. To identify the afferents responsible for these effects, we recorded the impulse activity of vagal afferents with endings in the left lung, while we slowly inflated that lung to 30-45 cm H2O. We found that 12 slowly adapting receptors fired at significantly lower inflation pressures than did 10 rapidly adapting receptors (5.8 +/- 1.5 vs. 13.5 +/- 2.2 cm H2O, respectively). We also found that 13 pulmonary C-fibers fired at significantly lower inflation pressures than did 10 bronchial C-fibers (16.4 +/- 1.8 vs 26.5 %/- 2.9 cm H2O, respectively). We conclude that slowly adapting receptors are likely to be responsible for the cardioacceleration evoked by low levels of inflation, and that both pulmonary and bronchial C-fibers are likely to be responsible for the cardiodeceleration evoked by high levels of inflation.
No takes yet. Share an insight, caveat, or question.
Kaufman et al. (1982) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: