Cardiovascular responses to stimulation of pulmonary C fibres in the cat: their modulation by changes in respiration.

Abstract

SUMMARY1. In cats anaesthetized with a mixture of chloralose and urethane, stimulation of pulmonary C fibres by right atrial injections of phenylbiguanide caused, after a latency of about 3 s, a reduction in pulmonary ventilation or apnoea, bradyeardia and systemic hypotension, confirming previous work.2. A decrease in femoral artery perfusion pressure also occurred under conditions in which the hindlimb was vascularly isolated, the blood flow was maintained constant and the inferior vena caval pressure did not change. This indicates a reduction in vascular resistance due to vasodilatation. The response was unaffected by atropine and propranolol, but was reduced or abolished by guanethidine, hexamethonium and denervation of the limb, indicating that it is due to a reduction in activity in sympathetic vasoconstrictor fibres.3. Similar cardiovascular responses were observed when the arterial blood pressure was maintained constant, and also in artificially ventilated animals.4. Evidence is presented that the receptors responsible for the respiratory and cardiovascular responses to right atrial injections of phenylbiguanide lie in the pulmonary vascular bed.5. When the pulmonary C fibres were excited during a period of apnoea which was induced reflexly by electrical stimulation of the central end of a superior laryngeal nerve, there were no consistent differences in the size of the cardiac or vascular responses compared to the control responses in the absence of the laryngeal input. This result occurred irrespective of the size of the control ventilatory response to phenylbiguanide.6. By contrast in the same experiments, the cardio-inhibitory and vasoconstrictor responses to excitation of the carotid body chemoreceptors were invariably potentiated by electrical stimulation of a superior laryngeal nerve, as found previously.7. The possible central mechanisms responsible for the differential modulation of pulmonary C fibre and carotid chemoreceptor reflexes by respiration are discussed.

Reflex Nature of the Cardiorespiratory Response to Primary Thoracic Blast Injury in the Anaesthetised Rat

“…Of these, the pulmonary C-fibre reflex is the most likely candidate since it produces the full range of cardiovascular and respiratory responses observed following thoracic blast. The afferent pathway can be stimulated by pulmonary oedema (Paintal, 1969) or by 5HT, released from platelets within the lungs, acting on pulmonary 5HT 3 receptors (Daly & Kirkman, 1988). The cardiac afferent C-fibre reflex could also be responsible for the cardiovascular component of the response to thoracic blast.…”

“…These are: the pulmonary afferent C-fibre reflex (pulmonary J receptors), causing apnoea, bradycardia and hypotension (Paintal, 1969;Willette et al 1982;Daly & Kirkman, 1988); the cardiac afferent C-fibre reflex, causing bradycardia and hypotension, (Dawes, 1947;Coleridge & Coleridge, 1979;Daly & Kirkman, 1988); the arterial baroreceptors producing bradycardia and hypotension, (Daly, 1983); the pulmonary stretch receptors (Hering-Breuer reflex), causing apnoea. Of these, the pulmonary C-fibre reflex is the most likely candidate since it produces the full range of cardiovascular and respiratory responses observed following thoracic blast.…”

“…The pulmonary afferent C-fibres are carried in the vagus nerve (Coleridge & Coleridge, 1984), which also carries the efferent limb of the reflex mediating the bradycardia (Daly & Kirkman, 1988). By contrast, the hypotension is the consequence of a sympathoinhibition leading to a fall in peripheral vascular resistance (Daly & Kirkman, 1988).…”

Reflex cardiac dromotropic responses to stimulation of the carotid and aortic chemoreceptors in the anaesthetized cat

“…As an index of the reflex activity of the preparations the changes in vascular resistance of the right hind limb were measured. The limb was vascularly isolated and perfused with blood from the blood pressure compensator at constant flow (Daly & Kirkman, 1988). All variables were recorded on a multi-channel high resolution thermal print-head recorder (model PAR2000B, TDM Tape Services Ltd, Nottingham, UK).…”

Effects of transcutaneous electrical diaphragmatic stimulation on the cardiac autonomic balance in healthy individuals: a randomized clinical trial

“…This phenomenon seems to be commanded by two major mechanisms involving respiratory and circulatory centers in the brainstem. First, the inhibition of cardiac vagal efferent activity by lung inflation, which evokes tachycardia by stimulating the pulmonary C-fiber afferents, i.e., pulmonary stretch receptors 14,15,17 ; second, the acetylcholine-mediated inhibitory postsynaptic potential in the cardiac vagal preganglionic neurons by central respiratory drive, which makes neurons less responsive to excitatory inputs during inspiration [18][19][20] . Over the last years, the analysis of HRV has been extensively used to evaluate the autonomic modulation of the cardiovascular system [21][22][23] .…”