H. D. Schultz

Stimulation of pulmonary vagal afferent C-fibers by lung edema in dogs.

In anesthetized, open-chest dogs we examined the effect of pulmonary edema on the firing frequency of afferent vagal fibers arising from the lung. We recorded impulses from slips of the cervical vagus nerves and infused isotonic Krebs-Henseleit solution (20% of body weight) intravenously to increase net filtration pressure in the lung microvasculature. Measurement of extravascular lung water (6.0 ± 0.4 g/g dry lung), and morphological examination of lung tissue (revealing various degrees of perivascular and peribronchial cuffing) confirmed that edema was present. At the end of the infusion when the lungs were congested (lung microvascular pressure, 37 cm water) and edematous, the impulse frequency of pulmonary and bronchial C-fibers and rapidly adapting receptors had increased 5–6 times. The only significant change in slowly adapting receptor activity was an increase during deflation. When lung water was still elevated but lung microvascular pressure had been restored to control by withdrawal of blood, impulse activity of rapidly and slowly adapting receptors reverted to or below control. Pulmonary C-fiber activity, although less than during congestion, remained significantly above control, several C-fibers being stimulated by interstitial edema in the absence of alveolar edema. Bronchial C-fibers were stimulated in severely edematous lung showing pronounced peribronchial cuffing and alveolar edema, but were not stimulated in milder grades of edema. Our results support the hypothesis (Paintal, 1969) that pulmonary C-fibers (J-receptors) are stimulated by an increase in interstitial pressure secondary to edema.

Afferent pathways involved in reflex regulation of airway smooth muscle

Our purpose in the present review is to give an account of the various sensory regions from which reflex effects on airway smooth muscle are known to arise, with some reference to the nature of the sensory structures involved, where this is known. We deal first with intrinsic afferent inputs-intrinsic in the sense that they arise from the airways themselves, although for convenience the term has been extended to include the upper airways that do not contain airway smooth muscle-and then with extrinsic afferent inputs that arise from regions remote from the airways and lungs.

Characteristics of C fibre baroreceptors in the carotid sinus of dogs.

1. We compared the pressure‐response characteristics of C fibre and A fibre baroreceptors in the carotid sinus of anaesthetized dogs, recording impulses from the sinus nerve and varying mean pressure in the vascularly isolated sinus, which was distended with a pulsatile pressure. Functional stimulus‐response curves were obtained by gradually increasing sinus pressure above and decreasing it below a set‐point of 100 mmHg. Baroreceptors were identified by a pulsatile discharge synchronous with the pulsations in sinus pressure. A and C fibre baroreceptors were identified by the conduction velocities and blocking temperatures of their axons. 2. The pressure‐response characteristics of C and A fibre baroreceptors differed in several respects. C fibres had a pulsatile firing threshold 50 mmHg higher than that of A fibres (105.8 +/‐ 1.8 and 54.6 +/‐ 2.9 mmHg, respectively), an average maximal sensitivity 35% of that of A fibres (0.39 and 1.12 impulses s‐1 mmHg‐1, respectively), and a maximal frequency (at 220 mmHg) 29% of that of A fibres (24.5 and 84.3 impulses/s, respectively). Although invariably pulsatile at pressures above threshold, the firing pattern of C fibre baroreceptors tended to be more irregular than that of their A fibre counterparts. 3. Impulses were also recorded from C fibres that were stimulated by increasing sinus pressure but had an irregular, non‐pulsatile discharge, a high pressure threshold (averaging 154.1 +/‐ 7.2 mmHg), and a low maximum frequency (10.8 +/‐ 2.4 impulses/s). 4. Cooling the sinus nerve progressively attenuated conduction in both A and C fibres, A fibres being blocked between 12 and 4 degrees C (mean 6.8 degrees C) and C fibres between 4 and ‐1.5 degrees C (mean 1.0 degree C). Although cooling the sinus nerve to 7 degrees C did not block conduction in all A fibres, impulse activity in baroreceptor A fibres at a carotid sinus pressure of 200 mmHg was no greater than that at a pressure of 75 mmHg. By contrast, at 7 degrees C baroreceptor C fibres still provided a signal proportional to sinus pressure. 5. Our results suggest that A and C fibre baroreceptors subserve different reflex functions, the former signalling changes in arterial pressure both above and below the normal set‐point, the latter only changes above. They also suggest that differential cold blockade may be a useful tool to determine the contribution of C fibre baroreceptors to cardiovascular reflexes.

Carotid sinus baroreceptors modulate tracheal smooth muscle tension in dogs.

Arterial baroreceptors are known to influence airway smooth muscle tone. Thus, increasing carotid sinus pressure from 20 to 200 mm Hg causes reflex tracheal dilation. However, the effects of changing sinus pressure around a normal arterial pressure set-point of 100 mm Hg have not been examined. In anesthetized, artificially ventilated dogs, we distended the vascularly isolated carotid sinuses with a pulsatile pressure and recorded isometric tension in an upper tracheal segment. The aortic nerves were cut. Increasing mean carotid sinus pressure in steps between 100 and 200 mm Hg decreased tracheal tension, heart rate, and arterial blood pressure; decreasing sinus pressure between 100 and 25 mm Hg had the opposite effect. Changing carotid sinus pressure still evoked tracheal responses when systemic arterial pressure was held constant. Increasing and decreasing carotid sinus pulse pressure around a constant mean pressure evoked similar changes in tracheal tension. All reflex effects were abolished by cutting or cooling (0 degree C) the carotid sinus nerves; tracheal responses were abolished by the carotid baroreflex were of comparable magnitude to those triggered by stimulating pulmonary stretch receptors, laryngeal receptors, and pulmonary C-fibers. Our results indicate that carotid sinus baroreceptors exert a tonic influence on the upper airways by a vagal cholinergic pathway, increasing and decreasing tracheal smooth muscle tension as blood pressure varies around the normal set-point.