The effect of emboli upon intrapulmonary receptors in the cat

1991

SUMMARY1. The responses of the rapidly adapting receptors (RARs) and the slowly adapting receptors (SARs) of the airways to changes in the Starling forces regulating fluid exchange in the pulmonary extravascular space were investigated in anaesthetized rabbits. The hydrostatic pressure in the pulmonary microvasculature was raised by partial obstruction of the mitral valve (mean left atrial pressure increased by approximately 5 and 10 mmHg above the control values) and the concentration of plasma proteins was reduced by plasmapheresis (the total plasma protein concentration reduced by 18 %).2. There was a significant correlation between the action potentials generated by RARs and mean left atrial pressure (n = 12). A similar response was not observed in SARs (n = 12).3. After plasmapheresis, there was an increase in the resting activity of the RARs (n = 5). In addition, the stimulus-response curve relating mean left atrial pressure and RAR activity was significantly shifted to the left compared to the one elicited before plasmapheresis. Plasmapheresis failed to influence the activity of SARs (n = 5).4. Obstruction of the pulmonary lymph flow by raising the afterload in the right external jugular vein caused a significant increase in the activity of RARs (n = 6). This response was also maintained during the entire period of lymphatic obstruction.5. The results show that manipulation of the Starling forces within the lung influences the RAR activity profoundly. It is suggested that the stimulus for the RARs may be a function of the fluid fluxes in the pulmonary extravascular space.

Section: Mechanisms For the Stimulation Of Rarsmentioning

confidence: 96%

Responses of slowly and rapidly adapting receptors in the airways of rabbits to changes in the Starling forces.

Hargreaves

Ravindran

1991

“…In the cat, it was found that injection of micro-emboli into the pulmonary arteries increased the peak intra-tracheal pressure and the activities of r.a.r., s.a.r. and pulmonary C-fibre receptors (Armstrong, Luck & Martin, 1976). Since the increase in peak intra-tracheal pressure persisted even after vagotomy, Armstrong et al (1976) attributed it to a decrease in dynamic compliance of the lung.…”

Section: Speculation On Mechanismsmentioning

confidence: 99%

“…and pulmonary C-fibre receptors (Armstrong, Luck & Martin, 1976). Since the increase in peak intra-tracheal pressure persisted even after vagotomy, Armstrong et al (1976) attributed it to a decrease in dynamic compliance of the lung. In their study, it was found that the activity of these receptors was not elevated in a persistent manner, until the peak airway pressure increased by more than 1 cmH2O (074 mmHg).…”

Section: Speculation On Mechanismsmentioning

confidence: 99%

Behaviour of canine pulmonary vagal afferent receptors during sustained acute pulmonary venous pressure elevation.

Man

Teo

1987

“…They are stimulated by a variety of pathophysiological changes in the airways e.g. pulmonary congestion (Mills, Sellick & Widdicombe, 1969;Kappagoda, Man & Teo, 1987;Hargreaves et al 1991), pulmonary oedema (Roberts, Bhattacharya, Schultz, Coleridge & Coleridge, 1986; and pulmonary embolism (Mills et al 1969;Armstrong, Luck & Martin, 1976). However, their role in increasing respiratory rate remains uncertain .…”

Section: Discussionmentioning

confidence: 99%

Effect of bradykinin on respiratory rate in anaesthetized rabbits; role of rapidly adapting receptors.

Hargreaves

Ravindran

1993

SUMMARY1. This study was performed in anaesthetized, spontaneously breathing rabbits: (a) to determine the effect of bradykinin administered into the right atrium on the respiratory rate, and (b) to elucidate the potential role of rapidly adapting receptors (RARs) in mediating this effect. The role of RARs was established by graded cooling of the cervical vagi. The respiratory rate was measured from an intrapleural pressure tracing.2. Dose-response curves relating right atrial injections of bradykinin (0 25, 0 5, 1 0 and 1-5 jug/kg) to the respiratory rate were established in the control state (i.e.vagi at 37°C). The respiratory rate increased significantly (P < 0.01, ANOVA) from a control value of 51'3 + 6-8 breaths/min by 12 + 3, 25 + 5, 43 + 7 and 58 + 11 % respectively. At doses of 1P0 and 1P5 jug/kg i.v., the increase in rate was preceded by apnoea.3. The dose-response curves were repeated with bolus injections of bradykinin (0-25, 0 5, 1P0 and 1-5 jug/kg) after cooling the cervical vagi to 8-9 'C. The increase in respiratory rate was attenuated significantly (P < 0-01 ANOVA). The rate increased from a control value of 27-2 + 2-1 breaths/min by 5 + 2, 6 + 2, 16 + 5 and 21 + 8 % respectively. With vagi cooled, apnoea was increased in duration and occurred at lower doses. On rewarming vagi, the original responses were reestablished. 4. When the study was repeated after bilateral vagotomy, apnoea was abolished but there was a small residual increase in rate. This increase was similar to that seen after cooling the vagi (P > 0 05). 5. RAR (n = 5) activity was recorded from the cervical vagus. Right atrial injections of bradykinin (0-25-1-0 jug/kg) stimulated RARs. On cooling the vagi to 8-9 'C caudal to the recording site, the increase in activity was blocked.6. These data support the proposition that bradykinin increases the respiratory rate in rabbits and that this response is, in part, a reflex mediated by RARs. In addition, bradykinin has other secondary effects on respiration: an apnoea which is mediated by non-myelinated vagal afferents and a small stimulatory effect on respiration which persists after bilateral vagotomy. MS 1660 17PHY 469