Rapidly adapting receptors in a rabbit model of mitral regurgitation.
1. Unlike in normal rabbits, pulmonary rapidly adapting receptors (RARs) in rabbits with chronic mitral regurgitation (MR) do not respond to small changes in extravascular fluid (EVF) volume in major airways. The present study examined the effect of shrinking the EVF volume in rabbits with chronic MR by infusing hypertonic albumin, to see whether this response of RARs is restored. The effect of raising the left atrial pressure (LAP) acutely above 25 mmHg (to cause pulmonary oedema) on RARs was also investigated. 2. Mean RAR activities in rabbits with MR (n = 6) at initial control, LAP +5 mmHg, LAP +10 mmHg and final control periods were 20.9 +/- 9. 5, 18.8 +/- 11.3, 27.0 +/- 11.2 and 17.2 +/- 9.8 action potentials min-1, respectively (P > 0.05, ANOVA). After infusion of 35 % bovine serum albumin i.v. these values were 9.4 +/- 3.2, 30.6 +/- 14.6, 48. 9 +/- 10.1 and 18.4 +/- 7.3 action potentials min-1, respectively (P < 0.01, ANOVA). In rabbits with chronic MR (n = 7) raising the LAP above 25 mmHg stimulated RARs. 3. EVF content of the airways and lungs was measured in rabbits with MR and in control rabbits, at baseline and after elevation of the LAP by 10 or 25 mmHg for 20 min. In control rabbits the EVF contents in the lower trachea, carina and bronchi at baseline and at LAP +10 mmHg were 52.1 +/- 1.2 and 57.8 +/- 1.7 %, respectively (P < 0.05, Student's t test). In rabbits with MR these values were 58.3 +/- 1.5 and 56.9 +/- 1.9 %, respectively. When the LAP was elevated by 25 mmHg the EVF content increased to 62.4 +/- 1.1 % (P < 0.05, t test compared with baseline and LAP +10 mmHg). 4. We concluded that in rabbits with chronic MR, RARs are unable to respond to acute, small elevations of LAP because there is no concomitant increase in EVF content in the vicinity of these receptors. Furthermore, these receptors can be activated in these animals by elevating the LAP above 25 mmHg or can be made sensitive to acute small elevations of LAP by shrinking the chronically expanded EVF compartment.
Gunawardena
S
S
Division of Cardiovascular Medicine, University of California, Davis 95616, USA.
Bravo
E
E
Kappagoda
C T
CT
D000200:Action Potentials / Q000502:physiology; D000222:Adaptation, Physiological / Q000502:physiology; D000465:Algorithms; D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D001980:Bronchi / Q000378:metabolism; D018618:Echocardiography, Doppler, Color; D004594:Electrophysiology; D015633:Extravascular Lung Water / Q000502:physiology; D006352:Heart Ventricles / Q000378:metabolism; D006982:Hypertonic Solutions; D008168:Lung / Q000378:metabolism / Q000503:physiopathology*; D008465:Mechanoreceptors / Q000502:physiology*; D008944:Mitral Valve Insufficiency / Q000503:physiopathology*; D011652:Pulmonary Circulation / Q000502:physiology; D011817:Rabbits; D014132:Trachea / Q000378:metabolism; D014630:Vagus Nerve / Q000502:physiology
D006982:Hypertonic Solutions