Abstract

We tested the hypothesis that altering the pattern and/or magnitude of discharge of pulmonary stretch receptors (PSRs) would alter baroreceptor reflexes in anesthetized aortic-denervated cats. Carotid baroreceptor control of mean arterial pressure (MAP), heart rate (HR), and hindlimb perfusion pressure (PPhl) was examined by changing carotid sinus pressure (CSP) from 50 to 225 mmHg. The pattern of PSR discharge was changed by switching conventional mechanical ventilation (CMV) to high-frequency ventilation (HFV). Magnitude of PSR discharge was altered by changing positive end-expiratory pressure (PEEP). Altering the discharge pattern of PSR had no effect on CSP-MAP or CSP-PPhl relationships; small changes in HR were observed. Increasing PSR activity by increasing PEEP during CMV (from 3 to 9 cmH2O) depressed CSP-MAP relationship, set point, and threshold pressure. However, the depression in CSP-MAP relationship and set point during PEEP was unrelated to PSR activation, because these changes were not abolished after bilateral vagotomy. CSP-PPhl relationship was significantly elevated during PEEP before and after vagotomy, suggesting activation of a nonvagally mediated vasoconstrictory mechanism instead of PSR-mediated depressor reflex. CSP-HR relationship during PEEP showed a slight elevation, which was abolished after vagotomy. We conclude that despite minor increases in HR, altering the pattern of magnitude of PSR activity with HFV and PEEP has no significant effect on carotid baroreceptor regulation of systemic circulation. Hemodynamic changes observed during PEEP were likely due to its mechanical effect on cardiac output and activation of other cardiopulmonary receptors rather than to the increase in PSR activity.

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