Neural and humoral factors in control of tracheal caliber

Abstract

To assess the contributions of neural (vagal) and humoral (blood borne) mechanisms in the tracheal constriction that occurs when pump ventilation is transiently withheld, experiments were conducted on decerebrate dogs. The dogs were paralyzed and thoracotomized, and each lung was independently ventilated. Pressure changes within an isolated tracheal segment (Ps) were monitored as an index of tracheal caliber. In series I, pump ventilation was withheld 20 s at the prevailing end-expiratory pressure (3–5 cmH2O) from both lungs or either lung alone when 1) both lungs were intact; or 2) the left lung was vascularly isolated (VIL) by occluding the pulmonary artery and the right gas exchange lung (GEL) was vagally denervated. In series II, steady-state pressure changes in the VIL were made with constant GEL ventilation. With both lungs intact, 20-s apnea elicited a 17.3 +/- 2.6 cmH2O increase in Ps; the left and right lungs contributed equally to this response. Following vagotomy and pulmonary arterial occlusion, a 7.8 +/- 2.6 cmH2O increase in Ps was elicited from two lungs; the VIL response was 60 +/- 11% and the GEL 41 +/- 15%. Onset and one-half response times were faster from the VIL than GEL. Prolonged maneuvers elicited progressively larger responses from the GEL, but the VIL response plateaued within 30 s and then adapted towards the control level. In series II, steady-state increases or decreases in VIL pressure elicited small decreases or increases in Ps, respectively, which showed nearly complete adaptation within several minutes.