Unilateral hypoventilation produced in dogs by occluding one pulmonary artery

Abstract

Temporary unilateral pulmonary artery occlusion resulted within 1 minute in a shift of tidal volume away from unperfused lungs in 14 anesthetized closed-chest dogs. The shift of ventilation was caused by bronchoconstriction following the decrease of CO2 on the occluded side. It was prevented by inhalation into that side of 6% CO2 in air, isoproterenol aerosol or 100% N2, but not by atropine or vagotomy. Airway resistance on the occluded side was doubled, and compliance fell 25%. Functional residual capacity fell variably (0–25%), and anatomic dead space decreased. When blood flow was restored, shunting was detected and ventilation returned slowly with normal inflation or immediately after hyperinflation of that lung. This suggests that terminal and respiratory bronchiolar smooth muscle constriction may lead to airway closure and atelectasis and that the gas exchange of the smooth muscle in smaller airways is carried out by direct diffusion to and from the airway rather than with blood. Submitted on June 9, 1960

Cardiorespiratory Effects of Experimental Lung Embolism*

“…In the distal segments the same contraction would cause widespread closure of the terminal airways with a fall in ventilated lung volume and CL. This appears to be the "unknown mechanism" (41) that produces a shift of ventilation toward the unaffected parts of the lungs, as demonstrated by fluoroscopy (42) and bronchospirometry (43) and by means of a ballooncatheter (44,45).…”

Mechanisms underlying gas exchange alterations in an experimental model of pulmonary embolism

“…Actually, the increase in dead space per se does not induce hypoxemia. For this reason, hypoxemia is attributed to a significant alteration of the V A /Q ratio (3,5,10,14,15,17,25), with alveolar ventilation being slightly increased but with perfusion being markedly increased.…”

“…Indeed, Levy and Simmons (15) observed that in PE there is a partial auto-regulation of the alveolar ventilation and perfusion at the lobar and segmental levels in order to maintain the equilibrium of the V A /Q (4,16). This phenomenon has only recently been confirmed with technology based on positron emission tomography scan that quantifies the redirection of the ventilation to alveoli with maintained perfusion, called effective or regional alveolar ventilation (V A eff) (14,17,18). Most studies attribute the redirection of alveolar ventilation to regional bronchoconstriction induced by alveolar hypocapnia (14,15,17,19,20).…”

“…This phenomenon has only recently been confirmed with technology based on positron emission tomography scan that quantifies the redirection of the ventilation to alveoli with maintained perfusion, called effective or regional alveolar ventilation (V A eff) (14,17,18). Most studies attribute the redirection of alveolar ventilation to regional bronchoconstriction induced by alveolar hypocapnia (14,15,17,19,20). However, this redistribution of alveolar ventilation varying from nonexistent to highly significant has been frequently reported in the literature (8,9,15), probably because of the different approaches and models used (3).…”

Relaxation of tracheomotor tone by PEEP: Influence of hypocapnia and acidemia

“…The PEEP effect on tracheomotor tone depends on the resting level of airway smooth muscle tone. Severinghaus et al 12 suggested that local mechanisms control airway smooth muscle tone, and hence ventilation: perfusion matching. Our data suggest that systemic acid-base balance also contributes to the magnitude of the tracheomotor response to PEEP.…”