Location and mechanism of airway constriction after barium sulfate microembolism

Abstract

Injection of barium sulfate microemboli into the right side of the heart of paralyzed, artificially ventilated cats increased pulmonary resistance, decreased pulmonary compliance and functional residual capacity, and increased end-expiratory transpulmonary pressure and anatomic dead space. These effects could be due to constriction of terminal respiratory units without significant narrowing of the large airways, which may actually enlarge. Anatomic studies, performed after rapid freezing of the lungs in the open thorax, showed that the principal site of constriction was the alveolar ducts. Intravenous isoproterenol partially or completely prevented the changes following microembolism, suggesting that they were due to smooth muscle contraction. Vagotomy, injection of heparin or atropine or guanethedine, or inhalation of 6% carbon dioxide did not prevent the changes; prior injections of 48/80 decreased the changes. These studies suggest that the embolism-induced changes depend on histamine release. The varied manifestations of barium sulfate microembolism, including the shift of ventilation to the unaffected areas, atelectasis of embolized areas, anoxemia, and abnormal breathing pattern may depend on the presence and extent of contraction of peripheral respiratory units induced by liberation of histamine. terminal airway constriction; histamine release; lung compliance; pulmonary resistance; airway anatomy; alveolar duct; muscle Submitted on August 30, 1963