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

Lessons From the World Trade Center Disaster

“…Subsequently, Miller and Palecki 3,33 reported reduced TLC with preservation of FEV 1 /VC in patients with asthma. Since distal airways constrict in response to a variety of stimuli, 45,46 these studies postulated closure/collapse of distal airways and alveolar ducts as the underlying mechanism. Kaminsky and Irvin 5 obtained pathologic specimens in a patient with reversible restriction due to asthma and demonstrated terminal airway infl ammation.…”

Role of Histamine in Hypoxic Pulmonary Hypertension in the Rat

“…Microembolization has been associated with histamine release (14), and circulating platelets were decreased rapidly in the course of a perfusion. If platelets or other formed elements help mediate histamine release, they may do so either directly or possibly via effects associated with plasma reactions, such as complement activation or formation of slow-reacting substance (15).…”

The role of prostaglandins in the bronchoconstriction induced by pulmonary micro‐embolism in the guinea‐pig.

“…A decrease in lung compliance has been frequently seen after BaSO4 induced pulmonary embolism (Halmagyi & Colebatch, 1961;Nadel, Colebatch & Olsen, 1964), and evidence that peripheral airway closure is the cause of such compliance change was supplied by the work of Clarke, Graf & Nadel (1970). The decrease in pulmonary compliance has been shown to be dependent on the release of humoral substances (Halmagyi, Starzecki & Homer, 1964).…”

“…The decrease in pulmonary compliance has been shown to be dependent on the release of humoral substances (Halmagyi, Starzecki & Homer, 1964). Such humoral agents, with known bronchoconstrictor actions have been thought to be histamine (Nadel, et al 1964), 5-hydroxytryptamine (5-HT); (Thomas, Stein, Tanabe, Rege & Wessler, 1964) or prostaglandin-like substances (Nakano & McCloy, 1973). In addition, platelet aggregation, occurring as a result of microsphere embolization, may lead to the release of humoral agents such as 5-HT (Zucker & Grant, 1974) and prostaglandins (Bo, Hognestad & Vaage, 1974;Vaage & Piper, 1975).…”