Roentgenographic evaluation of bronchial size following pulmonary embolization.

Abstract

Estimates of the changes in bronchial dimensions following pulmonary embolization have largely been derived from measurements of total lung resistance, anatomic dead space, lung compliance, and other parameters that are assumed to change with bronchoconstriction. Surprisingly, only one group, Jesser and de Takats (6), has attempted to visualize the bronchial response directly by instilling radiopaque material into the bronchial tree prior to embolization. With the use of bronchography, these investigators believed that they could demonstrate bronchoconstriction with pulmonary embolization by the appearance of radiopaque material “squeezed into the terminal radicals.” They did not measure any changes in bronchial dimensions, however, nor can any be definitely recognized in the published roentgenograms. Also, their report that these changes could be prevented by vagotomy, a procedure more recently shown to have no effect in preventing embolism-induced bronchoconstriction (1, 4, 8), suggests that their method was open to question. The development of newer pharmacologically inert contrast media and more refined roentgen technics led us to this investigation in an attempt to visualize directly the bronchial response to pulmonary embolization. To aid in determining the location and extent of bronchoconstriction, histamine and serotonin, two agents thought to mediate bronchoconstriction with pulmonary embolization, were employed, together with balloon occlusion of the left pulmonary artery and with pulmonary embolism itself. Materials and Methods Healthy mongrel dogs weighing 17 to 23 kg were selected for the study. The animals were lightly anesthetized by the intravenous administration of 20 to 25 mg/kg sodium pentobarbital and then intubated with a cuffed tracheal tube 1.2 cm in diameter. Total lung resistance was measured in 20 of 25 animals by technics described by Mead and Whittenberger (7). Briefly, these consisted of introducing a No. 10 Malecot catheter through one of the lower intercostal spaces into the intrapleural cavity, evacuating any pneumothorax, and then suturing the catheter in place. Transpulmonary pressure was measured with a Statham differential transducer, with one side connected to the intrapleural catheter and the other side to a connection in the tracheal cannula. Air flow was measured by a pneumotacho-pretation and should be identified. The contrast medium may itself produce alterations in bronchial width either by its pharmacological effects or by blocking air flow at critical points. This interference with air flow could prevent bronchial distention proximal to the blockage. Probably more important, it could interfere with distal gas exchange and lead to alterations in blood gas composition and pH, as well as prevent the more distal bronchi from contributing to the measurement of total lung resistance. For these reasons special effort was made only to coat the bronchial lumens, rather than to fill them completely.