The Respiratory Factor in Angiographic Media Toxicity

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Abstract
EARLIER LITERATURE concerning angiographic media toxicity suggests that the harmful effect of these agents is primarily due to an allergic or anaphylactic mechanism. Disbelief of the allergic reaction theory was voiced by Sandstrom in 1953 (30) and again in 1955 (31). Subsequent clinical and experimental observations support his thesis. Clinical reports of death following the injection of relatively small doses of such agents (for intravenous pyelography) cite pulmonary edema, pulmonary hemorrhage, and atelectasis as common pathologic findings. In 1955, Mudd et at. (24) clearly demonstrated that intravenous Urokon caused histologic changes in the lung, with alternate areas of ischemia and congestion, and smallvessel thrombosis. Such reactions were more common and more severe as the site of injection was advanced from the great veins to the right atrium, right ventricle, and pulmonary artery. The next year, Rowe and his co-workers (29) described a clinical syndrome, which included hypotension, tachycardia, increased venous pressure, and electrocardiographic changes, in 5 fatalities following angiocardiography. A similar cardiovascular response was observed by Eldridge et at. (16), Finby et at. (17), Weigen and Thomas (33), and Guzman and West (18). In most of these clinical observations, a relatively prolonged period of apnea was also associated with the rapid intravenous injection of the radiopaque media. Other experimental studies revealed a similar physiologic and pathologic response (5, 19, 20). In the course of earlier studies concerning the toxicity of Hypaque (3-5), a similar syndrome of apnea followed by rapid, shallow tachypnea and associated with pulmonary edema and hemorrhage was observed in dogs. This response to intravenous diatrizoates was proportional to the dosage employed and frequently appeared to be the major factor in the animal's death. Similar observations were subsequently recorded during toxicity studies of Ditriokon (7) and Angio-Conray (8). In addition, low molecular weight dextran, a substance which diminished the toxicity of these contrast media, also prevented this respiratory response when administered prophylactically (3, 4, 6). These initial observations have led to a more detailed study of the respiratory reflex, its pathways, and its physiologic implications (9). Methods Experiments were performed upon mongrel dogs anesthetized with pentobarbital. In a number of these studies, blood pressure was monitored with a catheter in the femoral artery connected to a Sanborn 267B pressure transducer and recorded on a multi-channel Sanborn recorder. Lead II of the electrocardiogram was also recorded. Respiratory rate and depth were measured by connecting a cuffed endotracheal tube to a Benedict-Collins Metabolator filled with 100 per cent oxygen and a closed circuit CO2 absorber to obtain measurements of oxygen consumption.