BRONCHIAL VASODILATORY RESPONSE TO IONIC AND NONIONIC CONTRAST-MEDIA

It has recently been shown that bronchial arterial injection of conven tional contrast medium causes a significant increase in bronchial bloo d flow (Qbr) and that this response is partially attenuated after infu sion of N-omega-nitro-L-arginine (L-NNA). However, the precise mechani sm for this increase in Qbr is unknown. In this study we examined the effect of bronchial arterial injection of conventional ionic as well a s nonionic contrast media. We measured Qbr in nine anesthetized, venti lated, open-chest sheep. Qbr was recorded before (baseline) and at the peak response to injection of 0.5 ml of either 0.9% saline (control; isosmolar with plasma), Omnipaque 300 (iohexol; nonionic), Conray 66 ( sodium iothalamate; ionic), or 50% dextrose (viscous control). Measure ments were made during a control period, after infusion of the a-agoni st phenylephrine (5 x 10(-6) to 5 x 10(-7) M), and after bronchial art erial infusion of L-NNA (10(-2) M). The results were as follows: bronc hial arterial injection of saline, Omnipaque, Conray, and dextrose cau sed an increase in Qbr (P < 0.05). During the control period, increase s in peak Qbr on injection of saline, Omnipaque, Conray, and dextrose were 55 +/- 29, 112 +/- 62, 280 +/- 99, and 388 +/- 125% of baseline, respectively. Bronchial arterial infusion of L-NNA lowered baseline Qb r and partially attenuated the response to injection of saline, Omnipa que, and Conray (P < 0.05). Phenylephrine, in doses that decreased bas eline Qbr to the same extent as did L-NNA, did not attenuate the bronc hial vasodilation. There was a linear relationship between osmolality and the percentage increase in bronchial blood flow We conclude that a n osmolar stress is the trigger for the contrast-induced bronchial vas odilation and that the response is partially mediated by endothelial r elease of nitric oxide.