Bronchial vasodilatory response to ionic and nonionic contrast media

Area of Science:

• Cardiovascular Physiology
• Pulmonary Circulation
• Pharmacology

Background:

• Bronchial arterial injection of contrast media increases bronchial blood flow (Qbr).
• The exact mechanism behind this increase in Qbr remains unclear.
• Previous studies suggest a partial attenuation by N omega-nitro-L-arginine (L-NNA), indicating a potential role for nitric oxide.

Purpose of the Study:

• To investigate the effect of conventional ionic and nonionic contrast media on Qbr.
• To elucidate the mechanism responsible for contrast-induced bronchial vasodilation.
• To determine the role of osmolality and nitric oxide in this response.

Main Methods:

• Qbr was measured in anesthetized, ventilated sheep before and during peak response to injections of saline, nonionic (Omnipaque), ionic (Conray) contrast media, and dextrose.
• Measurements were taken during control periods, after phenylephrine infusion, and after L-NNA infusion.
• The relationship between osmolality and Qbr increase was analyzed.

Main Results:

• Injection of saline, Omnipaque, Conray, and dextrose significantly increased Qbr.
• L-NNA infusion reduced baseline Qbr and attenuated the response to saline, Omnipaque, and Conray.
• Phenylephrine did not attenuate the vasodilation, and a linear relationship existed between osmolality and Qbr increase.

Conclusions:

• Osmolar stress is the primary trigger for contrast-induced bronchial vasodilation.
• The response is partially mediated by the endothelial release of nitric oxide.
• Alpha-adrenergic mechanisms are not involved in this contrast-induced vasodilation.