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ANESTHETIC PHARMACOLOGY

An Analysis of Remifentanil in the Pulmonary Vascular Bed of the Cat

Alan D. Kaye, MD, PhD^*, Amir Baluch, BS, James Phelps, MPT, Syed R. Baber, BS, Ikhlass N. Ibrahim, DVM^*, Jason M. Hoover, BS, Cuihua Zhang, MD, PhD^*, and Aaron Fields, MD^||

Departments of *Anesthesiology and Pharmacology, LSU Health Sciences Center, New Orleans, Louisiana; Texas Tech University Health Sciences Center School of Medicine, Lubbock, Texas and El Paso, Texas; Tulane University, New Orleans, Louisiana; and ||Department of Anesthesiology, Yale University School of Medicine, New Haven, Connecticut

Address correspondence and reprint requests to Alan D. Kaye, MD, PhD, DABPM, Professor and Chairman, Department of Anesthesiology, Professor, Department of Pharmacology, Louisiana State University School of Medicine, 1542 Tulane Ave. T6M5, New Orleans, LA 70112. Address e-mail to akaye{at}lsuhsc.edu.

In this investigation we sought to identify the role of remifentanil in the feline pulmonary vascular bed. Using adult mongrel cats in separate experiments, the effects of glibenclamide (adenosine triphosphate-sensitive K⁺ channel blocker), diphenhydramine (histamine H₁-receptor antagonist), L-N⁵-(1-Iminoethyl) ornithine hydrochloride (nitric oxide synthase inhibitor), and naloxone (opioid receptor antagonist) were investigated in pulmonary arterial responses to remifentanil (opioid agonist), pinacidil (adenosine triphosphate-sensitive K⁺ channel activator), and bradykinin (nitric oxide synthase inducer). Under increased tone conditions in the isolated left lower lobe vascular bed of the cat, remifentanil induced a dose-dependent vasodepressor response that was not significantly altered after administration of glibenclamide and L-N⁵-(1-Iminoethyl) ornithine hydrochloride. Responses to remifentanil were significantly attenuated after administration of diphenhydramine and naloxone. The results suggest that remifentanil has potent vasodepressor activity in the feline pulmonary vascular bed and that these responses are mediated by histamine and opioid receptor sensitive pathways.