Pulmonary vasodilation by ketamine is mediated in part by L-type calcium channels
| Autor: | Philip J. Kadowitz, Chang J. Feng, Alan D. Kaye, Ronald E. Banister, Muhammad Anwar, Bobby D. Nossaman |
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| Rok vydání: | 1998 |
| Předmět: |
Male
medicine.medical_specialty Cromakalim Potassium Channels Thromboxane Morpholines chemistry.chemical_element Vasodilation Adamantane Blood Pressure Calcium Pulmonary Artery Arginine Nitric oxide Rats Sprague-Dawley chemistry.chemical_compound Internal medicine Medicine Animals L-type calcium channel Cyclooxygenase Inhibitors Lung Meclofenamic Acid Anesthetics Dissociative Arachidonic Acid biology Dose-Response Relationship Drug business.industry 3-Pyridinecarboxylic acid 1 4-dihydro-2 6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)- Methyl ester Calcium Channel Blockers Potassium channel Rats Nitric oxide synthase Anesthesiology and Pain Medicine Endocrinology chemistry Verapamil biology.protein Ketamine Calcium Channels business medicine.drug |
| Zdroj: | Anesthesia and analgesia. 87(4) |
| ISSN: | 0003-2999 |
| Popis: | MD Departments of Anesthesiology and Pharmacology, Tulane University Medical School, New Orleans, Louisiana We studied the effects of ketamine in the isolated rat lung under conditions of increased pulmonary arterial pressure using the thromboxane A, mimic, U46619, and in response to ventilatory hypoxia. Ketamine caused dose-dependent vasodilation, and possible mechanisms were evaluated using verapamil, meclofe- namate, N”-L-nitro-L-arginine benzyl ester (an inhibi- tor of nitric oxide synthase), and U-38883A (an ATP- sensitive potassium channel antagonist) in the isolated blood-perfused rat lung. Under increased tone condi- tions, N’“-L-nitro-L-arginine benzyl ester, meclofe- namate, and U-38883A had no significant effect in at- tenuating ketamine-induced vasodilator responses. In a final series of experiments, verapamil significantly attenuated ketamine-induced vasodilator responses. These data suggest that ketamine has significant vaso- dilator activity in the pulmonary vascular bed of the rat, which seems to be mediated by an L-type calcium channel-sensitive pathway. These responses are not mediated or modulated by the release of nitric oxide, the activation of K+ATP channels, or the release of va- sodilator cyclooxygenase products. Implications: In this study, we examined the mechanism of the vasodi- lator effects of ketamine in the blood-perfused rat lung. The results of the present study suggest that ketamine- induced vasodilator responses are mediated by an L-type calcium channel-sensitive pathway. (Anesth Analg 1998;87:956-62) |
| Databáze: | OpenAIRE |
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