Inhaled furosemide inhibits behavioral response to airway occlusion in anesthetized cats.

BACKGROUND: A recent study showed that inhaled furosemide greatly improves experimentally induced dyspnea in humans. The objective of the current study is to test the hypothesis that inhaled furosemide suppresses the behavioral response to airway occlusion without changing the behavioral response to a somatic noxious stimulus in anesthetized animals. METHODS: In 10 spontaneously breathing cats anesthetized with isoflurane, anesthetic ED(50) was determined by measuring an end-tidal anesthetic concentration while observing escape behavior. The monitored behavior consisted of purposeful movement of the head and forearm after endotracheal tube occlusion. The duration from the start of airway occlusion to the onset of the positive response (DOCCL) was measured at the highest concentration of isoflurane permitting the positive motor response to airway occlusion before pretreatment. ED(50) values (minimum alveolar concentration) for the suppression of a somatic motor response to a noxious stimulus induced by toe pinch (toe-pinch ED(50)) were also determined. Then, the effects of inhaled furosemide or vehicle on the ED(50) for the suppression of the behavioral response to airway occlusion, DOCCL, and toe-pinch ED(50) were evaluated in a randomized, cross-over design. RESULTS: The ED(50) for the suppression of the behavioral response to airway occlusion significantly decreased (P < 0.01) and DOCCL was significantly prolonged (P < 0.01) after furosemide inhalation, whereas vehicle inhalation did not change these measurements. The decrease in ED(50) for the suppression of the behavioral response to airway occlusion after furosemide inhalation lasted 3 h. Furosemide inhalation did not affect the toe-pinch ED(50). CONCLUSION: Inhaled furosemide suppressed the behavioral response to airway occlusion in anesthetized animals without affecting the response to somatic noxious stimulus. The authors' animal model of respiratory distress may be applicable to the study of dyspnea in regard to its mechanism and treatment.

The effect of epidural anesthesia on respiratory distress induced by airway occlusion in isoflurane-anesthetized cats.

UNLABELLED: The role of afferent information from the chest wall in the genesis of dyspnea is not fully elucidated. We have developed an animal model for the study of airway occlusion (AO) and proposed new concepts of minimum alveolar anesthetic concentration for AO (MACAOR) and the duration from the start of AO to the onset of the positive motor response (DOCCL) to evaluate respiratory distress quantitatively. We examined the effects of thoracic epidural anesthesia on respiratory distress by using our animal model. Adult cats (n = 24) were anesthetized with isoflurane, and an epidural catheter was placed after T9 laminectomy. After determination of MACAOR, DOCCL was measured. Animals were then randomly assigned into three groups: the EPD Group (n = 12) received epidural 1% lidocaine (0.4 mL/kg), IM saline (0.4 mL/kg), and saline infusion. The IM Group (n = 6) received epidural saline (0.4 mL/kg), IM 1% lidocaine (1 mL/kg), and saline infusion. The PHE Group (n = 6) received epidural 1% lidocaine (0.4 mL/kg) and IV phenylephrine (0.5-1 microg. kg(-1). min(-1)) to maintain a stable arterial blood pressure. DOCCL and MACAOR were measured in each animal at 15 min after the administration of drugs. Plasma lidocaine concentrations were measured before and after epidural or IM injection. DOCCL was significantly longer after epidural injection in all groups than before the injection. Although there was no significant difference in the values of MACAOR between before and after the epidural injection in the EPD Group, the IM administration of lidocaine in the IM Group significantly reduced MACAOR. Plasma concentrations of lidocaine were similar in all groups at all measurement points. Our data indicate that thoracic epidural anesthesia using 1% lidocaine significantly reduced respiratory distress induced by AO. This effect is most likely caused by a systemic effect of lidocaine rather than by reduced afferent information from the chest wall. IMPLICATIONS: Thoracic epidural anesthesia reduced respiratory distress induced by airway occlusion. This effect is most likely caused by the systemic effect of lidocaine, rather than by the reduced afferent information from the chest wall.