Epidural clonidine suppresses the baroreceptor-sympathetic response depending on isoflurane concentrations in cats.
Epidural administration of clonidine induces hypotension and bradycardia secondary to decreased sympathetic nerve activity. In this study, we sought to elucidate the change in baroreflex response caused by epidural clonidine. Thirty-six cats were allocated to six groups (n = 6 each) and were given either thoracic epidural clonidine 4 micro g/kg or lidocaine 2 mg/kg during 0.5, 1.0, or 1.5 minimum alveolar anesthetic concentration (MAC) isoflurane anesthesia. Heart rate (HR), mean arterial blood pressure (MAP), and cardiac sympathetic nerve activity (CSNA) were measured. Depressor and pressor responses were induced by IV nitroprusside 10 micro g/kg and phenylephrine 10 micro g/kg, respectively. Baroreflex was evaluated by the change in both CSNA and HR relative to the peak change in MAP (deltaCSNA/deltaMAP and deltaHR/deltaMAP, respectively). These measurements were performed before and 30 min after epidural drug administration. Epidural clonidine and lidocaine decreased HR, MAP, and CSNA by similar extents. deltaCSNA/deltaMAP and deltaHR/deltaMAP for depressor response were suppressed with epidural lidocaine and clonidine in all groups but the clonidine 0.5 MAC isoflurane group (0.197 +/- 0.053 to 0.063 +/- 0.014 and 0.717 +/- 0.156 to 0.177 +/- 0.038, respectively, by epidural lidocaine [P < 0.05] but 0.221 +/- 0.028 to 0.164 +/- 0.041 and 0.721 +/- 0.177 to 0.945 +/- 0.239, respectively, by epidural clonidine during 0.5 MAC isoflurane). Those for pressor response were suppressed in all groups. We conclude that thoracic epidural clonidine suppresses baroreflex gain during isoflurane anesthesia >1.0 MAC but may offer certain advantages compared with epidural lidocaine during 0.5 MAC isoflurane by virtue of preserving baroreflex sensitivity when inadvertent hypotension occurs.
Ikeda
Yoshikazu
Y
*Department of Anesthesiology and Intensive Care Medicine, Osaka City University Medical School, Osaka, Japan; and †Department of Anesthesia, Hoshigaoka Kosei-nenkin Hospital, Osaka, Japan.
Nishikawa
Kiyonobu
K
Ohashi
Kenji
K
Mori
Takashi
T
Asada
Akira
A
D000138:Acidosis / Q000139:chemically induced / Q000378:metabolism; D000316:Adrenergic alpha-Agonists / Q000008:administration & dosage / Q000494:pharmacology*; D018685:Anesthetics, Inhalation / Q000494:pharmacology*; D000779:Anesthetics, Local / Q000494:pharmacology; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D002415:Cats; D003000:Clonidine / Q000008:administration & dosage / Q000494:pharmacology*; D004824:Epidural Space; D005260:Female; D006321:Heart / Q000187:drug effects / Q000294:innervation; D006339:Heart Rate / Q000187:drug effects; D007267:Injections; D007530:Isoflurane / Q000494:pharmacology*; D008012:Lidocaine / Q000494:pharmacology; D008297:Male; D011311:Pressoreceptors / Q000187:drug effects*; D013564:Sympathetic Nervous System / Q000187:drug effects*
D000316:Adrenergic alpha-Agonists; D018685:Anesthetics, Inhalation; D000779:Anesthetics, Local; D008012:Lidocaine; D007530:Isoflurane; D003000:Clonidine