T. Ide et al., The effect of epidural anesthesia on respiratory distress induced by airway occlusion in isoflurane-anesthetized cats, ANESTH ANAL, 92(3), 2001, pp. 749-754
Citations number
22
Categorie Soggetti
Aneshtesia & Intensive Care","Medical Research Diagnosis & Treatment
The role of afferent information from the chest wall in the genesis of dysp
nea is not fully elucidated. We have developed an animal model for the stud
y of airway occlusion (AO) and proposed new concepts of minimum alveolar an
esthetic concentration for AO (MACAOR) and the duration from the start of A
O to the onset of the positive motor response (DOCCL) to evaluate respirato
ry distress quantitatively. We examined the effects of thoracic epidural an
esthesia 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. A
nimals 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 sa
line infusion. The IM Group (n = 6) received epidural saline (0.4 mL/kg), I
M 1% lidocaine (1 mL/kg), and saline infusion. The PHE Group (n = 6) receiv
ed epidural 1% lidocaine (0.4 mL/ kg) and IV phenylephrine (0.5-1 mug . kg(
-1) . min(-1)) to maintain a stable arterial blood pressure. DOCCL and MACA
OR were measured in each animal at 15 min after the administration of drugs
. Plasma lidocaine concentrations were measured before and after epidural o
r IM injection. DOCCL was significantly longer after epidural injection in
all groups than before the injection. Although there was no significant dif
ference in the values of MACAOR between before and after the epidural injec
tion in the EPD Group, the IM administration of lidocaine in the IM Group s
ignificantly reduced MACAOR. Plasma concentrations of lidocaine were simila
r in all groups at all measurement points. Our data indicate that thoracic
epidural anesthesia using 1% lidocaine significantly reduced respiratory di
stress induced by AO. This effect is most likely caused by a systemic effec
t of lidocaine rather than by reduced afferent information from the chest w
all.