ELEVATED PLASMA ALPHA(1)-ACID GLYCOPROTEIN LEVELS - LACK OF CONNECTION TO RESISTANCE TO VECURONIUM BLOCKADE INDUCED BY ANTICONVULSANT THERAPY

This study was designed to investigate the relationships among anticon vulsant therapy, plasma alpha(1)-acid glycoprotein (AAG) levels, and r esistance to vecuronium blockade. Thirty-one patients scheduled for ro utine neurosurgery were included in the study. The patients were treat ed (TG; n = 20) with phenytoin (n = 15) and/or carbamazepine (n = 4) a nd/or phenobarbital(n = 3) for greater than or equal to 6 days or were left untreated (UG; n = 11, control group). TG patients were further assigned to one of two subgroups according to the plasma anticonvulsan t level measured the day before surgery and found to be within (TG(W), n = 10) or below (TG(B), n = 10) the therapeutic range. Finally, the 31 patients were divided into two more groups according to their plasm a AAG levels: higher than (HAAG, n = 17) or within (NAAG, n = 14) the normal range (25-94 mg dl(-1)). Anesthesia was induced and maintained with propofol and sufentanil. Muscle relaxation was obtained with vecu ronium 0.1 mg kg(-1). A train-of-four (TOF) stimulation mode at 2 Hz w as applied to the ulnar nerve every 15 s, and neuromuscular transmissi on was assessed using a TOF-Guard accelograph monitor. Plasma AAG conc entrations (means +/- SEM) were 103.7 +/- 7.6 mg dl(-1) in TG, 80.7 +/ - 6.7 mg dl(-1) in UG, 95.9 +/- 13.2 mg dl(-1) in TG(W), 111.6 +/- 7.6 mg dl(-1) in TG(B), 114.9 +/- 7.4 mg dl(-1) in HAAG, and 71.4 +/- 3.8 mg dl(-1) in NAAG groups. The differences in plasma AAG concentration s between UG and TG and between HAAG and NAAG groups were statisticall y significant. No significant relationship was found between plasma AA G levels and phenytoin concentrations (r = -0.26). The time (mean +/- SEM) to recovery of T1 to 25% of control was significantly shorter in TG (28.2 +/- 1.4 min) than in UG (42.2 +/- 3.1 min) but did not differ significantly according to the plasma anticonvulsant level (27.3 +/- 2.0 min in TG(W); 29.1 +/- 1.9 min in TG(B)) and the plasma AAG level 31.7 +/- 1.9 min in HAAG; 35.3 +/- 3.3 min in NAAG). The time for the TOF ratio to recover to 25% yielded similar profiles and statistical s ignificance levels: TG, 32.9 +/- 2.2 min; UG, 51.2 +/- 4.0 min; TG(W), 35.0 +/- 3.9 min; TG(B), 30.7 +/- 1.8 min; HAAG, 38.1 +/- 3.1 min; NA AG, 42.0 +/- 4.1 min. We conclude that anticonvulsant therapy induces an increase in plasma AAG independently of the plasma anticonvulsant l evel. However, duration and recovery of vecuronium blockade do not dif fer according to plasma AAG levels. Consequently, elevated AAG does no t contribute to the resistance to vecuronium blockade induced by antic onvulsants.