Effect of ulinastatin on the rocuronium-induced neuromuscular blockade

Abstract

Background: Ulinastatin is a glycoprotein derived from human urine and a serine protease inhibitor found in human urine and blood. Ulinastatin increases both liver blood flow and urine output. Rocuronium is eliminated mainly through the liver and partly through the kidney, hepatic elimination of rocuronium might be enhanced by ulinastatin. We examined the effect of ulinastatin on the neuromuscular block caused by rocuronium.

Methods: Forty four adult patients were randomly divided into two groups of 22 patients each, i.e. the study group and the control group. In the study group, a bolus dose of ulinastatin 5,000 U/kg was administered 2 min before the injection of rocuronium 0.6 mg/kg. In the control group, normal saline was administered instead of ulinastatin. For the monitoring of both onset and recovery from neuromuscular blockade, train-of-four (TOF) and post-tetanic count were used with TOF-Watch Sx. All patients underwent general anesthesia with total intravenous anesthesia (TIVA) of remifentanil and propofol, using the effect site target infusion system.

Results: In the study group, the onset of neuromuscular block was significantly slower than in the control group (P < 0.05). The recovery time from the rocuronium injection to the return of PTC was also significantly shorter in the study group than in the control group (P < 0.05). Similarly, times to the return of T1, T2, T3, and T4 (i.e. the first, second, third, and fourth response of TOF) were significantly shorter in the study group than in the control group (P < 0.05).

Conclusions: Ulinastatin significantly delays the onset of neuromuscular block and accelerates the recovery from the block caused by rocuronium.

Keywords: Neuromuscular junction; Rocuronium; Ulinastatin.