To observe the effects of urapidil on the cardiovascular responses to tracheal intubation, forty-six patients (ASA Ⅰ - Ⅱ) were randomly divided into group A (n=23) and group B(n=23). Anesthesia was induced with valium 0.2mg/kg, 2.5% thiopental sodium 5mg/kg and tracheal intubation was facilitated with succinylcholine 1.5mg/kg. Urapidil 0.5mg/kg was intravenously given immediately after administration of succinylcholine in group A. After intubation. SP, DP,MAP,HR and RPP increased by 6%,12%, 15%, 24% and 28% in group A and increased by 30%,37%,33%,48% and 95% in group B respectively. Compared correspondingly with those in group B, the values of the parameters mentioned above decreased significantly in 5 minutes after intuhation in group A(P

Objective: To study pharmacokinetics of lidocaine during superior laryngeal nerve block (SLNB) combined with topical anesthesia to endotracheal mucosa by thyrocricocentesis(TCC). Method: Eight patients (ASA Ⅰ-Ⅱ grade)scheduled for general anesthesia and operation were performed bilateral SLNB with 2% lidocaine 2mg/kg and TCC with 5 % lidocaine 2mg/kg within 1 min,The internal jugular venous blood samples were taken at 1,5,10,20,30, 60,120 and 180 minutes after lidocaine administrations to determine lidocaine serum concentrations using a fluoresence polarization immunoassy. Pharmacokinetics were calculated with a procedure (3p87) by computer. Result: The pharmacokinetics could be described as two-compartment model. Absorption rates of lidocaine were fast,values of t_(1/2) Ka and Tpeak were 5.0?2.5 min and 7.5?2.1 min respectively。Maximal concentrations (Cmax) of lidocaine were 3.8?0. 6?g/ml, which were within safety ranges. Conclusion: It may be safe that 2% lidccaine 2mg/kg superior laryngeal nerve block is combined with 5% lidocaine 2mg/kg topical anesthesia to endotracheal mucosa by thyrocricocentesis.

The concept of the Bezold-Jarisch reflex(BJR)has experienced more than 100 years,which is that the left ventricular unmyelinated vagus nerve input receptors are stimulated by drugs or me-chanical pull,the stimulation was then integrated by the vagus nerve afferent brain stem nucleus and trans-mitted to the vascular movement center to form vagal nerve output enhancement,leading to severe bradycar-dia,peripheral vasodatation,hypotension and even cardiac arrest,e.g,a cardiovascular inhibitory reaction.Although BJR is applied in clinical anesthesia,insufficient attention has been paid to it,resulting in absence of the mechanism analysis of related sudden severe bradycardia,hypotension,and even cardiac ar-rest in perioperative period.