Role of XXXX in suppression of cardiovascular responses following endotracheal intubation.

@entity1 @entity101 @entity943 @entity551 @entity6305 @entity2899 @entity2900
The role of @entity2899 in blocking the @entity101 tachycardiac response following laryngoscopy and endotracheal intubation was evaluated in 45 female @entity1 aged 20-40 yr. The @entity1 belonging to grade I (of American Society of Anaesthesiologists) and undergoing elective surgical procedures under general anaesthesia were allocated in 3 equal groups. @entity1 in the 3 groups received 1.5 mg/kg @entity2900 , 0.6 mg/kg @entity2899 and 0.12 mg/kg @entity6305 , respectively for intubation. There were no @entity943 in any of the groups following endotracheal intubation. There was significant (P less than 0.01) fall in blood pressure following induction prior to intubation in all the three groups. Maximum fall was noted in group II (23.53 +/- 7.21 mmHg in mean arterial pressure). Following endotracheal intubation, blood pressure and heart rate increased significantly (P less than 0.01) in all 3 groups. Maximum increase was observed in group I (26.4 +/- 4.95 mmHg in mean arterial pressure and 19.07 +/- 6.54 beats/min in heart rate). Blood pressure and heart rate increases in groups II and III were comparable. Our findings indicate that @entity551 produced by @entity2899 through ganglion blockade is not effective in attenuating the cardiovascular responses following endotracheal intubation. It is also possible that increased cardiovascular response following endotracheal intubation may not be due to sympathetic ganglion stimulation.
