CJA
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

This Article
Right arrow Full Text (PDF)
Right arrow Submit a scholarly reply
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Nishina, K.
Right arrow Articles by Obara, H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Nishina, K.
Right arrow Articles by Obara, H.

Canadian Journal of Anesthesia, Vol 43, 678-683, Copyright © 1996 by Canadian Anesthesiologists' Society


ARTICLES

Prostaglandin E1 attenuates the hypertensive response to tracheal extubation

K Nishina, K Mikawa, M Shiga, N Maekawa and H Obara
Department of Anaesthesiology, Kobe University School of Medicine, Japan.

PURPOSE: Tracheal extubation causes hypertension and tachycardia, which may cause imbalance between myocardial oxygen demand and supply in patients at risk of coronary artery disease. We conducted a randomized, controlled study to evaluate the effects of 0.05 or 0.1 microgram.kg-1.min-1 prostaglandin E1 (PGE1) iv on haemodynamic variables occurring during tracheal extubation and emergence from anaesthesia and compared them in patients receiving either lidocaine or saline. METHODS: Eighty ASA physical status 1 patients undergoing elective surgery were enrolled in the current study. Anaesthesia was maintained with sevoflurane 1.0%-2.5% (ET concentration) and nitrous oxide 60% in oxygen. Muscle relaxation was achieved with vecuronium. The patients were randomly assigned to receive one of four treatments (n = 20 each): saline (control), 0.05 microgram.kg-1.min-1 PGE1, 0.1 microgram.kg-1.min-1 PGE1, or 1 mg.kg-1 lidocaine. PGE1 was infused from completion of surgery until five minutes after tracheal extubation. Changes in heart rate (HR) and blood pressure (BP) were measured during and after tracheal extubation. RESULTS: In the control group, the HR, systolic BP, and diastolic BP increased during tracheal extubation. Administration of 0.1 microgram.kg-1.min-1 PGE1 and 1 mg.kg-1 lidocaine attenuated the increases in BP although 0.05 microgram.kg-1.min-1 PGE1 failed to do so. The inhibitory effect of the 0.1 microgram.kg-1.min-1 PGE1 on BP was similar to that of lidocaine 1 mg.kg-1 iv. The increase in HR was attenuated by lidocaine but not by PGE1. CONCLUSION: The intravenous infusion of 0.1 microgram.kg-1.min-1 PGE1 given during emergence from anaesthesia and tracheal extubation is a useful method for attenuating the hypertension associated with noxious stimuli during this period.





HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1996 by the Canadian Anesthesiologists' Society.