Effects of Dexamethasone on Neuromuscular Transmission in a Phrenic Nerve-Hemidiaphragm Preparation in the Rat.
10.4097/kjae.2003.44.3.377
- Author:
Bon Nyeo KOO
1
;
Yong Taek NAM
;
Yang Sik SHIN
;
Jeong Mi HAN
;
Jeong Seok LEE
;
Sung Yell KIM
Author Information
1. Department of Anesthesiology and Pain Medicine, Yonsei University College of Medicine, Seoul, Korea. ytnam@yumc.yonsei.ac.kr
- Publication Type:Original Article
- Keywords:
Dexamethasone;
dose-response curve;
phrenic nerve-hemidiaphragm Preparation;
vecuronium
- MeSH:
Adenosine Triphosphatases;
Animals;
Atrophy;
Dexamethasone*;
Diaphragm;
Humans;
Muscles;
Muscular Atrophy;
Neuromuscular Blocking Agents;
Neuromuscular Junction;
Quadriplegia;
Rats*;
Rats, Sprague-Dawley;
Status Asthmaticus;
Vecuronium Bromide
- From:Korean Journal of Anesthesiology
2003;44(3):377-385
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: MacFarlane and Rosenthal reported a case of acute quadriplegia after nondepolarizing muscular blocking agents in status asthmaticus patient treated with high doses of corticosteroid. Reports regarding the reactions of glucocorticoid treated muscles to neuromuscular blocking agents are sparse and inconsistent. The aims of this study were to examine the degree of muscle atrophy and its effects on sensitivity to neuromuscular blocking agents in relation to the dose and duration of dexamethasone. METHODS: Sixty Sprague-Dawley rats were divided into six groups. They were treated daily with dexamethasone 0.4 mg/kg and 4 mg/kg daily for 1 week or 3 weeks. The two control groups were treated with normal saline. The day after treatment, the dose-response curves of vecuronium were measured using a phrenic nerve-hemidiaphragm preparation. To classify muscle fiber, the diaphragm was stained for myofibrillar adenosine triphosphatase after alkaline and acid preincubation, and a morphometric examination was carried out. RESULTS: The diaphragmatic muscle in rats treated with long term, high dose dexamethasone showed significant atrophy. For the short term, low dose dexamethasone group, the ED50 and ED95 of vecuronium decreased 41.5% and 26.8% compared to those of the control group, respectively (P<0.05). However, the ED50 of vecuronium in the long term, high dose dexamethasone group increased 22.2% compared to that of the control group (P<0.05). CONCLUSION: This study suggests that sensitiviy to vecuronium was not modulated by dexamethasone-induced muscle atrophy. Quantitative changes of receptors at the neuromuscular junction or some anoother process might be responsible for this change.
