| Item type: | Article | ||||
|---|---|---|---|---|---|
| Journal or Publication Title: | Anesthesia & Analgesia | ||||
| Publisher: | LIPPINCOTT WILLIAMS & WILKINS | ||||
| Place of Publication: | PHILADELPHIA | ||||
| Volume: | 112 | ||||
| Number of Issue or Book Chapter: | 5 | ||||
| Page Range: | pp. 1174-1178 | ||||
| Date: | 2011 | ||||
| Institutions: | Medicine > Lehrstuhl für Anästhesiologie | ||||
| Identification Number: |
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| Keywords: | INDUCED CA2+ RELEASE; SKELETAL-MUSCLE; SARCOPLASMIC-RETICULUM; SUSCEPTIBLE SWINE; MG2+ DEPENDENCE; HALOTHANE; DANTROLENE; INVIVO; ATP; | ||||
| Dewey Decimal Classification: | 600 Technology > 610 Medical sciences Medicine | ||||
| Status: | Published | ||||
| Refereed: | Yes, this version has been refereed | ||||
| Created at the University of Regensburg: | Yes | ||||
| Item ID: | 64991 |
Web of ScienceAbstract
BACKGROUND: Malignant hyperthermia (MH) is a potentially lethal hypermetabolic syndrome. Volatile anesthetics and/or succinylcholine lead to an increase of the intracellular calcium concentration resulting in activation of various intracellular processes. A production of carbon dioxide, and later lactate, are early signs of increased cellular energy consumption. On a cellular level, magnesium ...
Abstract
BACKGROUND: Malignant hyperthermia (MH) is a potentially lethal hypermetabolic syndrome. Volatile anesthetics and/or succinylcholine lead to an increase of the intracellular calcium concentration resulting in activation of various intracellular processes. A production of carbon dioxide, and later lactate, are early signs of increased cellular energy consumption. On a cellular level, magnesium acts as a physiological calcium inhibitor resulting in less-intense calcium liberation from the sarcoplasmic reticulum. In this study, we examined the effects of IV magnesium administration on the clinical course of an MH crisis. METHODS: Sixteen Pietrain pigs (10 MH-susceptible [MHS] and 6 MH-nonsusceptible [MHN]) were anesthetized without an MH trigger substance. Invasive hemodynamic monitoring was established before 4 mg/kg succinylcholine was administered. Four of the MHS pigs received 10 mg/kg magnesium sulfate 10 minutes later. Hemodynamic changes (heart rate, mean arterial blood pressure, and oxygen saturation as measured by pulse oximetry) were continuously monitored. Venous and arterial blood gases (pH, PCO2, PO2, base excess, and lactate) were taken at 15-minute intervals. The H test and U test were used with P < 0.05 for significant differences among the groups. RESULTS: No differences among the groups were seen for weight, hemodynamic, and metabolic variables before administration of succinylcholine. In all MHS animals, succinylcholine led to a marked decrease of mean arterial blood pressure and increase of heart rate. Animals in both MHS groups developed combined metabolic and respiratory acidosis. Succinylcholine had no effect on animals in the MHN group. Hemodynamic and metabolic values were not different between the 2 MHS groups but were between groups MHS and MHN. CONCLUSION: Succinylcholine led to a hemodynamic and metabolic reaction in only MHS pigs. Treatment with magnesium did not influence the clinical course. The intervention had no beneficial effect in the acute phase of an MH crisis. (Anesth Analg 2011; 112: 1174-8)
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