This Article  • References  • Full text PDF  • Send to a friend  • Save in My Folder  • Save to citation manager  • Permissions  Citing Articles  • Contact me when this article is cited  Related Content  • Similar articles in JAMA  Social Bookmarking   What's this?

Charles H. Williams, PhD
Texas Tech University Health Sciences Center El Paso

JAMA. 1986;255(24):3362-3363.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

To the Editor.—

A recent article in MEDICAL NEWS & PERSPECTIVES entitled "Malignant Hyperthermia: Nightmare for Anesthesiologists—and Patients"¹ presents a one-sided and inaccurate view of the basic fundamental genetic defect that causes malignant hyperthermia (MH).

My laboratory has been using a colony of MH-susceptible pigs as an animal model for MH studies for the past 16 years. Our most recent experimental data clearly demonstrate that a 100- to 300-fold increase of plasma norepinephrine (up to 108 ng/mL) precedes by five to ten minutes the development of the classic MH syndrome symptoms.² We have also published data showing that an intense peripheral vasoconstriction and severe hypertension are also part of the MH syndrome.^3-6 The vasoconstriction is so severe that heat loss via radiation from the skin is completely shut down. The severe hypertension (>400 mm Hg), intense peripheral vasoconstriction, and severe tachycardia (>180 beats per minute) that develop . . . [Full Text PDF of this Article]

CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter     What's this?