title: Dysfunctional metabolism induced by the systemic effects of burn trauma: the role of rates of polyinositol and glycerophosphate formation in diaphragm.
abstract: Common complications among patients with burns are respiratory problems. Inspiration for breathing normally is facilitated by diaphragmatic contractility. However, in burn trauma numerous factors impose on skeletal muscle activity and chest wall function. These present limitations to surgical procedures requiring anesthesia. The hypothesis of this study was that the systemic effects of increasing burn size may result in metabolic changes in the polyinositol part of the phosphatidyl inositol signal transduction system in diaphragm. In this report, rate changes in polyinositol phosphates (i.e., inositol triphosphate (IP3), inositol 1,4 biphosphate (I1,4P2), inositol 1 phosphate (I1P), and inositol) that occurred in diaphragm subjected to the systemic effects of burn trauma were examined. Third-degree burn injury was applied by scalding predefined areas (i.e., 0%, 20%, and 50% body surface area) on the dorsal and ventral surfaces of mice. At postburn day 21 tissues were harvested and the levels of the polyinositol phosphates were measured by incorporation of myo-[2-3H]-inositol with separation of the phosphates by anion-exchange chromatography. All actual levels and rates of formation were analyzed with standard statistical tests and curve-fitting routines. Rate changes of the labelled [3H]-polyinositol phosphates were determined for the control, 20%, and 50% groups. These data show that rate changes occur in the polyinositol part of the phosphatidyl signal transduction system and are caused by the systemic effects of large percent body surface area burns. The changes that occur in the polyinositol phosphates provide insight into dysfunctional processes that can affect skeletal muscle physiology. The long-term goal of these studies is that they will lead to therapeutic advancements in the treatment of respiratory dysfunction in patients with burns.
authors.affiliation: Clinical Pharmacology Laboratory of the Anesthesia, Shriners Burns Institute, Boston.
authors.forename: J F
authors.initials: JF
authors.lastname: Tomera
authors.forename: K
authors.initials: K
authors.lastname: Lilford
authors.forename: S P
authors.initials: SP
authors.lastname: Kukulka
mesh_terms: D000818:Animals; D001830:Body Surface Area; D002056:Burns / Q000150:complications / Q000378:metabolism*; D003964:Diaphragm / Q000503:physiopathology; D005994:Glycerophosphates / Q000096:biosynthesis* / Q000502:physiology; D007294:Inositol / Q000096:biosynthesis; D007295:Inositol Phosphates / Q000096:biosynthesis* / Q000502:physiology; D008297:Male; D051379:Mice; D009132:Muscles / Q000378:metabolism*; D012120:Respiration Disorders / Q000209:etiology / Q000503:physiopathology; D015290:Second Messenger Systems / Q000502:physiology*; D015398:Signal Transduction / Q000502:physiology*
chemical_list: D005994:Glycerophosphates; D007295:Inositol Phosphates; D007294:Inositol