Myocardial [3H]polyinositol phosphates and their response to burn trauma

Polyinositol phosphates comprise a portion of the phosphatidyl signal transducing system. The most well known is IP3 which stimulates Ca2+ release from Ca2+ sequestering organelles within cells. In this study, polyinositol phosphate changes in the heart subjected to the systemic effects of burn trauma were examined. The hypothesis was that systemic trauma induced by large body surface area (% BSA) burn may perturb the phosphatidylinositol signal transducing system. At postburn day 21 left ventricular tissues were harvested from mice with varying burn sizes (i.e. 0, 20 and 50 per cent). Levels of the polyinositol phosphates were measured by incorporation of myo-[2-3H]inositol with separation of the phosphates by anion-exchange chromatography. Analysis of variance was used for statistical evaluation. Multivariate relationships between the independent polyinositol forms (inositol, Il,4P2 and I1P) existed for control (r2 = 0.71 and 50 per cent burn groups (r2 = 0.78). Numerous interdependent relationships existed within each of the multivariate tests. These analyses confirm that several independent polyinositol phosphates contribute to changes in the second messenger IP3 in ventricular tissue subjected to the systemic effects of burn trauma. Disruption of the polyinositol phosphates may underlie either the cause, or exacerbation, of heart dysfunction and cellular damage in burn patients.