It has been presumed that alteration in the concentrations of second messengers leads to alterations in the function of the ryanodine receptor. Consequently, we have determined the basal content of cyclic AMP and inositol phosphates in skeletal and cardiac muscle of malignant hyperthermia (MH) susceptible (MHS) and healthy normal control (MHN) swine. Since alpha 1- and beta-adrenoceptors are linked to these second messenger systems, the densities of alpha 1- and beta-adrenoceptors were also determined. In skeletal as well as cardiac muscle, a higher basal concentration of almost all of the inositol phosphates was found. Of all inositol phosphates measured, the presumed second messenger inositol 1,4,5-trisphosphate (1,4,5-IP3) was mostly concentrated in both tissues. Each MHS sample contained more 1,4,5-IP3 than the highest value observed in MHN muscle, indicating that a threshold of 1,4,5-IP3 concentration for determination of MHS or MHN status can be defined. In addition, MHS skeletal muscle contained more cAMP than MHN, whereas there was no difference between MHS and MHN in cardiac muscle. The changes observed in the different inositol phosphate and cAMP contents were not accompanied by an altered alpha 1- or beta-adrenoceptor density in skeletal or cardiac muscle between MHS and MHN. However, the total number of beta-adrenoceptors of MHN and MHS was significantly higher in cardiac (about 80 fmol/mg protein) than skeletal muscles (about 30 fmol/mg protein). The cardiac muscles revealed about 80% beta 1- and beta 2- and 20% beta 2-adrenoceptors, whereas skeletal muscles were characterized by over 95% beta 2-adrenoceptors.(ABSTRACT TRUNCATED AT 250 WORDS)
Bei 9 Patienten mit posttraumatischer Katabolie wurde ein Abfall des Linolsäuregehaltes im Serum innerhalb von 7 Tagen bis um 80% des Ausgangswertes gemessen. Die höchste Abfallrate fand sich zwischen dem ersten und fünften Tag. Analoges Verhalten ergab sich für das Stoffwechselfolgeprodukt der Linolsäure, die Arachi-donsäure. Als weiterer Ausdruck der Fettstoffwechselentgleisung muβ das Auftreten einer anomalen Eikosatriensäure gewertet werden. Der Linolsäuremangel im Postaggressionsstoffwechsel ist durch han-delsübliche Fettemulsionen oder gezielter durch Konzentrate essenti-eller Fettsäuren zu beheben.
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