PubMed · 8753421
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S Shoji. 1995. [Creatine kinase (CK)].. https://pubmed.ncbi.nlm.nih.gov/8753421/
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The method of vectorisation and of summation of biochemical quantity vectors (SV), complemented by models, is suggested for description of data involving three or more quantities. By the SV method, the data of sample quantities are transformed into a vector which preserves sample quantity information. Examples are presented to demonstrate patient monitoring after acute myocardial infarction (AMI) by the SV method and by variously ordered sets of LD and CK patterns. Furthermore, compared with MM3/MM1 isoform ratios, the set of CK quantities (MM3, MM2, MM1) together with the basic model SV3 is able to monitor the processes of CK isoform changes and to indicate unusual quantity values compared with reference values. Similarly, the translation model SV3 with the set of MM3, MB2, MB1 quantities and dSV3 vectors, obtained by subtraction of the control vector from all resultant SV3 vectors, monitors individual deviations from the control values. In the case of inadequate SV ¿c¿ values, the SV3 translation model indicates a possibility of excess MM3 release from non-cardiac tissues. The SV method, with basic model SV5 and ordered set of LD quantities (1-5) enables AMI to be proved in the group of patients whose LD1/2 < 0.76 and activity of LD5 > 10%. In general, apart from isoenzyme data processing, the SV method can also be applied for processing other data object quantities.
BACKGROUND: The purpose of this study was to determine whether transient ischemic preconditioning protects human myocardium against normothermic ischemic injury. METHODS: Isolated human right atrial trabeculae were suspended in an organ bath with oxygenated Tyrode's solution at 37 degrees C and field stimulated at 1 Hz. Developed force was recorded. Trabeculae (Warm I/R) received normoxic perfusion before 45 minutes of normothermic simulated ischemia (hypoxic, substrate-free buffer with pacing at 3 Hz) and 120 minutes of reperfusion. Preconditioned trabeculae (Warm IPC) were subjected to 5 minutes of normothermic simulated ischemia and 10 minutes of perfusion before normothermic simulated ischemia-reperfusion injury. Trabeculae (Cold I/R) were subjected to hypothermic (4 degrees C) ischemia (hypoxic buffer) for 4 hours and 60 minutes of reperfusion (37 degrees C). Preconditioned trabeculae (Cold IPC) were pretreated with 5 minutes of normothermic simulated ischemia before hypothermic ischemia and 60 minutes of reperfusion. At the end of reperfusion, trabeculae were frozen at -70 degrees C and assayed for tissue creatine kinase activity. RESULTS: At the end of reperfusion, warm preconditioned trabeculae (Warm IPC) recovered 51% +/- 5% of baseline developed force, whereas warm I/R trabeculae recovered 24% +/- 3% (p < 0.05). Tissue creatine kinase levels reflecting preserved tissue viability were sustained in Warm IPC trabeculae (1,183 +/- 204 U/g), whereas nonpreconditioned control trabeculae (Warm I/R) exhibited lower levels of enzymatic activity (403 +/- 32 U/g) (p < 0.05). In contrast, Cold IPC trabeculae recovered 47% +/- 5% and Cold I/R, 56% +/- 8% of baseline developed force at the end of reperfusion (p > 0.05). CONCLUSIONS: We conclude that transient ischemic preconditioning protects human myocardium against normothermic ischemic injury.