phosphocreatinine and Acute-Disease

In order to investigate the changes in phosphoglucose metabolism in acute experimental pancreatitis, the authors utilized the measuring cell NMR spectroscopy. The experimental pancreatitis had been evoked by both the method of ligature of lateral pancreas ducts and that of the duodenal blind loop. These methods evoke a morphological response, namely edematous and necrotizing pancreatitis. Gradual reduction of macroergic phosphate binds and augmentation of anorganic phosphates represent the principal change in NMR spectrum. The clinical picture provides evidence of the exhaustion of highly energetic phosphate compounds which are necessary for the maintenance of integrity of the pancreas tissue in acute experimental pancreatitis. The discussion includes the possibilities and limitations of the NMR spectroscopy.

Topics: Acute Disease; Adenosine Triphosphate; Animals; Female; Magnetic Resonance Spectroscopy; Male; Pancreas; Pancreatitis; Phosphocreatine; Rats; Rats, Wistar

The effect of phosphocreatine and phosphocreatinine disodium salts on excitation conduction in acute myocardial ischemia was investigated, using repeated short-term ischemia exposures of the isolated rabbit ventricular septum as a model. Considerable improvement of excitation conduction through ischemized myocardium, seen after the administration of phosphocreatine and phosphocreatinine salts, was shown to be associated with Na+ added to the perfusion medium. Phosphocreatine and phosphocreatinine effects on excitation conduction time and the septal force in control perfusion were related to both the addition of Na+ and the binding of Ca2+ by these agents in the perfusion medium.

Topics: Acute Disease; Animals; Arrhythmias, Cardiac; Calcium; Coronary Disease; Culture Media; Electric Stimulation; Heart Conduction System; In Vitro Techniques; Male; Phosphocreatine; Rabbits; Sodium

Using isotope-labeled microspheres (diameter 15 microns) it was shown that phosphocreatine at a dose of 300 mg/kg does not affect the myocardial blood flow in the ischemic zone during acute occlusion (5 min) of the left anterior descending coronary artery (LAD) in dogs. Intravenous administration of NaCl hypertonic solution which contained the same amount of Na+ as 300 mg/kg of phosphocreatinine disodium salt prevented the development of ventricular fibrillation during acute LAD occlusion in dogs. Under these conditions excitation conduction velocity significantly increased. Experiments in isolated intraventricular rabbit septum have showed that the addition of phosphocreatine or phosphocreatinine to the perfusion medium at a concentration of 10 mmole/liter increased excitation conduction velocity in ischemic myocardium. However, when changes in perfusate Na+ and Ca2+ concentration produced by addition of phosphocreatine or phosphocreatinine were compensated, these compounds do not affect excitation conduction velocity. On the other hand, the alterations similar to those produced by the addition of phosphocreatine or phosphocreatinine led to the same increase of excitation conduction velocity. The results obtained indicate an important role of the changes of blood plasma ionic composition on intravenous administration of phosphocreatine in electrophysiological and antiarrhythmic effects of this substance during acute myocardial ischemia.

Topics: Acute Disease; Animals; Blood Pressure; Calcium; Coronary Circulation; Coronary Disease; Coronary Vessels; Dogs; Heart; Heart Rate; In Vitro Techniques; Myocardial Contraction; Phosphocreatine; Reference Values; Sodium

The association between phosphocreatine's antifibrillatory action and its effect on the excitement propagation processes in the ischemic area was investigated under acute coronary arterial occlusion in dogs. Ischemia considerably reduced the amplitude, and increased the duration and time of onset, in local electrograms, and provoked cardiac fibrillation at the time of occlusion or during the recovery of coronary flow. A single intravenous injection of 300 mg/kg phosphocreatine eliminated cardiac fibrillation and largely prevented electrographic changes in the ischemized area. Phosphocreatinine, phosphocreatine's structural analogue, produced a similar effect. It is suggested that antiarrhythmic action of phosphocreatine and phosphocreatinine is mediated by their membrane effects.

Topics: Acute Disease; Animals; Anti-Arrhythmia Agents; Coronary Disease; Dogs; Drug Evaluation, Preclinical; Heart Conduction System; Kinetics; Phosphocreatine; Ventricular Fibrillation

We analyzed brain tissue for adenosine and its metabolites, inosine and hypoxanthine, in rats during acute (30 s) hypoxia and during sustained (5 min) hypoxia and hypocarbia. Within 30 s of the onset of hypoxia, adenosine levels were increased from 0.34 +/- 0.08 (SE) to 1.65 +/- 0.33 nmol/g (P less than 0.005), paralleling temporally the changes in cerebral blood flow. During sustained hypoxia and hypocarbia, brain tissue was sampled by a fast (freeze-blow) or slow (in situ) freezing method. With the freeze-blow technique, adenosine concentrations remained stable between arterial partial pressure of O2 (PaO2) greater than 200 and 100 mmHg, doubled at PaO2 = 50 mmHg, and increased sevenfold (P less than 0.005) when PaO2 reached 30 mmHg. No increases in adenosine or its metabolites were noted with the in situ technique. During hypocarbia (arterial CO2 partial pressure less than 20 mmHg), adenosine concentrations increased with both sampling techniques. Freezing times in brain were measured during in situ freezing and were increased during hypoxia and decreased during hypocarbia. In conclusion, 1) adenosine concentrations in brain are increased during hypoxia, and 2) the in situ technique in rat does not appear to be optimal for sampling brain tissue for subsequent measurement of adenosine under conditions where cerebral blood flow is increased.

Topics: Acute Disease; Adenine Nucleotides; Adenosine; Animals; Arteries; Blood; Brain Chemistry; Carbon Dioxide; Freezing; Hypoxia, Brain; Lactates; Lactic Acid; Oxygen; Partial Pressure; Phosphocreatine; Rats; Time Factors