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V Döring

Publications and source records attributed to V Döring.

41 records · Page 3Linked to original sources
PubMedDate not supplied

Metabolism and fine structure of the Mg++-procaine-arrested perfused heart.

Arrested rabbit hearts were perfused in normothermia for up to two hours by a cardioplegic erythrocyte-containing solution having an increased Mg++-, procaine-, and a reduced NaCl-content. After this time, hearts did not reveal any sign of anoxic or toxic damage in their metabolic pattern, in their ultrastructural picture, and in their functional capacity after reanimation. Despite a small loss in adenine nucleotide content, the ATP/ADP ratio and the PC content were raised. The contents of glycogen and glycolytic intermediates were normal or slightly reduced. After two hours of perfusion mitochondria showed no swelling, their membrane structure was unaltered. The myofibrils were well aggregated. The number of glycogen granules was increased. Hearts were reanimated after two hours of cardioplegia and could be loaded by pressure and volume.

Adenosine Diphosphate↗
PubMedDate not supplied

Metabolism and structure of the magnesium aspartate-procaine-arrested ischaemic heart of rabbit and man.

The fine structure and the content in energy-rich phosphate compounds, glycogen, and metabolites of the Embden-Meyerhoff-pathway in rabbits hearts or human papillary muscles arrested by magnesium aspartate-procaine are investigated in normothermia and mild or deep hypothermia. In all experimental conditions the break-down of adenine nucleotides and glycogen was distinctly retarded in cardioplegia compared to ischaemic arrest. While e.g. an ATP-content of 3.6 mumole/g wet weight was found after 40 min. at 32 degrees C in the magnesium asparate-procaine arrested heart, it dropped down to 1.3 mumole/g in the ischaemically arrested heart. In cardioplegia after 60 min at 15 degrees C the in vivo contents of ATP and glycogen were determined. The rate in metabolic changes in the magnesium aspartate-procaine arrested human papillary muscle was in the range of that recorded in the arrested rabbit heart. The ultrastructural appearance of the cardioplegically arrested heart did not differ from that of the controls after 20 min at 32 degrees C or 120 min at 15 degrees C. In hearts arrested by cardioplegia 40 min at 32 degrees C first signs of ischaemic lesions e.g. mild swelling of mitochondria and few rarefications in mitochondrial matrix were observed. Because of the significantly improved preservation of the fine structure of the heart and retardation of ischaemically provoked changes in cardiac metabolism, the method of inducing heart arrest by cardioplegia should also clinically be given preference to methods of arresting the heart by ischaemia.

Adenosine Triphosphate↗
PubMedDate not supplied

Induced ischemic cardiac arrest. Clinical and experimental results with magnesium-aspartate-procaine solution (Cardioplegin).

The risk of open heart surgery can be lowered by combination of different methods of myocardial protection. 1. Cardioplegia with a potassium free Mg-1-aspartate and Procaine-solution (Cardioplegin). 2. Coronary perfusion after ischemia longer than 35-40 minutes in case of excessive left ventricular hypertrophy or failure. 3. Hypothermia. Surface cooling gives an additional safety if coronary perfusion is not ideal possible in case of multiple coronary stenoses. For patients with this dispositions a continuous coronary perfusion with cardioplegic solution might be advisable, as it was presented by Gercken in his paper. This method was used three times already in human, but is still in an experimental stage.

Animals↗