A method based on the principle of thermodilution was developed for a quasi non-invasive permeability control of aortocoronary bypass. An epivascularly-attached thermistor records the cooling of the bypass wall when, following the intravenous injection of 5 to 10 ml of a NaCl solution at 4 degrees C, a bolus of cooled blood passes through the bypass. During cardiosurgical intervention, the thermistor is attached to the venous bridge by one or 2 sutures. The efferent cable goes through the thorax wall and is coupled to a subcutaneously implanted telemetric amplifier unit. The influence of the vessel wall on the perivascular temperature signal, as compared to the intravascular one, was studied in acute and chronic animal experiments. In acute experiments the perivascular peak of temperature was found to be lower than the intravascular one. Continuous measurements over 9 days showed variations in the perivascular signals which must have been due to changes in the thermal capacity of the tissue coupled to the thermistor as well as to changes in resistance caused by a variable extent of scarred area and by the varying water content of the wound bed. These variables will continue to keep rheothermia within the limitations of a method with primarily binary results (= bypass: open or closed). Given stable coupling conditions after full development of the scar around the thermistor, the signal falsification by the then constantly coupled tissue capacity becomes calculable such as to obtain semiquantitative results which, theoretically should vary predominantly with cardiac output.

To determine the cardio-protective effect of heavy water on the ischemic myocardium, a thoracotomy was performed on 18 mongrel dogs. The animals were connected to the extracorporeal circulation in a standardized experimental procedure. Following total cardiopulmonary bypass, 2,000 ml of a standard cardioplegic solution (LK 352) was infused at the aortic root of 10 dogs, which served as controls (group I), and the same solution containing 20% of 99.8% deuterium oxide was given at the aortic root of the remaining animals (group II). At the end of 60 minutes of ischemia, 1,000 ml of the solutions was again administered at the aortic root of the corresponding animals. Myocardial biopsies were taken from the apex of the left ventricle of each dog before cardiopulmonary bypass, immediately after the infusion of the cardioplegic solutions, following 90 minutes of ischemia, and after 30 minutes of reperfusion, and studied ultrastructurally. Whereas the ultrastructure of the myocardium of group I was well preserved at the end of the ischemic period, deuterium-oxide-treated hearts showed extensive focal and global myofilamentolysis and lysis of whole myocytes. Structural damage to glycogen, nuclear chromatin dispersal, severe intracellular edema and complete rupture of the intercalated discs were characteristic findings. At the end of ischemia, all the hearts of group I could be resuscitated. During the ischemia, all the hearts of group II developed into stone hearts. Biochemical studies on a second series showed a higher ATP depletion and a significantly higher lactate accumulation in group II than in group I.(ABSTRACT TRUNCATED AT 250 WORDS)