Affiliations: Department of Cardiac Surgery, University of Technology, Dresden, Germany | Center for Biomaterial Development and Berlin-Brandenburg Center for Regenerative Therapies, Institute of Polymer Research, Helmholtz-Zentrum Geesthacht, Teltow, Germany | Center for Medical Basic Research, Martin-Luther-University Halle-Wittenberg, Halle (Saale), Germany
Note: [] Corresponding author: Prof. Dr. F. Jung, Center for Biomaterial Development and Berlin-Brandenburg Center for Regenerative Therapies, Institute of Polymer Research, Helmholtz-Zentrum Geesthacht, Kantstrasse 55, 14513 Teltow, Germany. Tel.: +49 3328 352269; Fax: +49 3328 352452; E-mail: friedrich.jung@hzg.de
Abstract: During extracorporeal circulation (ECC) controlled hypothermia is a common method of myocardial protection due to a reduction of the myocardial oxygen consumption. Although the beneficial aspects of hypothermia on the myocardial metabolism have been widely demonstrated the effect of hypothermia on the myocardial oxygen tension (PmyO2) is unclear. For this reason the PmyO2 of German Landrace pigs (male, three months of age) during ECC was analysed under mild hypothermia (32°C, n = 6 pigs) and under normothermia (n = 10 pigs, control group) within a time period of 23 min (1400 sec). Flexible invasive Clark type microcatheters were used to measure the PmyO2 in the beating heart. During normothermal ECC a continuous PmyO2 increase from 36.5 ± 15.8 mmHg to 52.6 ± 27.2 mmHg (+44.1%) after 1400 sec was measured (p = 0.02). In contrast, mild hypothermia caused a continuous PmyO2 decrease from initially 46.9 ± 17.5 mmHg to 36.7 ± 20.8 mmHg (−21.8%, p < 0.013) in the test period. Electrocardiography revealed no signs of ischemia or arrhythmia during normo- and hypothermic ECC. It seems obvious that mild hypothermia results in a reduction of the oxygen transfer to the myocardial cells and that this effect outweighs the beneficial effects of hypothermia in the myocardium which are related to reduced oxygen consumption. However, in mild hypothermia oxygen supply to the myocardium remained sufficient for normal myocardial function.
