In parallel to the energetics, cardiac pump function can be determined via a balloon introduced into the left ventricle and attached to a pressure transducer. A characteristic pressure registration obtained with this setup is illustrated in the upper part of the ³¹P NMR spectrum. The zoomed area shows clearly the periodical pressure alterations during the heart action. The minima of the trace reflect the end-diastolic and the maxima the end-systolic pressure, respectively – the difference [maximum - minimum] yields the developed pressure of the heart. The distance between the minima or maxima can be used to calculate the heart rate, which is found to be tenfold higher in the mouse (~600 beats per minute) than in man.

In parallel to the exhaustion of cardiac energy stores left ventricular pressure development dwindles and thereby also the pump function of the heart (figure at the right). Very quickly contractile function completely grinds to a halt, and a bit later the so-called contracture develops (pressure increase during ischemia), which is attributed to the inundation of the cytosol by Ca²⁺ ions. The latter is caused by breakdown of the membranous ion gradients and failure of ATP-driven ion pumps, respectvely, as a consequence of the impaired energy state.

To what extent the original heart function can be recovered depends from the duration of ischemia and the applied "therapy" in terms of additionally infused drugs or the transgenic model used. For example, we could show that hearts without endothelial nitric monoxid synthase (eNOS knockout mice) recover better from an ischemic period than the corresponding control hearts, whereas on the other hand the lack of myoglobin has an adverse effect (compare also the original publications given below). Thus, by an appropriate combination of transgenic animal model and pharmacologic intervention experimental series can be carried out, that may give a clue for a more effient therapy of heart attack in man.

Compared with the approach described in the first chapter, where ³¹P NMR spectra were simply acquired over the full sensitive volume, the main difficulty herein consists in ensuring an exact localization of the spectra within the heart and avoiding contaminations of signals from adjacent tissue. For this, the thorax of the mouse is "covered" with a spectroscopic grid, which exactly correlates with the anatomical ¹H MR image. The figure at the left exemplary illustrates the superimposing of such a 2D ³¹P CSI dataset (Chemical Shift Imaging → theory) and the corresponding proton image. Despite the low resolution of the image it can be clearly recognized that only there, where tissue is present, ³¹P signals are detected. Strong signals are especially found in the skeletal muscle of the animals back (in the upper part of the figure) and the area of the heart.

By the combined use of ¹H MRI and ³¹P CSI a rather complete picture about heart function and energetics of genetic modified mouse strains generated as models for the exploration of the underlying causes of human cardiomyopathies can be obtained. Due to the noninvasive nature of these investigations, it will be possible via repetitive measurements to monitor the progession of the induced heart diseases and to assess the success of suitable therapies.