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Introduction It is known that in patients with ischaemic vascular diseases col- Abstract The development of a collateral circulation (arteriogenesis), bypassing an arterial occlusion, is important for tissue survival, but it remains functionally defective. Micro array data of growing collateral vessels, exposed to chronically elevated fluid shear stress (FSS), showed increased transcription of the transient receptor potential cation channel, subfamily V, member 4 (Trpv4). Thus, the aim of this study was to investigate the role of the shear stress sensitive Trpv4 in transmitting this physical stimulus into an active growth response. qRT-PCR at different time points during the growth of collateral vessels after femoral artery ligature (FAL) in rats showed a strong positive correlation of Trpv4 transcription and the intensity of FSS. An increased protein expression of Trpv4 was localized in the FSS-sensing endothelium by means of confocal immunohistochemistry. Cultured porcine endothelial cells showed a dose-dependent expression of Trpv4 and an increased level of

Cellular degeneration rather than adaptation is present in hibernating myocardium. The consequence is progressive diminution of the chance for complete structural and functional recovery after restoration of blood flow. The practical consequence from this study should be early revascularization in patients showing areas of hibernating myocardium.

Myocytes can die by necrosis or by apoptosis and the characteristics of both kinds of cell death are so typical that a differentiation can be made by histological and molecular-biological methods using electron microscopy, dUTP labeling with fluorescence or peroxidase staining (TUNEL) and the DNA laddering method. However, the problem of quantification of apoptotic cells has not been completely solved because of lack of standardization as well as uncritical use and interpretation of the TUNEL method. Equally, quantification of apoptotic cells is not optimal until now because of three reasons: methodological (overinterpretation of results, no differentiation between myocytes and non-myocytes), experimental (global or regional acute ischemia, chronic conditions such as heart failure or hibernating myocardium), and interpretation (unknown time period for the completion of apoptosis). This problem is reflected in the large differences in incidence of apoptosis reported. Our own data show that in dog myocardium made globally ischemic for 90 min, 8% of the myocytes showed a positive staining for apoptosis (TUNEL method) after 6 h of reperfusion. Despite these results the question of reperfusion injury and the influence of apoptosis still remains open, because it can not be excluded until now that the apoptotic process is initiated during the ischemic period. Studies in hibernating myocardium and chronic heart failure show a similar situation, because of a wide variation of numbers of apoptotic cells and the limited possibility to investigate human tissue. There is no doubt that apoptosis plays an important role in chronic pathophysiological situations such as heart failure and hibernating myocardium but the importance of apoptosis in the acute situation of ischemia/reperfusion still has to be clarified.