Histological and SEM Assessment of Blood Stasis in Kidney Blood Vessels after Repeated Intra-Arterial Application of Radiographic Contrast Media

Background: After application of iodinated contrast media (CM), a pronounced deterioration of the microcirculation in skin and myocardium was reported. Clinically, the repeated application of CM, especially, led to an increase of the renal resistance index (RRI). With respect to the transiency of the RRI increase, it is reasonable to assume that the deterioration of blood flow could be due to transient blood stasis caused by reversible morphologic cell alterations due to osmotic discrepancies between CM and human blood. Therefore, the hypothesis was investigated whether CM are able to induce in vivo such blood stasis and cell deformations in the renal vasculature of well-hydrated pigs. Methods: The in vivo study was performed as a prospective randomized examination to compare the effects of two different CM in 16 pigs (German Landrace). Pigs were randomized to receive either Iodixanol (n= 8), or Iopromide (n= 8). Each animal received 10 injections separated by 5-min intervals via the suprarenal aorta at a rate of 10 mL/s according to the usual procedure during a cardiac catheter examination. Finally, the kidneys were explanted and processed for histology (H & E staining and fibrin staining according to Weigert) as well as for scanning electron microscopy (SEM) with regards to morphologic correlates explaining the changes in the microcirculation. Results: In each of the predefined four categories of vascular diameters, blood stasis were found, but clearly more often after application of Iopromide than after application of Iodixanol (p< 0.001). In addition, Iopromide induced more blood stasis in all of the examined kidney regions compared to Iodixanol (p= 0.0001). There were no obstructive events in the middle cortex following the application of Iodixanol. Except for the region around a puncture channel of a placed-in catheter probe, no fibrin was detected in Weigert's fibrin-stained samples, neither around the histologically assessed thrombi nor in vessels with blood stasis. Complementary SEM analyses revealed in a few cases only a slight generation of fibrin and thrombi and deformations, such as echinocyte and "box-like" deformations. Conclusions: According to previous in vitro studies, pathological erythrocyte deformations, such as echinocyte and box-like formation of erythrocytes, were observed also in vivo. In addition, blood stasis and/or thrombi could be detected in histological samples from explanted kidneys from young pigs after repeated in vivo administration of CM. In only a few cases, mural platelet aggregates within minimal fibrin meshes occurred only after the application of Iopromide

The great Sumatra-Andaman earthquakes : imaging the boundary between the ruptures of the great 2004 and 2005 earthquakes

Segmentation along convergent margins controls earthquake magnitude and location, but the physical causes of segment boundaries, and their impact on earthquake rupture dynamics, are still poorly understood. One aspect of the 2004 and 2005 great Sumatra-Andaman earthquakes is their abrupt termination along a common boundary. This has led to speculation on the nature of the boundary, its origin and why it was not breached. For the first time the boundary has been imaged and, with newly acquired marine geophysical data, we demonstrate that a ridge on the subducting Indo-Australian oceanic crust may exert a control on margin segmentation. This suggests a lower plate influence on margin structure, particularly its segmentation. The ridge is masked by the sedimentary cover in the trench. Its most likely trend is NNE-SSW. It is interpreted as a fracture zone on the subducting oceanic plate. A ramp or tear along the eastern flank of the subducting fracture zone beneath Simeulue Island may be considered as an intensification factor in terms of rupture propagation barrier