Objective To evaluate blood flow structure within left ventricle,quantify the variation of the flow at infarct segments,and assess the impact of myocardial infarction.Methods Twenty-eight patients with chronic myocardial infarction(CMI)and 30 healthy controls were involved.The flow vector images on the section plane of the flow within the left ventricle were acquired by vector flow mapping(VFM).Timeflow(T-F)curve and all other peak systolic and diastolic flow curve include normal velocity profile,parallel velocity profile,vector profile were analyzed by DSA-RSI program.Results Ventricular ejction peak S,rapid ventricular filling peak E and atrial systole peak A were relatively lower in CMI group at infarct segment than normal control group,the time duration from bottom to peak was relatively longer in CMI group.Normal velocity profile,parallel velocity profile,vector profile,flow profile at peak S and E were lower in CMI group than normal group.Conclusions The velocity of CMI group was lower and the time to peak was longer than that of control group.VFM is a new noninvasive and clinically useful parameter for the evaluation of regional left ventricular segment flow dynamics.

Myelinated Schwann cells in the peripheral nervous system express the p75 nerve growth factor receptor (p75NGFR) as a consequence of Schwann cell dedifferentiation during Wallerian degeneration. p75NGFR has been implicated in the remyelination of regenerating nerves. Although many studies have shown various mechanisms underlying Schwann cell dedifferentiation, the molecular mechanism contributing to the re-expression of p75NGFR in differentiated Schwann cells is largely unknown. In the present study, we found that lysosomes were transiently activated in Schwann cells after nerve injury and that the inhibition of lysosomal activation by chloroquine or lysosomal acidification inhibitors prevented p75NGFR expression at the mRNA transcriptional level in an ex vivo Wallerian degeneration model. Lysosomal acidification inhibitors suppressed demyelination, but not axonal degeneration, thereby suggesting that demyelination mediated by lysosomes may be an important signal for inducing p75NGFR expression. Tumor necrosis factor-alpha (TNF-alpha) has been suggested to be involved in regulating p75NGFR expression in Schwann cells. In this study, we found that removing TNF-alpha in vivo did not significantly suppress the induction of both lysosomes and p75NGFR. Thus, these findings suggest that lysosomal activation is tightly correlated with the induction of p75NGFR in demyelinating Schwann cells during Wallerian degeneration.
Axons ; Cell Dedifferentiation ; Chloroquine ; Demyelinating Diseases ; Lysosomes ; Myelin Sheath ; Nerve Growth Factor ; Peripheral Nervous System ; RNA, Messenger ; Schwann Cells ; Tumor Necrosis Factor-alpha ; Wallerian Degeneration