Magnetic resonance imaging characteristics of ischemic brain infarction over time in a canine stroke model

This study describes magnetic resonance imaging (MRI) results and changes in lateral ventricular size over time in a canine ischemic stroke model. T1- and T2-weighted (T1W, T2W) imaging and fluid-attenuated inversion recovery (FLAIR) sequence MRI were performed at 3 h and 3, 8, and 35 days after brain infarct induction. Diffusion-weighted imaging (DWI) and apparent diffusion coefficient (ADC) mapping were performed at 8 and 35 days. A total of 29 brain lesions were induced successfully in 12 of 14 beagle dogs. At 3 h, T2W and FLAIR detected hyperintense lesions in three randomly selected dogs. On T1W, all lesions appeared hypointense to isointense at 3 h, isointense (18/29) or hypointense (11/29) at 3 days, hypointense to isointense with peripheral hyperintensity (24/26) at 8 days, and hypointense (18/26) at 35 days. Infarcts on DWI/ADC were hypointense to isointense centrally, with the periphery hyperintense/hyperintense (17/26) at 8 days and hypointense/hyperintense (19/26) at 35 days. A marked increase in lateral ventricular size was observed in dogs with cerebral infarcts. In conclusion, T2W and FLAIR were useful for detecting early stage (3 h to 3 days) brain infarction. T1W and DWI were useful for detecting neuronal necrosis and providing supplemental information for phase evaluation.

Lysophosphatidylcholine Increases Ca2+ Current via Activation of Protein Kinase C in Rabbit Portal Vein Smooth Muscle Cells

Lysophosphatidylcholine (LPC), a metabolite of membrane phospholipids by phospholipase A(2), has been considered responsible for the development of abnormal vascular reactivity during atherosclerosis. Ca2+ influx was shown to be augmented in atherosclerotic artery which might be responsible for abnormal vascular reactivity. However, the mechanism underlying Ca2+ influx change in atherosclerotic artery remains undetermined. The purpose of the present study was to examine the effects of LPC on L-type Ca2+ current (ICa(L)) activity and to elucidate the mechanism of LPC-induced change of ICa(L) in rabbit portal vein smooth muscle cells using whole cell patch clamp. Extracellular application of LPC increased ICa(L) through whole test potentials, and this effect was readily reversed by washout. Steady state voltage dependency of activation or inactivation properties of ICa(L) was not significantly changed by LPC. Staurosporine (100 nanometer) or chelerythrine (3 micrometer, which is a potent inhibitor of PKC, significantly decreased basal ICa(L), and LPC-induced increase of ICa(L) was significantly suppressed in the presence of PKC inhibitors. On the other hand, application of PMA, an activator of PKC, increased basal ICa(L) significantly, and LPC-induced enhancement of ICa(L) was abolished by pretreatment of the cells with PMA. These findings suggest that LPC increased ICa(L) in vascular smooth muscle cells by a pathway that involves PKC, and that LPC-induced increase of ICa(L) might be, at least in part, responsible for increased Ca2+ influx in atherosclerotic artery.