We report the synthesis of N‐methylimidazolium chloride‐modified iron oxide nanoparticles (MImCl‐NPs) by condensation of an imidazolium cation‐containing silane coupling agent (1) with the iron oxide nanoparticles which were prepared by the coprecipitation of FeCl2 and FeCl3 by alkaline hydrolysis. The modified iron oxide nanoparticles exhibited a superparamagnetic behavior at the room temperature. For a given weight concentration, MImCl‐NPs showed a darker (T2‐weighted) image than Resovist®, which is commercially available and used for MRI imaging in practice. When mice were given a daily intravenous injection of 5% glucose aqueous solution of MImCl‐NPs for two weeks, MImCl‐NPs showed no significant difference in body weight and blood biochemistry of serum in all samples compared to controls. DLS measurements of the aqueous solutions of the modified iron oxide nanoparticles after the addition of NaPF6 and NaI indicated the presence of particle aggregates. In contrast, no aggregation was observed after the addition of NaCl. A higher degree of adsorption of DNA onto MImCl‐NPs was observed in comparison to that onto amino‐functionalized magnetic nanoparticles (NH2‐NPs). Copyright © 2008 John Wiley & Sons, Ltd.

Fibrotic lesion is formed by myofibroblasts capable of producing collagens. The myofibroblasts are characterized by immunoexpressions of vimentin, desmin and α-smooth muscle actin (α-SMA) in varying degrees. The cellular characteristics remain investigated in myocardial fibrosis. We analyzed immunophenotypes of myofibroblasts appearing in isoproterenol-induced myocardial fibrosis in rats until 28 days after injection (10 mg/kg body weight); the lesions developed as interstitial edema and inflammatory cell reaction on 8 hr and days 1 and 3, and fibrosis occurred on days 1, 3, 7, 14, and 21 by gradual deposition of collagens, showing the greatest grade on day 14; the lesions gradually reduced with sporadic scar until day 28. Myofibroblasts expressing vimentin and α-SMA increased with a peak on day 3, and then, gradually decreased onwards. Interestingly, Thy-1 expressing cells appeared in the affected areas, apparently being corresponding to the grade similar to vimentin- and α-SMA-positive cells. Thy-1 is expressed in immature mesenchymal cells such as pericytes with pluripotent nature. The immunoreactivity for A3-antigen, a marker for immature mesenchymal cells, was seen in some surrounding cells. There were no cells reacting with antibodies to nestin or glial fibrillary acidic protein, although hepatic myofibroblats have been reported to react with these antibodies. Collectively, myofibroblasts appearing in rat myocardial fibrosis may have been derived from immature mesenchymal cells positive for Thy-1 or A3-antigen, with thereafter showing expressions of vimentin and α-SMA in differentiation.

His-bundle pacing gives a more physiological ventricular contraction in comparison to right ventricular apical pacing. However the problems of lead fixation and stability of long-term His-bundle pacing are yet unsolved. We used six adult beagles, in which a screw-in lead was anchored in the His-bundle region for observation of the pacing conditions and histopathologic changes of the conduction system over the course of 2 months. In the results, a satisfactory fixation was obtained using a conventional screw-in lead and no histological influence on the conduction system was observed. The pacing threshold at the time of implantation was 1.15 +/- 0.69 V (3.23 +/- 3.08 mA) in the pulse width of 0.5 ms. R wave amplitude, the impedance and slew rate were 7.28 +/- 2.04 mV, 409 +/- 102 Ohm, and 0.65 +/- 0.41 V/s, respectively. Two months later, these parameters changed to 2.83 +/- 1.06 V (10.4 +/- 5.71 mA), 5.63 +/- 1.62 mV, 310 +/- 71.3 Ohm, and 0.49 +/- 0.22 V/s, respectively. These results suggest the feasibility of clinical application of permanent His-bundle pacing.

Active drainage of cardiac lymph using hyaluronidase was attempted in dogs. The results were satisfactory and the ischemic myocardium was salvaged. The infract risk area (I/R) ratio decreased after drainage.Regional myocardial ischemia and infarction were provided by means of ligature of the left coronary artery for 120 and 240 minutes respectively. Cardiac lymph was collected by conventional procedures. Enzymes released from the myocardium increased significantly in the cardiac lymph. The volume of cardiac lymph gradually increased after ligature of the coronary artery. Administration of hyaluronidase further increased the cardiac lymph flow and significantly decreased the I/R ratio as determined by triphenyl tetrazolium chloride (TTC) and methylene blue staining. Drainage of the cardiac lymph salvaged the ischemic myocardium. Reduction of interstitial edema and augmentation of cardiac lymph flow with the hyaluronidase prevented the development of the infarction. This is the first documentation of the effect of active drainage of cardiac iymph on the development of infarction through observation of the I/R ratio.