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To investigate whether cilostazol, a cyclic adenosine monophosphate (cAMP) phosphodiesterase inhibitor, suppresses intimal hyperplasia in canine vein grafts, and to elucidate its mechanisms in terms of cell proliferation and apoptosis. Bilateral reversed jugular vein interposition grafts of the common carotid artery were performed in 12 beagle dogs. Starting from 7 days before surgery, either cilostazol (30 mg/day; n = 6) or a placebo (n = 6) was given orally twice daily. Vein grafts were harvested at 1 or 4 weeks, and fixed under pressure for histological examination. By 1 week after implantation, the cilostazol group showed significantly less cell proliferation than the placebo group. By 4 weeks after implantation, intimal and medial thickness was significantly thinner in the cilostazol group than in the placebo group. There was significantly more apoptosis in the placebo group than in the cilostazol group at both time points. Cilostazol suppressed the development of intimal hyperplasia in canine autogenous vein grafts. Thus, it may be associated with the modulation of cell proliferation and apoptosis.

Conventional surgery for aortoesophageal fistula (AEF) is technically difficult, and is associated with high morbidity and mortality. We report a case of primary AEF caused by a descending thoracic aortic aneurysm, which was successfully treated with an endovascular stent-graft technique. The patient has been followed up for 3 years with no signs of infection.

The etiology of femoral artery aneurysms is believed to involve the interaction of a genetic alteration that predisposes to the loss of arterial wall integrity. This is precipitated by local forces such as repeated flexion of the arteries at the hip. We describe herein a case of bilateral femoral and right internal iliac artery aneurysms that developed in a patient with long-standing paraplegia. This could suggest that alterations in the arterial wall caused by stress and kinking during hip flexion may not play a principal role in the pathogenesis of nonspecific femoral artery aneurysms.

A variety of mechanisms have been proposed for the regulation of ion channel molecules. As integral membrane proteins, ion channels may interact with the cytoskeleton. Regulation of channels by the actin network may therefore be important. In the present study we used cytochalasin D and exogenous actin to test this possibility. The Cl- channel of the apical membrane of renal proximal epithelium was detected in its active state after prolonged depolarization. Within 6 sec after its addition, cytochalasin D (0.05 microgram/ml) significantly decreased the number of open channels and mean open probability (NPo) of the Cl- channel. Colchicine (1 mM), which affects microtubules, did not influence channel activation. Cytochalasin D is known to not only disrupt the F-actin network but to inhibit polymerization of F-actin as well. The latter effect is also produced by DNaseI. Cytochalasin D, but not DNaseI, inactivated Cl- channels in cell-free membrane patches, suggesting that cytochalasin D inactivated the channel by disrupting the actin network. Cytochalasin D appeared to specifically affect the channel, as opposed to membrane permeability, since only the activated whole-cell Cl- currents were altered by cytochalasin D. Addition of actin polymer, but not actin monomer, reactivated the cytochalasin-D-depressed channel. Thus, repair of the disrupted F-actin network with actin polymer apparently restored the activity and number of open Cl- channels. We therefore conclude that the F-actin network interacts with and possibly regulates the Cl- channel of renal proximal tubule epithelia.