[Intraoperative evaluation of visceral arteries by transesophageal echocardiography during aortic fenestration].

76-year-old man was diagnosed with DeBakey type IIIb acute aortic dissection, for which he underwent axillo-femoral bypass surgery. Two days postoperatively, hematochezia developed suddenly. Laboratory data revealed AST 5,088 IU x l(-1), ALT 3,822 IU x l(-1), and CK 27,746 IU x l(-1) suggesting intestinal malperfusion due to stenosis of the celiac artery (CEA) and superior mesenteric artery (SMA). The abdominal aorta and visceral arteries were evaluated by transesophageal echocardiography (TEE). Color Doppler imaging revealed increased blood flow velocity (4.0 m x sec(-1)) in CEA due to the stenosis, while that in SMA was decreased. Open abdominal aortic fenestration was performed. The aorta was clamped at the level of the infra-renal and inferior mesenteric arteries, and the septum between the false and true lumens was resected. On postoperative TEE assessment, CEA stenosis was resolved, and flow velocity was improved (3.0 m x sec(-1)). Color Doppler imaging demonstrated that fenestration resulted in recovery of SMA perfusion. Aortic fenestration is useful in the treatment of ischemic complications of aortic dissection. Its advantages include minimal invasiveness and short operative time. Bypass surgery and reoperation were avoided by evaluating visceral arteries by TEE in the case reported here.

Ultrastructural studies on the phenotypic modulation of human intimal smooth muscle cells.

The present study was carried out to clarify the mechanism of intimal thickening at the ostia of celiac and superior mesenteric arteries. The cell components involved in the process were analyzed under electron microscope. Autopsy samples from cases without significant atherosclerotic diseases were examined and the percentages of smooth muscle cells in either synthetic or contractile state, macrophages, and foam cells in the intima of mesenteric and celiac arteries were calculated. Smooth muscle cells in the synthetic state were predominant in the proximal region and those in the contractile state were predominant in the distal region. Few macrophages were present in both regions. The intima in the proximal and distal regions of celiac arteries in autopsy samples was further divided into three layers and the percentages of various smooth muscle cell phenotypes in each layer were calculated and compared in patients at different ages. In the proximal region, the phenotype of the smooth muscle cells changed from the synthetic to the contractile state from the deeper to the superficial layers with the advance of age. In the distal region, the contractile state was dominant regardless of the age. These results suggest that the phenotypic modulation of human intimal smooth muscle cells is reversible dedifferentiation-redifferentiation process; this phenomenon plays an important role in the initiation of atherosclerosis.

The role of vascular smooth muscle cell phenotypic modulation at the aortic branch in atherogenesis.

To elucidate the mechanism of the development of atherosclerosis, we have investigated the cell population of phenotypes of contractile (C-SMC) and synthetic (S-SMC) states of SMCs at proximal and distal areas of bifurcation of the celiac and superior mesenteric arteries in children and young persons by transmission electron microscopy. The previous studies in patients with hypercholesterolemia and who were young indicated that percentages of proximal area at bifurcation of both arteries were greater than that of C-SMC (P 0.01), and that C-SMCs at distal area were less than that of S-SMC (P 0.05). Ultrastructurally, SMCs at proximal area were S-SMCs containing many synthetic organelles and intermediate filaments. On the other hand, those at distal area were C-SMCs containing actin, myosin, dense bodies and microtubules. In the present study, we have ascertained that the phenotypic modulation of SMCs in the intima and media might correlate to the physico-medial relationship between SMCs and elastic tissues. In this communication, we have observed that the intimal SMCs transformed their phenotypes from the internal elastic layer (S-SMC) to the superficial layer (C-SMC), and that the medial SMCs in the arteries of the young clearly consisted of two types: one type adhered to the elastic layer and the other type existed with the separated one. The difference between both areas in the relatively young need to be observed in detail from now on. In summary, the vascular SMCs and the elastic lamina are considered to contribute to the subsequent phenotypic modulation and their migration of SMCs.

The role of vascular smooth-muscle cells in atherogenesis: phenotypic modulation of the medial smooth-muscle cells in the aortic bifurcation.

To elucidate the mechanism of migration of vascular smooth-muscle cells (SMCs) from media to intima, we have investigated the phenotypic modulation of the medial SMC at bifurcation of the celiac artery in 5 children and 3 young persons using a transmission electron microscope. We counted the number of separated SMCs from the elastic layers, although the medial SMCs are fundamentally attached to the elastic fibers, and are still contractile in their phenotypes. Both proximal and distal portions revealed that SMCs in the media were more or less present in the separated state and were ultrastructurally consistent with the synthetic state of SMC in the proximal area and the contractile state in distal areas. In order to migrate from media to intima, medial SMC should separate from the elastic layers and transform their phenotypes. In this paper, we examined the relationship between vascular SMCs and elastic layers in the media and ascertain that it was responsible for the contribution to the subsequent phenotypic modulation and their migration of medial SMCs.

Lipid accumulation and ultrastructural change within the aortic wall during early spontaneous atherogenesis.

To identify the initial period and type of lipid accumulation during spontaneous atherosclerosis, quantitative chromatographic profiles of major lipid classes in upper thoracic aortas (non-lesion areas) and celiac artery cushions (lesion areas) were obtained from atherosclerosis-susceptible White Carneau (WC) and atherosclerosis-resistant Show Racer (SR) pigeons from 1 day to 6 months of age. Thoracic aortas of WC and SR pigeons contained similar amounts of cholesterol, nonesterified fatty acids, triacylglycerols, cholesteryl esters, phospholipids, and hydrocarbon at each age studied. However, celiac sites in WCs contained more total lipid than corresponding SR sites at 6 weeks and 6 months of age. This initial increase at 6 weeks in WCs was characterized by invreased concentrations of nonesterified saturated fatty acids. By 6 months of age, WC celiac cushions had greater concentrations of each lipid class except hydrocarbon than did SR cushions. This initial lipid accumulation was accompanied by ultrastructural changes within the arterial wall, which included the presence of extracellular, vesiclelike structures and extensive accumulation of basal lamina-like material between cells. This material was not present in aortic regions that are not predisposed to lesion formation. This material increased by 6 months of age in the enlarging WC fibromuscular intimal cushions. These morphologic changes paralleled the quantitative lipid increases and represented the first morphologic changes detectable at this site. Age-related changes in arterial lipid content and ultrastructure in SRs are different from those related to early spontaneous atherogenesis in WCs.