Three tesla magnetic resonance angiography with ultrashort echo time describes the arteries near the cerebral aneurysm with clip and the peripheral cerebral arteries.

BACKGROUND: The assessment of the clipped cerebral aneurysm and the cerebral arteries after the treatment of subarachnoid hemorrhage (SAH) is important to find aneurysm regrowth or postoperative cerebral vasospasm. Usually, contrast-enhanced computed tomography angiography is performed for the evaluation of the arteries, but it has side effects of contrast medium. Time-of-flight magnetic resonance angiography (MRA) is a fast and non-invasive method, but clip-induced artifact limits assessment of the artery in the vicinity of the clip. 1.5T MRA with ultrashort echo time (UTE) reduces metal artifact, but the obtained image is too rough to evaluate the aneurysm remnant, and the description range is too narrow to assess the cerebral vasospasm. We routinely use SIGNA Pioneer 3.0T (GE Healthcare Life Sciences, Buckinghamshire, England) and perform SILENT SCAN with UTE-MRA for the postoperative assessment of the clipped aneurysm and cerebral arteries for SAH patients treated by clipping. It has better image quality and describes arteries with a wide description range, so it possesses the potential to overcome the disadvantages of 1.5T UTE-MRA. CASE DESCRIPTION: We presented a representative SAH patient who postoperatively underwent 3.0T UTE- MRA after clipping. The artery near the clipped aneurysm was evaluated in detail, and the cerebral arteries were described from the main trunk to the peripheral parts with a wide description range, which enabled the assessment of cerebral vasospasm. CONCLUSION: 3.0T UTE-MRA may be helpful for the usual assessment of the arteries after clipping and cerebral vasospasm in the future.

Perivascular Adipose Tissue-Enhanced Vasodilation in Metabolic Syndrome Rats by Apelin and N-Acetyl⁻l-Cysteine-Sensitive Factor(s).

Perivascular adipose tissue (PVAT) can regulate vascular tone. In mesenteric arteries of SHRSP.Z-Leprfa/IzmDmcr rats (SHRSP.ZF) with metabolic syndrome, vascular dysfunction is compensated by PVAT-dependent mechanisms that disappear with increasing age. In this study, we investigated the mechanisms of the age-related changes and responsible factor(s) involved in the enhancing effects of mesenteric arterial PVAT in SHRSP.ZF. Acetylcholine- and sodium nitroprusside-induced relaxations of isolated arteries were greater with PVAT than without PVAT at 17 and 20 weeks of age (wks), and as expected, this enhancement by the presence of PVAT disappeared at 23 wks. PVAT mRNA levels of angiotensin II type 1 (AT1) receptor-associated protein was less and AT1 receptor was unchanged at 23 wks when compared to 20 wks. At 20 wks, the enhanced acetylcholine-induced relaxation by the presence of PVAT was inhibited by N-acetyl-l-cysteine (NAC). Acetylcholine-induced relaxation of arteries without PVAT was increased in the presence of exogenously added apelin. PVAT mRNA level of apelin was higher in SHRSP.ZF than in control Wistar-Kyoto rats, and the level was decreased with aging. These results suggest that AT1 receptor activation in PVAT, and changes in the regulation of apelin and a NAC-sensitive factor are related to the age-dependent deterioration of the vasodilation enhancing effects of mesenteric arterial PVAT in SHRSP.ZF.

Time-Dependent Differences in the Influence of Perivascular Adipose Tissue on Vasomotor Functions in Metabolic Syndrome.

BACKGROUND: Metabolic syndrome (MetS) facilitates the development of cardiovascular disease due to atherosclerosis, which is accelerated by defects of the vascular endothelium. Vascular dysfunction in response to nitric oxide (NO) occurs in the mesenteric arteries of an animal model of MetS, SHRSP.Z-Leprfa/IzmDmcr (SHRSP.ZF) rats. Vascular responses to vasodilators are affected by perivascular adipose tissue (PVAT) that surrounds the outsides of arteries. In this study, we assessed the role of PVAT in vascular dysfunction observed in SHRSP.ZF. METHODS: To determine the effects of PVAT on vasodilators in SHRSP.ZF and control Wistar-Kyoto (WKY) rats, we used organ bath bioassay techniques to assay acetylcholine and nitroprusside-induced relaxations of isolated mesenteric arterial ring preparations with PVAT intact or removed. RESULTS: A PVAT-mediated enhancement of relaxations induced by acetylcholine and nitroprusside occurred in SHRSP.ZF at 20 weeks of age, but not at 10 and 30 weeks, and did not occur in WKY. Furthermore, the enhancing effects of PVAT from SHRSP.ZF at 20 weeks could not be substituted by replacement with PVAT from either WKY or 30-week-old SHRSP.ZF, was inhibited by NO synthase inhibitor, and abolished by removal of the arteries' endothelium. Cyclic guanosine monophosphate (cGMP) accumulation elicited by nitroprusside was higher in SHRSP.ZF arteries with PVAT than arteries without PVAT at 20 weeks, but the enhancement of cGMP accumulation did not occur at 30 weeks. CONCLUSIONS: PVAT may regulate arterial tone by releasing diffusible vasorelaxing factor(s), which, through endothelium-derived NO production, compensates for impaired vasodilations at early stages of MetS.

Functional Relationship between Arterial Tissue and Perivascular Adipose Tissue in Metabolic Syndrome.

Metabolic syndrome is a complex of disorders that includes visceral obesity, insulin resistance, hypertension, and dyslipidemia. It is characterized by an increased risk for serious cardiovascular events. Adipocytes are now recognized to contribute to the development of cardiovascular complications in metabolic syndrome via the release of several bioactive substances (adipocytokines). Obesity induces an increase in the volume of perivascular adipose tissue (PVAT), which is located outside the blood vessels. In recent years, PVAT has been reported to produce/release vasoactive adipocytokines. Thus, PVAT can modulate vasomotor function by releasing vasorelaxing/vasocontracting factors, resulting in the development of cardiovascular disease due to metabolic syndrome. By using animal models (SHR/NDmcr-cp rats, SHRSP.Z-Lepr(fa)/IzmDmcr rats, and B6.BKS (D)-Lepr(fa)/J mice), we have demonstrated that chronic oxidative-nitrative stress is closely linked to the development of vascular dysfunction in response to nitric oxide (NO) in resistant arteries with increasing age/exposure to metabolic abnormalities. Further, our recent findings have led us to believe that PVAT helps in the regulation of vasodilation to compensate for the impaired vasodilation observed in pathophysiological conditions in the mesenteric arteries of SHRSP.Z-Lepr(fa)/IzmDmcr rats. However, a breakdown of the compensatory system occurs with long-term exposure to metabolic abnormalities. We propose the concept of the functional regulation of vascular tissue by PVAT in metabolic syndrome.