Butylated hydroxytoluene (BHT) can inhibit experimental atherosclerosis in animals. Although the agent is an antioxidant, the exact mechanism of the reaction in atherosclerosis is still unknown. To investigate the effects of BHT on expression of P-selectin (PADGEM, GMP-140), intercellular adhesion molecule-1 (ICAM-1) and class II MHC (Ia) antigen, we proposed an experiment on rats. Male rats (n=18 per group) were fed either a normal cholesterol control diet, a normal cholesterol diet containing 0.5% BHT (BD), a high cholesterol diet containing 1.5% cholesterol and 0.1% sodium cholate (CD), or the CD diet containing 0.5% BHT (BCD). Rats were sacrificed after 3 days, and after 1, 2, 4, 10, and 17 weeks of dietary treatment. Although there was no gross or light microscopic atherosclerotic lesions, scanning electron microscopy revealed monocytic adhesion to aortic endothelium and mild endothelial injuries in CD and BCD groups. Immunohistochemically, the addition of BHT to a high cholesterol diet inhibited P-selectin expression but not in ICAM-1 and Ia antigen. These findings suggest that in rats, high cholesterol diets induce expression of ICAM-1, P-selectin and Ia antigen. In addition, the antiatherogenic effect of BHT may play a role in the inhibition of P-selectin.
Animal ; Antioxidants/pharmacology ; Antioxidants/metabolism* ; Aorta, Abdominal/ultrastructure ; Aorta, Abdominal/pathology ; Aorta, Thoracic/ultrastructure ; Aorta, Thoracic/pathology ; Butylated Hydroxytoluene/pharmacology ; Butylated Hydroxytoluene/metabolism* ; Cholesterol/metabolism ; Cholesterol, Dietary/metabolism* ; Male ; Microscopy, Electron, Scanning ; P-Selectin/biosynthesis* ; Rats ; Rats, Sprague-Dawley

The presence of elastin layers in the aortic walls of twelve human fetuses was confirmed with scanning electron microscope pictures after hot alkali treatment and histochemical examination. In addition, the number of elastin layers in aortic walls of 5 different segments were compared in fetuses of varying ages. Aldehyde fuchsin stained slides of elastin ascending aortas showed a range between 27 and 55 layers of elastin in fetuses of 8 weeks to 32 weeks. However, in the lower abdominal aortas, elastin layers decreased from 28 to only 3 layers for fetuses of the same age. Furthermore, as elastin layers decreased from ascending aorta to abdominal aorta with the progression of fetal life, similar changes in the elastin lamellae were observed. These results suggest that while aortas grow rapidly in length, the medial elastin thickens slowly, perhaps due to slow development of hydrodynamic forces and pressures. Also the adventitial elastin appears to lose out gradually along the length from ascending aorta to abdominal aorta.
Aorta/*embryology/metabolism/ultrastructure ; Elastin/*metabolism ; Fetus/anatomy & histology/*metabolism/physiology ; Human

BACKGROUNDThe expression of TES, a novel tumor suppressor gene, is found to be down-regulated in the left anterior descending aorta of patients with coronary artery disease (CAD) compared with non-CAD subjects. This study aimed to investigate the expression of TES during the development of atherosclerosis in rabbits.

METHODSThirty-two New Zealand rabbits were randomly divided into a normal diet (ND) and high-fat diet (HFD) groups. Body weight and serum lipid levels were measured at 0, 4, and 12 weeks after diet treatment. The degree of atherosclerosis in thoracic aortas was analyzed by histological examinations. The expression of Testin in the tissue samples was inspected via immunohistochemical and immunofluorescence confocal microscopy. Real time-polymerase chain reaction and Western blot analysis were performed to evaluate the expression of TES/Testin at mRNA and protein levels in the aortic tissues.

RESULTSAfter 12 weeks postenrollment, rabbits in HFD group had a higher level of serum lipids and atherosclerotic plaque compared to ND group (P < 0.05). Testin expression was detected at high levels in the endothelium and a weak expression on the subendothelium area. The expression of TES mRNA was markedly reduced by 10-fold in the aortic tissues in the HFD group compared with the ND group (P = 0.015), and the protein level was also significantly decreased in the HFD group (P < 0.05).

CONCLUSIONSReduced TES/Testin expression is associated with the development of atherosclerosis, implicating a potentially important role in the pathogenesis of atherosclerosis.

Animals ; Aorta ; metabolism ; Atherosclerosis ; etiology ; metabolism ; Diet, High-Fat ; adverse effects ; Proteins ; genetics ; metabolism ; Rabbits

OBJECTIVE: To explore the effect of Kuanxiong Aerosol (KXA) on isoproterenol (ISO)-induced myocardial injury in rat models. METHODS: Totally 24 rats were radomly divided into control, ISO, KXA low-dose and high-dose groups according to the randomized block design method, and were administered by intragastric administration for 10 consecutive days, and on the 9th and 10th days, rats were injected with ISO for 2 consecutive days to construct an acute myocardial ischemia model to evaluate the improvement of myocardial ischemia by KXA. In addition, the diastolic effect of KXA on rat thoracic aorta and its regulation of ion channels were tested by in vitro vascular tension test. The influence of KXA on the expression of calcium-CaM-dependent protein kinase II (CaMK II)/extracellular regulated protein kinases (ERK) signaling pathway has also been tested. RESULTS: KXA significantly reduced the ISO-induced increase in ST-segment, interventricular septal thickness, cardiac mass index and cardiac tissue pathological changes in rats. Moreover, the relaxation of isolated thoracic arterial rings that had been precontracted using norepinephrine (NE) or potassium chloride (KCl) was increased after KXA treatment in an endothelium-independent manner, and was attenuated by preincubation with verapamil, but not with tetraethylammonium chloride, 4-aminopyridine, glibenclamide, or barium chloride. KXA pretreatment attenuated vasoconstriction induced by CaCl₂ in Ca²⁺-free solutions containing K⁺ or NE. In addition, KXA pretreatment inhibited accumulation of Ca²⁺ in A7r5 cells mediated by KCl and NE and significantly decreased p-CaMK II and p-ERK levels. CONCLUSION KXA may inhibit influx and release of calcium and activate the CaMK II/ERK signaling pathway to produce vasodilatory effects, thereby improving myocardial injury.
Aerosols ; Animals ; Aorta, Thoracic ; Calcium/metabolism* ; Endothelium, Vascular/metabolism* ; Myocardial Ischemia/metabolism* ; Rats ; Vasodilation

MicroRNAs (miRNAs) are genomically encoded non-protein-encoding small RNAs, which negatively regulate target gene expression at post-transcriptional level. The present study aimed to investigate whether disorders of miRNAs system were involved in the pathogenesis of hypertension in spontaneously hypertensive rats (SHR). MiRanda, Target Scan and PicTar were utilized for predictive analysis of miRNAs and target genes. MiR-1, miR-133a, miR-155 and miR-208 were selected as the candidate miRNAs potentially related to blood pressure. The expression levels of miR-1, miR-133a, miR-155 and miR-208 in the aorta of 4-, 8-, 16- and 24-week-old SHR and age-matched Wistar-Kyoto (WKY) rats were detected by real-time RT-PCR. The mRNA levels of angiotensin II receptor type 1 (AGTR1a), angiotensin II receptor associated protein (AGTRAP), divalent metal transporter 1 (DMT1), low-density lipoprotein-related protein 1B (LRP1B), fibroblast growth factor-7 (FGF-7), protocadherin 9 precursor (PCDH9), chloride channel protein 5 (CLCN-5), small conductance calcium activated potassium channel protein 3 (KCNN3) and thyroid hormone receptor associated protein 1 (THRAP1), which were predicted to be target genes of differentially expressed miRNAs, were further detected by real-time RT-PCR. The results obtained showed that the expression levels of miR-1, miR-155 and miR-208 in the aorta were significantly different from those in the heart of WKY rats. The miR-155 level was significantly lower in aorta of 16-week-old SHR than that of age-matched WKY rats (P<0.05), but there was no difference between SHR and WKY rats in other age groups. In addition, miR-155 level was negatively correlated to blood pressure (r=-0.525, P<0.05). Both in WKY rats and SHR, miR-208 was most abundantly expressed in 4-week-old rats, but declined significantly in 8-, 16- and 24-week-old rats (P<0.05). No difference in miR-208 levels was observed between age-matched SHR and WKY rats. Moreover, miR-208 expression in aorta was negatively correlated with blood pressure (r=-0.400, P<0.05) and age (r=-0.684, P<0.0001). Neither miR-1 nor miR-133a was differentially expressed in SHR and WKY rats in different age groups. The mRNA levels of predicted target genes were not correlated to miR-155 or miR-208 levels. These results indicate that miR-155 is less expressed in the aorta of adult SHR compared with that of WKY rats and is negatively correlated with blood pressure, suggesting it is possibly involved in the development and pathologic progress of hypertension. The miR-208 expression in rat aorta declines with aging and it may play a role in the blood vessel development.
Animals ; Aorta ; metabolism ; Blood Pressure ; Hypertension ; metabolism ; MicroRNAs ; metabolism ; RNA, Messenger ; Rats ; Rats, Inbred SHR ; Rats, Inbred WKY

Animals ; Aorta ; metabolism ; Hyperlipidemias ; metabolism ; Mice ; Mice, Inbred C57BL ; Nitric Oxide Synthase ; metabolism ; Physical Conditioning, Animal ; Physical Endurance

BackgroundOutflow tract (OFT) septation defects are a common cause of congenital heart disease. Numerous studies have focused on the septation mechanism of the OFT, but have reported inconsistent conclusions. This study, therefore, aimed to investigate the septation of the aortic sac and the OFT in the early embryonic human heart.

MethodsSerial sections of 27 human embryonic hearts from Carnegie stage (CS) 10 to CS19 were immunohistochemically stained with antibodies against α-smooth muscle actin (α-SMA) and myosin heavy chain.

ResultsAt CS10-CS11, the OFT wall was an exclusively myocardial structure that was continuous with the aortic sac at the margin of the pericardial cavity. From CS13 onward, the OFT was divided into nonmyocardial and myocardial portions. The cushion formed gradually, and its distal border with the OFT myocardium was consistently maintained. The aortic sac between the fourth and sixth aortic arch arteries was degenerated. At CS16, the α-SMA-positive aortopulmonary septum formed and fused with the two OFT cushions, thus septating the nonmyocardial portion of the OFT into two arteries. At this stage, the cushions were not fused. At CS19, the bilateral cushions were fused to septate the myocardial portion of the OFT.

ConclusionsData suggest that the OFT cushion is formed before the aortopulmonary septum is formed. Thus, the OFT cushion is not derived from the aortopulmonary septum. In addition, the nonmyocardial part of the OFT is septated into the aorta and pulmonary trunk by the aortopulmonary septum, while the main part of the cushion fuses and septates the myocardial portion of the OFT.

Actins ; metabolism ; Alkaline Phosphatase ; metabolism ; Aorta ; embryology ; Heart ; embryology ; Heart Valves ; embryology ; Humans ; Immunohistochemistry ; Myosin Heavy Chains ; metabolism

OBJECTIVETo identify gene expression differences between abdominal aorta aneurysm (AAA) and normal abdominal artery.

METHODSFive AAA specimens and five normal abdominal artery specimens were collected. Total RNA was extracted and purified from the samples independently. Then isolated RNA was labeled and hybridized onto the Affymetrix Genechip.

RESULTSOne thousand nine hundreds and sixty-two differently expressed genes were identified in AAA compared with normal abdominal artery, of which 554 genes were up-regulated and 1408 genes were down-regulated. Functional analysis revealed that genes involved in immune response, inflammatory response and chemokines were significantly up-regulated in AAA.

CONCLUSIONThe differently expressed genes may be useful in providing new insights and foster a better understanding of the mechanism of AAA.

Aorta, Abdominal ; metabolism ; Aortic Aneurysm, Abdominal ; genetics ; Gene Expression Profiling ; Humans ; Oligonucleotide Array Sequence Analysis

BACKGROUND: Hypothermia protects the brain by suppressing the cerebral metabolism and it is performed well enough before the total circulatory arrest(TCA) in the operation of aortic disease. Generally, TCA has been performed depending on the rectal or nasopharyngeal temperatures; however, there is no definite range of optimal temperature for TCA or an objective indicator determining the temperature for safe TCA. In this study, we tried to determine the optimal range of temperature for safe hypothermic circulatory arrest by using the intraoperative electroencephalogram(EEG), and studied the role of EEG as an indicator of optimal hypothermia. MATERIAL AND METHOD: Between March, 1999 and August 31, 2000, 27 patients underwent graft replacement of the part of thoracic aorta using hypothermia and TCA with intraoperative EEG. The rectal and nasopharyngeal temperatures were monitored continuously from the time of anesthetic induction and the EEG was recorded with a ten-channel portable electroencephalography from the time of anesthetic induction to electrocerebral silence(ECS). RESULT: On ECS, the rectal and nasopharyngeal temperatures were not consistent but variable(rectal 11degree C -25degree C, nasopharynx 7.7degree C -23degree C). The correlation between two temperatures was not significant(p=0.171). The cooling time from the start of cardiopulmonary bypass to ECS was also variable(25-127min), but correlated with the body surface area(p=0.027). CONCLUSION: We have found that ECS appeared at various body temperatures, and thus, the use of rectal or nasopharyngeal temperature were not useful in identifying ECS. Conclusively, we can not fully assure cerebral protection during hypothermic circulatory arrest in regards to the body temperatures, and therefore, the intraoperative EEG is one of the necessary methods for determining the range of optimal hypothermia for safe circulatory arrest.
Aorta, Thoracic ; Aortic Diseases ; Body Temperature ; Brain ; Cardiopulmonary Bypass ; Electroencephalography* ; Humans* ; Hypothermia ; Metabolism ; Nasopharynx ; Transplants

Objective: To investigate the expression pattern of tropomyosin 2(TPM2) in aorta of patients with aortic dissection and explore its clinical implication. Methods: Thirteen cases with acute type A aortic dissection(TAAD) diagnosed by transabdominal aortic angiography from 2015 in Tongji Hospital were included. During the operation, the aortic wall tissues of these patients were collected. Ten patients with heart transplantation were selected as control group, and normal aortic wall tissues were taken. The hematoxylin-eosin (HE) and Verhoeff's Van Gieson (EVG) staining were performed to observe the morphological changes of aorta. The mRNA expression level of TPM2 was measured by real-time fluorescent quantitative-PCR, and the protein levels of TPM2 were detected by Western blot and immunohistochemical staining. Image The J software was used to collect the optical density values of each point on the image, obtain the integrated optical density(IOD) value, and calculate the average density(%, IOD/area of the target distribution area). Results: HE and EVG staining revealed medial degeneration and broken elastic fiber in aorta of TAAD patients. The mRNA expression levels of TPM2 were significantly upregulated in aorta of TAAD patients as compared to the control group (P<0.05), so as the TPM2 protein expression levels ((9.73±1.20)% vs. (0.11±0.04)%, P<0.05). And TPM2 was mainly expressed in cytoplasm. Conclusion: The increased expression of TPM2 in TAAD patients hints that TPM2 might be involved in the pathogenesis of aortic dissection.
Aneurysm, Dissecting/genetics* ; Aorta ; Aortic Aneurysm, Thoracic/genetics* ; Gene Expression ; Humans ; RNA, Messenger ; Tropomyosin/metabolism*