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[Histological study on the arterial wall of Göttingen miniature swine].

In order to clarify the histological aspects of arterial walls of miniature swine, 41 arterial segments removed from each of 17 Göttingen miniature swines/csk at 6-12 months after birth were examined by light microscopy. Every segment was classified into three types--elastic, transitional, and muscular--according to its histological architecture. Each type was identified on the basis of relative volume and disposition of elastic tissues, collagenous fibers, and smooth muscles in three coats, Tunica intima, Tunica media, Tunica externa. The distribution of each type was demonstrated in a transition from the elastic to the muscular type. The transitional type was designated as a representative type of artery in transitional regions between elastic and muscular types and had some characteristic structures like a mixture of both of them. This type also had longer regions in the back district with the heart as the starting point, such as the Aorta abdominalis, than that of the front. Every artery belonging to the three types had some different structures at different levels, respectively. It was supposed that the histological arrangement of tissues in the walls of a vessel from various parts of the arterial tree would respond properly to the functional demand.

Animals↗

[Mitogen-activated protein kinase regulated hypoxia-inducible factor 1alpha in hypoxia-induced pulmonary hypertension in rats].

OBJECTIVE: To investigate the dynamic expression of hypoxia-inducible factor 1alpha (HIF-1alpha) and mitogen-activated protein kinase (MAPK) in pulmonary arteries of rats with hypoxia-induced pulmonary hypertension. METHODS: Forty male adult Wistar rats were randomly divided into five groups:a control group (C group) and groups with hypoxia for 3, 7, 14 and 21 days (H(3), H(7), H(14) and H(21) group), eight rats per group. Mean pulmonary pressure (mPAP), right ventrical hypertrophy index (RVHI) and vessel morphometry were measured. The levels of HIF-1alpha mRNA expression in lung tissue was measured by in site hybridization (ISH). The protein expression of HIF-1alpha and p-ERK, p-JNK, p-P38 were observed by immunohistochemistry or Western blot. RESULTS: The level of mPAP [(23.5 +/- 1.8) mm Hg], the ratio of vascular wall thickness to external diameter [WT, (45.5 +/- 3.1)%] and the ratio of vascular wall area to the total area [LA, (54.7 +/- 3.2)%] were significantly higher in H(7) group than those in C group [(16.2 +/- 2.0) mm Hg, (36.8 +/- 2.5)% and (63.2 +/- 2.5)% respectively, all P < 0.05]. These parameters reached a high level and remained stable on H(14) group, RVHI was significantly higher [(26.9 +/- 1.3)%] on H(14) group than in C group [(23.0 +/- 1.5)%, P < 0.05]. Expression of p-ERK protein in C group was barely positive, but was up-regulated in pulmonary arterial tunica intima and tunica media of all hypoxia rats. Expression of p-JNK and p-P38 in C group and hypoxia groups were barely positive. Expression of HIF-1alpha protein in C group was barely positive, but was up-regulated in pulmonary arterial tunica intima of all hypoxic rats. In pulmonary arterial tunica media, the levels of HIF-1alpha protein was markedly up-regulated in H(3) group (0.209 +/- 0.009, P < 0.05), reaching its peak at H(7) group (0.232 +/- 0.008, P < 0.05), then tended to decline in H(14) group and H(21) group. HIF-1alpha mRNA staining was barely positive in C group, H(3) group and H(7) group, but began to increase significantly at H(14) group (0.305 +/- 0.104, P < 0.05), then remained stable in pulmonary arterial tunica intima. Linear correlation analysis showed that p-ERK, HIF-1alpha mRNA and mPAP were correlated with vessel morphometry and RVHI (P < 0.01); p-ERK was positively correlated with HIF-1alpha mRNA and protein (tunica intima). CONCLUSION: MAPK as a signal transduction may play an important role in the development of hypoxia-induced pulmonary hypertension.

Animals↗

Systemic atherosclerosis in dogs: histopathological and immunohistochemical studies of atherosclerotic lesions.

Histopathological and immunohistochemical studies were carried out on five cases of canine systemic atherosclerosis. The five animals were male, and showed hypercholesterolaemia and hypertriglyceridaemia on biochemical analysis of plasma. Histopathologically, atherosclerotic lesions were seen in the aorta and muscular arteries in many organs, including the heart, spleen, kidneys, lungs, pancreas, alimentary tract, urogenital organs, eyes, prostate and urinary bladder. The lesions were characterized by the deposition of lipids and infiltration of lipid-laden foamy cells in the tunica intima and tunica media, sometimes forming fibrofatty plaques, containing abundant sudanophilic material, cholesterol clefts and mineralized material. The lesions started in the tunica intima and extended to the tunica media and tunica adventitia. Immunohistochemical examination with canine apolipoprotein B-100 (CApoB-100) antibody identified the lipids containing low density lipoprotein. Immunoreactivity to CApoB-100 antibody was recognized in the tunica intima, lipid-laden foamy cell cytoplasm and smooth muscle cells in the tunica media, and fibrofatty plaque. These histopathological and immunohistochemical features were similar to those of human atherosclerotic lesions.

Age Factors↗

[Apoptosis of pathological tissues and expression of apoptosis-related genes in hepatic venous stricture Budd-Chiari syndrome].

OBJECTIVE: To investigate the pathogenesis of hepatic venous stricture Budd-Chiari syndrome from the point of view of hepatic venous intimal proliferation, apoptosis and apoptosis-related genes. METHODS: Thirty samples resected from patients with hepatic venous stricture Budd-Chiari syndrome and 21 samples of normal hepatic vein and vena cava obtained from necropsy of fresh corps as controls were examined. The paraffin sections of the samples were stained with hematoxyline and eosin and diaminobenzidine respectively and observed under light microscope to examine the pathology and calculate the apoptotic cells. SP immunohistochemistry was used to detect the expression of Bcl-2 and Bax. Proliferating cell nuclear antigen (PCNA) expression was detected by SABC immunohistochemistry. RESULTS: Light microscopy showed irregular proliferation in the tunica intima and tunica media, especially in the former. Incomplete elastic fiber, spotted smooth muscle cells, proliferation of fibrous connective tissue, and degeneration of partial tissues, and infiltration of inflammatory cells, etc. were observed. In the endothelial tissue TUNEL positive cells was 1.94 +/- 0.64 in the Budd-Chiari syndrome patients, significantly higher than that in the controls (0.56 +/- 0.21, P < 0.002); and PCNA positive cells was 3.46 +/- 0.51 in the Budd-Chiari syndrome patients, significantly higher than that in the controls (0.78 +/- 0.16, P < 0.0005). The bcl-2 expression rate was 8.56 +/- 1.17 in the Budd-Chiari syndrome patients, significantly higher than that in the normal controls (4.34 +/- 1.28, P < 0.0005); Bax expression was 3.95 +/- 1.31 in the Budd-Chiari syndrome patients, significantly lower than that in the normal controls (5.06 +/- 1.21, P < 0.001); and the bcl/Bax ratio of the cells in the tunicae intima and media of the normal hepatic veins was 0.914 +/- 0.334, significantly lower than that in the Budd-Chiari syndrome patients (2.402 +/- 1.021, P < 0.01). Electron microscopy showed that in comparison with the normal tissues the pathological tissues had more synthesized smooth muscle cells and lacked normal myoendothelial structure. CONCLUSION: Irregular proliferation of tunica intima of hepatic vein and apoptosis may be one of the mechanisms of hepatic venous stricture Budd-Chiari syndrome.

Adult↗

Pre-eclampsia associated alterations of the elastic fibre system in umbilical cord vessels.

Although pre-eclampsia (PE) is often associated with fetal hypoxia, hypertension and/or disturbed function of the fetal circulation, the effect of these altered hemodynamic parameters on the structure and composition of umbilical vessels has not been systematically investigated before. Therefore, this study focuses on PE-associated changes of the elastic fibre system in umbilical cord vessels investigated by light and electron microscopy, immunocytochemistry and biochemistry. In umbilical cord veins, no changes in thickness of the vessel wall or of any sublayer were observed. However, the internal elastic lamina of the veins was split in 80% of the PE-group in contrast to 20% in uncomplicated pregnancies. This effect was significant (alpha <0.01) from 36 weeks of gestation onwards. In umbilical cord arteries, the entire arterial vessel wall was found to be 15% thicker in PE than in uncomplicated pregnancies. The enlargement was caused by an increase of both the tunica intima and tunica media. The thickening of the tunica intima was attributed to a migration of smooth muscle cells towards the endothelium, accompanied by a splitting of the internal elastic lamina. Compared to uncomplicated pregnancies, smooth muscle cells of arteries and veins in PE showed a metabolic activation demonstrated by highly dilated endoplasmic reticulum. A semiquantitative score method as well as a quantitative dot blot assay indicated a PE-associated reduction of elastin expression in the arterial vessel walls. In summary, PE obviously induces a decrease of the elastin content accompanied by a thickening of the vessel wall in umbilical cord arteries. This remodeling of the elastic fibre system, together with an increased migration of smooth muscle cells, might represent part of the functional adaptation system of the umbilical cord arteries on the altered hemodynamic conditions in PE.

Adult↗

[Expression of early growth response gene-1 and its correlative genes in autogenous vein graft and significance thereof: an experiment with rats].

OBJECTIVE: To investigate the expression of early growth response gene-1 (Egr-1) and its correlative genes: platelet-derived growth factor-B (PDGF-B) gene and transforming growth factor-beta(1) (TGF-beta(1)) gene, in autogenous vein graft and the relationship of the expression of these genes to intimal hyperplasia (IH). METHODS: A segment of the right common jugular vein was transplanted to the infra-renal abdominal aorta of the same individual so as to establish an autogenous vein graft model in 90 Wistar rats. Vein samples were harvested 1, 2, 6, and 24 hours, 3 and 7 days, and 2, 4, and 6 weeks after the operation to undergo histological examination. In situ hybridization and RT-OCR were performed to examine the mRNA expression of Egr-1, PDGF-B, and TGF-beta(1). Western blotting and immunohistochemistry were used to detect the protein expression of Egr-1, PDGF-B, and TGF-beta(1). The contralateral common jugular vein was used as control. RESULTS: Histological examination showed a great amount of vascular smooth muscle cells (VSMCs) in the tunica intima and tunica media of the vein graft since the 7 th day after the transplantation. mRNA expression of Egr-1, PDGF-B, and TGF-beta(1) was not found in the normal veins. The expression of Egr-1 mRNA in the vein graft showed a biphasic manner: increased remarkably 1 h after the transplantation, decreased during the period 6 h approximately 3 d after, re-increased 7 d after, and peaked 4 weeks after. The mRNA expression of PDGF-B appeared 6 h after, and peaked 2 weeks after, and began to decrease since the 4 th week. The mRNA expression of TGF-beta(1) increased 6 h after, peaked 7d after, and began to decrease 2 weeks after. The protein expression of Egr-1 appeared 2 h after, and peaked 4 weeks after; the protein expression of PDGF-B appeared 6 h after and peaked 4 weeks after; and the protein expression of TGF-beta(1). Appeared 24 h after and peaked 2 weeks after. Immunohistochemistry showed that Egr-1 protein expression was mainly in the VSMCs and monocytes/macrophages in the tunica media in the early stage after transplantation, and peaked 4 weeks later with a positive cell rate of 40% +/- 9%; in the early stage after transplantation PDGF-B protein expression was mainly in the VSMCs in the tunica media, and peaked 4 weeks after with a positive cell rate of 45% +/- 4%; the TGF-beta(1) protein expression peaked 2 weeks after with a positive cell rate of 41% +/- 7%; and 4 weeks after transplantation the protein expressions of Egr-1, PDGF-B, and TGF-beta(1) were all mainly in the VSMCs in the newly-grown tunica intima. CONCLUSION: The IH of vein graft is affinitive with the expression of Egr-1, PDGF-B, and TGF-beta(1). The activation and expression of Egr-1, PDGF-B, and TGF-beta(1) depend on Egr-1 and may contribute to the high expression of Egr1 via a feedback mechanism.

Animals↗

Analysis of microsatellite instability and loss of heterozygosity in human aortic atherosclerotic lesions.

The aim of the present study is to investigate whether microsatellite instability (MSI) and loss of heterozygosity (LOH) are involved in atherogenesis. Paraffin-embedded tissues of thoracic and abdominal aortas were collected from 29 non-neoplastic autopsied cases. We selected two types of atherosclerotic lesions including fibrocellular intimal thickening and uncomplicated atheromatous lesions, and analyzed two sites such as the aortic tunica intima and tunica media in each case. The frequencies of MSI and LOH were highest in the aortic tunica intima of atheromatous lesions and lowest in the aortic tunica media of fibrocellular intimal thickening lesions. Our results suggest that genetic instabilities such as MSI and LOH may be involved in the development of atherosclerotic lesions.

Aged↗

Diabetic macroangiopathy. Quantitative histopathological studies of the extramural coronary arteries from type 2 (non-insulin-dependent) diabetic patients.

A morphometric study was performed on histological sections of the extramural coronary arteries from 10 Type 2 (non-insulin-dependent) diabetic patients and 10 non-diabetic subjects, matched for age and sex. Standardised samples were taken from the two coronary arteries and the fractional contents of Periodic Acid-Schiff-positive material, acid mucopolysaccharides and connective tissue was determined in the arterial tunica media from the two groups using a point-counting technique. The thickness of tunica intima and tunica media was obtained by micrometric measurements. There was no difference in the thickness of tunica intima with and without atherosclerotic plaque between the vessels from diabetic and nondiabetic hearts. However, the thickness of tunica media was significantly reduced in arteries from the diabetic patients (2p less than 0.01). In tunica media of the diabetic patients there was a significant increase (50%) in the amount of Periodic Acid-Schiff-positive material (2p less than 0.01), whereas the content of acid mucopolysaccharides (alcian-blue positive) was significantly reduced (2p less than 0.02). These changes in tunica media were similar in areas below and outside the intimal atherosclerotic plaques. The content of connective tissue was found to be significantly increased in the arteries from the diabetic patients, but only in areas outside atherosclerotic plaques (2p less than 0.025). There was no correlation between the observed changes in tunica media and the known duration of diabetes. The results obtained in the present study may be ascribed to the presence of a non-atherosclerotic diabetic macroangiopathy.

Aged↗

Immunohistochemical studies on the distribution of cellular myosin II isoforms in brain and aorta.

The distribution of nonmuscle myosin isoforms in brain and aorta was studied by using polyclonal antibodies against two synthetic peptides selected from a region near the carboxyl terminus of bovine brain (peptide IIB) and human macrophage (peptide IIA) myosin. Immunoblots of brain homogenates and purified myosin showed two major bands stained by anti-peptide IIB (MIIB1 and MIIB2) and a minor band stained by anti-peptide IIA (MIIA2). Polyclonal anti-human platelet myosin antibodies did not react with MIIB isoforms. In cryosections from bovine, rat, and mouse brains, anti-peptide IIB stained most neuronal cells. In bovine cryosections, glial staining was also observed. In contrast, anti-peptide IIA and anti-platelet myosin antibodies primarily stained blood vessels. In bovine aorta, the anti-peptide antibodies recognized four bands, MIIB3, MIIB4, MIIA1, and MIIA2. Only MIIA2 was recognized by anti-human platelet myosin antibodies. In bovine aorta cryosections, anti-peptide IIB stained smooth muscle cells in tunica intima and tunica media but did not stain endothelial cells. Anti-peptide IIA stained smooth muscle cells in the tunica media, and endothelial cells of vaso vasorum but not of aorta. Only polyclonal anti-platelet myosin antibodies stained the endothelial cells of aorta tunica intima. These results indicate that multiple isoforms of cellular myosins exist in mammals, that these isoforms are expressed in a cell specific manner, and that the major myosin isoforms isolated from whole brain originate from neurons and, at least in bovine brain, from glia, but not from blood vessels.

Amino Acid Sequence↗

A quantitative study of the aorta of the New Zealand rabbit (Oryctolagus cuniculus L.).

Ten segments of the aorta of the rabbit were studied quantitatively. The thoracic and abdominal aorta of the rabbit were measured from proximal to distal and parallel to the reduced diameter, demonstrating a decreasing thickness of the tunica intima and tunica media that becomes physiologically apparent during adulthood in these commonly used laboratory animals. The ratio of intimal to medial thickness, multiplied by 100, was calculated and found to be between 2.56 and 3.74 for the thoracic aorta and 4.03 and 5.62 for the abdominal aorta of the rabbit. These findings are important for the better understanding of the development of atherosclerosis.

Animals↗

Nerve growth factor is expressed in rat femoral vein.

PURPOSE: Entubulization is a well known method of nerve repair for defects too large to be reconstructed by direct suturing without tension. Vein grafts and alloplastic tubes have been used for entubulization in peripheral and cranial nerves, but the mechanism by which they promote healing is poorly understood. The overall hypothesis of this laboratory is that nerve growth factor (NGF) plays an important role in nerve regeneration after entubulization with a vein graft. The purpose of this pilot study was to localize NGF protein expression in the rat femoral vein. MATERIALS AND METHODS: Sciatic nerves and femoral veins were harvested from adult male Sprague-Dawley rats. Femoral arteries were also collected and used for comparison and validation of the analysis. All specimens were fixed in paraformaldehyde and embedded in paraffin. Specimens were either stained with hematoxylin and eosin or used for immunohistochemical reaction with anti-NGF antibody. RESULTS: Sciatic nerve was used as a positive control to identify the monofascicular architecture with hematoxylin and eosin and to document the positive immunohistochemical reaction. NGF immunoreactivity was present in the tunica intima and tunica adventitia of femoral vein and artery but not in the tunica media. CONCLUSION: The results of this pilot study indicate that NGF is detectable in both the intimal and adventitial layers of the rat femoral vein and artery but not in the smooth muscle wall. These findings suggest that vein grafts could potentially promote nerve regeneration by supplying NGF to the injured nerve.

Animals↗

Immunohistochemical detection of apolipoprotein A-I and B-100 in canine atherosclerotic lesions.

We attempt to determine and compare the localization of apolipoproteins (apo) apoA-I and B-100 in atherosclerotic lesions of canine aortas, coronary arteries, and the peripheral arteries, using immunohistochemical techniques. Histopathologically, atherosclerotic lesions were characterized by deposition of lipids and infiltration of lipid-laden foamy cells in the tunica intima and tunica media, sometimes forming fibrofatty plaques containing abundant sudanophilic and mineralized material. Canine apoA (CapoA)-I and canine apoB (CapoB)-100 immunopositive signals were simultaneously observed in mild and severe atherosclerotic lesions of the aorta, coronary arteries, splenic arteries, and renal arteries in the double-immunolabeled sections. Both CapoA-I and CapoB-100 positive signals were seen in the cytoplasm of endothelial cells, smooth muscle cells, and macrophages. The subendothelial space and extracellular matrix in the tunica intima and media were also positive. Neither CapoA-I nor CapoB-100 positive signals were seen in normal arteries. These findings closely resemble those of the localization of apoA-I and apoB-100 in human atherosclerotic lesions.

Animals↗

Remodelling of septal branch of coronary artery and carotid artery in L-NAME treated rats.

Coronary and carotid artery structure was studied in rats in order to analyze the processes in the cardiovascular system in NO-deficient hypertension model. Long-term inhibition of NO synthase was induced by L-nitro arginine methyl ester (L-NAME, 50 mg/kg/day p.o.) for a period of 8 weeks. An increase in blood pressure and heart/body weight ratio confirmed the reliability of the model. The wall thickness as well as the calculated wall area of the coronary artery increased by 70% and 50%, respectively, in comparison to control vessels. The wall thickness and the calculated wall area of the carotid artery increased by 73% and 70%, respectively. Further analysis indicated that both the tunica intima and tunica media in the coronary and the carotid artery increased quantitatively in a similar manner. Remarkable differences were found in the contribution of cellular and noncellular components in the tunica media of the coronary and carotid arteries of experimental animals. The calculated extracellular area increased by 116% in comparison to the control coronary artery and by 97% in comparison to the control carotid artery. The increase in extracellular matrix of the tunica media of coronary and carotid arteries seems to be basic cause of the remodelling of the vessels studied.

Animals↗

Autoradiographic localization of dopamine D1-like receptors in the rabbit pulmonary circulation.

The pharmacological characteristics and the anatomical localization of dopamine D1-like receptors were studied in sections of rabbit lung using [3H]SCH 23390 as a ligand. [3H]SCH 23390 was bound to sections of rabbit lung in a manner consistent with the labelling of dopamine D1-like receptors. The binding was time-, temperature-, and concentration-dependent belonging to a single class of high affinity sites. The dissociation constant value (Kd) was 2.05 nM, whereas the maximum density of binding sites (Bmax) averaged 85 +/- 4 fmol/mg tissue. The pharmacological profile of [3H]SCH 23390 binding to sections of rabbit lung is consistent with the labelling of dopamine D1 receptors. Light microscope autoradiography revealed the development of silver grains which correspond to [3H]SCH 23390 binding sites within the tunica intima and the tunica media of large intrapulmonary artery branches. The presence of silver grains was also observed in the tunica media, but not in the tunica intima of medium-sized pulmonary artery branches. No silver grains were observed in small-sized pulmonary artery branches or in the pulmonary veins. Dopamine D1-like receptors localized in the rabbit pulmonary circulation probably mediate vasodilatation. Further work is necessary to clarify the functional significance of the non-homogeneous distribution of dopamine D1-like receptor sites in the pulmonary circulation.

Animals↗

[Hypoxia-inducible factor 1alpha regulates vascular endothelial growth factor's roles on pulmonary arteries of rats with hypoxia-induced pulmonary hypertension].

OBJECTIVE: To investigate the dynamic expression of hypoxia inducible factor 1alpha (HIF-1alpha) and vascular endothelial growth factor (VEGF) in pulmonary arteries of rats with hypoxia-induced pulmonary hypertension. METHODS: Forty male adult Wistar rats were randomly divided into five groups: a control group (C group) and groups with hypoxia for 3, 7, 14 and 21 days (H(3), H(7), H(14) and H(21) group), eight rats per group. Mean pulmonary pressure (mPAP), vessel morphometry and right ventricle hypertrophy index (RVHI) were measured. Lungs were inflation fixed for in situ hybridization and immunohistochemistry. RESULTS: mPAP increased significantly after 7-day of hypoxia [(18.41 +/- 0.37) mm Hg, P < 0.05], reaching its peak after 14-day of hypoxia, then remained on the high level. Pulmonary artery remodeling index (outer diameter 100 - 150 micro m) and RVHI became evident after 14-day of hypoxia. Expression of HIF-1alpha protein in control group was poorly positive, but was up-regulated in pulmonary arterial tunica intima of all hypoxic rats. In pulmonary arterial tunica media, the levels of HIF-1alpha protein was markedly up-regulated after 3-day (0.178 +/- 0.017, P < 0.05), reaching its peak after 7-day of hypoxia (0.221 +/- 0.021, P < 0.05), then tended to decline after 14-day and 21-day of hypoxia. HIF-1alpha mRNA staining was poorly positive in control, hypoxia for 3 days and hypoxia for 7 days, but began to increase significantly after 14-day of hypoxia (0.203 +/- 0.024, P < 0.05), then remained stable. Expression of VEGF protein began to increase after 7-day of hypoxia (0.074 +/- 0.022, P < 0.05), reaching its peak after 14-day of hypoxia (0.147 +/- 0.017, P < 0.05), then remained on the high level. VEGF mRNA in control and hypoxia for 3 days was poorly positive, but began to increase after 7-day of hypoxia (0.138 +/- 0.010, P < 0.05), and remained on the high level thereafter. VEGF mRNA located mainly in tunica intima and tunica media, whereas VEGF protein located predominantly in tunica intima. Linear correlation analysis showed that HIF-1alpha mRNA, VEGF, and mPAP were correlated with vessel morphometry and RVHI (P < 0.01). HIF-1alpha protein (tunica intima) was positively correlated with VEGF mRNA and protein (P < 0.01). CONCLUSIONS: HIF-1alpha and VEGF are both involved in the pathogenesis of hypoxia-induced pulmonary hypertension in rats. HIF-1alpha protein may regulate the expression of VEGF gene by transcriptional activation, resulting in the occurrence and development of hypoxic pulmonary hypertension.

Animals↗

[Experimental study on cryopreservation of arterial allografts by vitrification].

OBJECTIVE: To evaluate the feasibility of preservation of arteries by vitrification and the effectiveness of vitrified arteries as allografts. METHODS: Sixty rabbits were used in the research. Forty-eight femoral arteries were harvested from 24 rabbits as the transplanted materials,and 24 femoral arteries were preserved by vitrification, 24 by freezing for 14 days, respectively. The other 36 rabbits were used as the transplanted subjects, and were divided into three groups, 12 rabbits including 24 femoral arteries per group: Group A (fresh arterial autografts), Group B (vitrified arterial allografts) and Group C (frozen arterial allografts). The morphologic changes of arterial grafts were observed macroscopically and histologically. The patent rate of arterial grafts were measured by angiography, and the rabbits were sacrificed on the 14th day, the 30th day, the 60th day and the 120th day after transplantation respectively. Arterial grafts were harvested to observe the morphological changes,and the immunological rejection was evaluated by measuring the ratio of tunica intima and tunica media. The results were compared between these groups. RESULTS: Before transplantation, the integrated rate of Group B was 91.67%, which was significantly better than that of Group C (54. 17%, P < 0.01). After transplantation, the accumulative patent rate of Group B was 87.50%, which was significantly better than that of Group C (66.67, P < 0.05). There was statistically significant difference in the ratio of tunics intima and tunica media between Group B and Groups A, C(P < 0.05). CONCLUSION: The above results show that vitrification does less damage to cells and tissues because of ice-free in the process of cryopreservation. So vitrification can be used to preserve arteries, and the arterial allografts preserved by vitrification are better than those preserved by freezing.

Animals↗

Hypoxia-inducible factor-1 alpha regulates the role of vascular endothelial growth factor on pulmonary arteries of rats with hypoxia-induced pulmonary hypertension.

BACKGROUND: Hypoxia-inducible factor-1alpha (HIF-1alpha) is one of the pivotal mediators in the response of lungs to decreased oxygen availability, and increasingly has been implicated in the pathogenesis of pulmonary hypertension. Vascular endothelial growth factor (VEGF), a downstream target gene of HIF-1alpha, plays an important role in the pathogenesis of hypoxic pulmonary hypertension and hypoxic pulmonary artery remodelling. In this study, we investigated the dynamic expression of HIF-1alpha and VEGF in pulmonary artery of rats with hypoxia-induced pulmonary hypertension. METHODS: Forty male Wistar rats were exposed to hypoxia for 0, 3, 7, 14 or 21 days. Mean pulmonary arterial pressure (mPAP), vessel morphometry and right ventricle hypertrophy index (RVHI) were estimated. Lungs were inflated and fixed for in situ hybridisation and immunohistochemistry. RESULTS: mPAP values were significantly higher than the control values after 7days of hypoxia [(18.4 +/- 0.4) mmHg, P < 0.05]. RVHI developed significantly after 14 days of hypoxia. Expression of HIF-1alpha protein increased in pulmonary arterial tunica intima of all hypoxic rats. In pulmonary arterial tunica media, HIF-1alpha protein was markedly increased by day 3 (0.20 +/- 0.02, P < 0.05), reached the peak by day 7, then declined after day 14 of hypoxia. HIF-1alpha mRNA increased significantly after day 14 of hypoxia (0.20 +/- 0.02, P < 0.05). VEGF protein began to increase markedly after day 7 of hypoxia, reaching its peak around day 14 of hypoxia (0.15 +/- 0.02, P < 0.05). VEGF mRNA began to increase after day 7 of hypoxia, then remained more or less stable from day 7 onwards. VEGF mRNA is located mainly in tunica intima and tunica media, whereas VEGF protein is located predominantly in tunica intima. Linear analysis showed that HIF-1alpha mRNA, VEGF and mPAP were correlated with hypoxic pulmonary artery remodelling. HIF-1alpha mRNA was positively correlated with VEGF mRNA and protein (P < 0.01). CONCLUSION: HIF-1alpha and VEGF are both involved in the pathogenesis of hypoxia-induced pulmonary hypertension in rats.

Animals↗

Comparison of left and right vertebral artery intracranial diameters.

BACKGROUND: The vertebral artery is vulnerable to mechanical injury, especially in the region of the first and second cervical vertebrae, with resultant thrombus and/or emboli formation, often found at the vertebro-basilar junction. Such vascular injuries and associated neurological insults have been documented repeatedly in the literature as following cervical spine manipulation, when movements of the head and neck can cause compression and/or stretching of the vertebral artery and alterations in its blood flow. This has particular clinical relevance if a patient has a hypoplastic vertebral artery. Such persons may be considered at risk as regards vascular accidents following manipulation of the cervical spine. The aim of this study was to measure and compare the intracranial diameters of the left and right vertebral arteries in groups of black and white male and female South African subjects. METHODS: Cadaver material from 58 specimens was processed for light microscopy, and measurements of inner (lumen only) and outer (lumen, tunica intima, and tunica media) diameters taken and compared, using the t-test. RESULTS: Data analysis revealed a significant difference between the left and right vertebral artery intracranial diameters in the white female group only (N = 8). CONCLUSIONS: Such a statistically significant difference implies a difference of biological importance and it is suggested that this particular group of subjects may be a high-risk group as regards vascular accidents following cervical spine manipulation.

Black People↗