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PubMed1988

Postnatal development of the innervation and paraganglia in the porcine pulmonary arterial bed.

The innervation of the pulmonary trunk and pulmonary arterial bed was studied in 17 pigs from birth to 6 months of age. After birth, the pulmonary trunk and extra- and intra-pulmonary arteries contained neurofilament and protein gene-product-immunoreactive nerve fibres in both the adventitia and media. The density of nerve fibres increased from birth to 2 months, this being most marked during the first 2 weeks of life. Most of the fibres in the media were presumed to be sympathetic in origin as they contained both neuropeptide tyrosine and tyrosine hydroxylase immunoreactivity. Fibres were associated with the vasa-vasorum and vascular smooth muscle running around the vessel, between the elastic laminae and smooth muscle cells, in the outer two-thirds of the media. Vasoactive intestinal polypeptide and calcitonin gene-related peptide-immunoreactive nerve fibres were found to be associated with the pulmonary trunk and extra-pulmonary artery, but generally not with the intra-pulmonary arteries. Tyrosine hydroxylase immunoreactivity was detected in the glomus cells at birth, but peptide immunoreactivity (enkephalin) was not demonstrated in paraganglia until 14 days of age. Adaptation to extra-uterine life is associated with rapid development changes in the innervation of the pig pulmonary trunk, extra- and intra-pulmonary arteries and in the expression of peptide immunoreactivity in both nerve fibres and glomus cells. These changes may have a role in the postnatal adaptation of the pulmonary circulation.

Aging↗
PubMed2001

Smooth muscle cell modulation and cytokine overproduction in varicose veins. An in situ study.

The exact aetiology and physiopathology of varicose disorders remain unclear. The aim of the present work was to study, in situ, the morphology and composition of cellular and matrix components in varicose veins compared with control veins and to identify factors that could contribute to varicose remodelling. A combined histological, immunohistochemical, and biochemical approach was used. Longitudinal sections of varicose (n=12) and control veins (n=9) were studied to assess the organization, structure, and phenotype of smooth muscle cells; the localization of microvascular endothelial cells; the distribution of connective tissue proteins; and the localization of cytokines. These cytokines were further quantified by ELISA. Considerable heterogeneity of the varicose vein wall was observed, with a succession of hypertrophic and atrophic segments, presenting severe disorganization of the medial layer and numerous areas of intimal thickening. In hypertrophic portions, medial smooth muscle cells showed marked alterations suggesting modulation from a contractile to a proliferative and synthetic phenotype; furthermore, the number of vasa vasorum was increased. In contrast, in atrophic portions, both cellular and matrix components were decreased. TGFbeta1 (p< or =0.005) and bFGF (p< or =0.001) were increased and VEGF was not significantly modified in varicose veins when the results were expressed per mg of DNA. These results show that phenotypic modulation of smooth muscle cells, altered extracellular matrix metabolism, and angiogenesis are the main mechanisms contributing to the morphological and functional modifications of varicose remodelling. The increased expression of bFGF and TGFbeta1 by varicose vein cells may play a pivotal role in the hypertrophy of the venous wall, but the exact mechanism leading to aneurysmal dilatations remains to be elucidated.

Adult↗
PubMed1997

Efficient in vivo gene transfer into the heart in the rat myocardial infarction model using the HVJ (Hemagglutinating Virus of Japan)--liposome method.

The lack of efficient treatment for myocardial infarction remains an unresolved problem in the field of cardiovascular disease. Gene therapy may be a potential therapeutic strategy for the treatment of myocardial infarction. However, current methods of in vivo gene transfer into the heart are limited by their low efficiency and/or potential toxicity. In the present study, we developed an efficient technique of gene transfer into the intact heart in vivo using the Sendai virus (HVJ: Hemagglutinating Virus of Japan)--liposome method. We used the beta-galactosidase gene, luciferase gene and human angiotensin converting enzyme (ACE) gene as markers. In vivo gene transfer into the rat heart was performed as follows: (1) direct injection into the rat heart, (2) incubation within the pericardium, and (3) infusion into a coronary artery. Direct injection of the HVJ-liposome complex containing the beta-galactosidase vector into the rat heart resulted in limited staining of beta-galactosidase 3 days after transfection. To compare transfection efficiency between "naked" plasmid DNA transfection and the HVJ-liposome method, we also transfected the luciferase reporter gene into the heart. Luciferase activity was significantly higher in hearts transfected by the HVJ-liposome method than that in hearts transfected by direct "naked" plasmid transfection (P < 0.01). To confirm the successful gene in the protein level, we measured ACE activity in the hearts. Cardiac ACE activity was significantly increased in hearts transfected with human ACE gene as compared to hearts transfected with control vector (P < 0.01). On the other hand, incubation of HVJ-liposome complex, containing beta-galactosidase vector, within the pericardium resulted in widespread staining of cardiac myocytes and fibroblasts, mainly located in several surface layers beneath the pericardium. More importantly, widespread stained areas of beta-galactosidase were also observed in the middle of the myocardium around the vasa vasorum. We also examined the efficiency of gene transfer by the HVJ-liposome method in a rat myocardial infarction model. In the infarction model, using the pericardium incubation approach, staining for beta-galactosidase was observed in the viable cells around the infarction area. Finally, direct infusion of the HVJ complex, containing the beta-galactosidase vector, into coronary artery also resulted in widespread staining of beta-galactosidase in cardiac myocytes around the microvasculature. Using direct injection, we found significant injury to the myocardium and severe fibrosis at the injection site, whereas no apparent injury was observed using pericardium incubation and coronary infusion. There was no evidence of cytotoxicity or inflammation caused by the HVJ-liposome complex itself. Overall, we have established an efficient in vivo gene transfer method into the heart using the HVJ-liposome method. Direct infusion into the coronary artery resulted in widespread transfection without damaging the myocytes; incubation within the pericardium demonstrated the usefulness of the HVJ-liposome method for studying cardiac function and as a means of gene therapy for cardiovascular diseases.

Animals↗
PubMed1995

Healing comparison of small intestine submucosa and ePTFE grafts in the canine carotid artery.

Continuing investigation of small-diameter vascular graft materials suggests that unacceptable graft complications continue and that the ideal material has not yet been found. We compared healing of xenogeneic small diameter grafts (3.5 to 5.0 mm diameter) made from porcine small intestine submucosa (SIS) implanted in the carotid artery to expanded polytetrafluorethylene (ePTFE) in the contralateral carotid in 8 dogs. Two dogs were sacrificed for graft evaluation at 7, 28, 90, and 180 days after surgery. Only one SIS graft was occluded at 28 days and the other 7 were patent. Six of 8 ePTFE grafts were occluded with thrombi. One was patent at 7 and one at 90 days. At 7 days post-implant, the luminal surface of the SIS graft was covered by a thick (30 microns), compact fibrin meshwork. By 28 days endothelial cells were seen completely covering the fibrin meshwork which stained for FVIII-related antigen. Smooth muscle cells were observed in the neo-intima. Most ePTFE grafts had fibrin on the luminal surface which formed fibrin thrombi with platelets and numerous red blood cells. Complete endothelial coverage of the ePTFE grafts was not observed by 180 days. There was not a pronounced neointima seen on the luminal surface of the graft. The vasa vasorum was present in the fibrous capsule surrounding the ePTFE graft, but it did not penetrate into the graft as seen in the SIS graft. At 90 days the SIS vascular graft had the histological appearance similar to a normal artery. The SIS graft potency and healing characteristics were superior to the synthetic ePTFE graft and warrant further investigation.

Animals↗
PubMed1992

IDL, VLDL, chylomicrons and atherosclerosis.

In humans with the lipoprotein lipase deficiency disorder large amounts of chylomicrons and large very low-density lipoprotein (VLDL) accumulate in plasma. In spite of this, atherosclerosis does not seem to develop at an accelerated rate, suggesting that these lipoproteins do not promote atherogenesis. In humans with dysbetalipoproteinemia remnant lipoproteins (intermediate density lipoprotein (IDL) plus beta-VLDL) accumulate in plasma and these particles may therefore be the factor causing accelerated atherosclerosis in this disorder. Epidemiological studies in humans suggest that IDL or remnant lipoproteins are predictors of the severity or progression of atherosclerosis. Similar studies in the St. Thomas' Hospital rabbit strain, an animal model with genetically elevated plasma levels of VLDL, IDL and low-density lipoprotein (LDL), showed that IDL or remnant lipoproteins were better predictors of the extent of atherosclerosis than were LDL or VLDL. Studies of lipoprotein/arterial wall interactions have demonstrated that the larger the lipoprotein particle, the lower the influx into intima. Very large VLDL and chylomicrons do not seem to enter intima. Although high-density lipoprotein (HDL) enters intima faster than other lipoproteins, the small HDL particles seem to penetrate the entire arterial wall and leave via lymphatics and vasa vasorum in the outer media and adventitia. In contrast, LDL, and possibly also IDL and smaller VLDL, may only leave the intima via the lumen of the artery. In conclusion, a substantial body of evidence suggests that remnant lipoproteins (IDL and smaller VLDL) share with LDL the potential for promoting atherosclerosis, whereas very large VLDL and chylomicrons do not seem to have this effect.

Animals↗
PubMed1978

Sympathetic innervation of the pulmonary artery, ascending aorta, and coronar glomera of the rabbit. A fluorescence microscopic study.

Adrenergic nerve fibres were demonstrated in the connective tissue of the rabbit coronar glomera by means of the formaldehyde-induced fluorescence technique for catecholamines. This type of innervation is similar to the adrenergic nerve supply to the rabbit and cat carotid body. Adrenergic fibres terminate subendothelially and only a few can be traced to type I cells in the glomera coronaria. The sympathetic innervation of the ascending aorta is exceedingly sparse in contrast to the pulmonary trunk, while vasa vasorum of the ascending aorta exhibit a dense sympathetic innervation.

Animals↗
PubMed1978

The innervation and fine structure of paraneuronic cells in an amphibian pulmonary artery.

The pulmonary artery of Bufo marinus contains large numbers of bipolar cells situated in the tunica adventitia and in the outer layers of the media. These cells show a bright green-yellow fluorescence (emission spectra 485 nm) after formaldehyde pre-treatment suggesting that they contain a primary monoamine. The most characteristic fine-structural feature of these cells is the presence of numerous dense-cored vesicles (80--300 nm diameter) in their cytopalsm. The cells are in close contact (20 nm gap) with both agranular and granular nerve fibres. Both EM-cytochemical and formaldehyde-induced fluorescence tests indicate that the granule-containing nerve fibres are adrenergic. The agranular nerve fibres form discrete synaptic contacts with pre and post-synaptic membrane thickenings on the cells. This was never observed with respect to the adrenergic fibres. Each process of the cells is about 45 micrometer long. The processes do not bear any special relationship to either vessels of the arterial vasa vasorum or medial smooth muscle cells. Their location in the wall of the artery suggests that they are functionally significant with respect to activity of the arterial media.

Animals↗
PubMed1978

Fine structural and cytochemical study of the innervation of smooth muscle in an amphibian (Bufo marinus) lung before and after denervation.

The innervation of the toad (Bufo marinus) lung was studied with transmission electron microscopy and fluorescence techniques, both before and after 12 or 20 days close vagosympathetic denervation. Four cytologically distinct types of neuronal processes were recognised, in relation to the visceral muscles of the lung. These were described as cholinergic, adrenergic, non-adrenergic/non-cholinergic (NANC) and sensory on the basis of the characteristics of their vesicular content and cytochemical reactions. An apparent efferent innervation of visceral smooth muscle was achieved by NANC (50%), cholinergic (25%) and adrenergic (25%) fibres. A few sensory fibres were also present. After denervation only NANC fibres persisted, showing that the cell bodies of these fibres were intrapulmonary. The vascular smooth muscle was supplied by cholinergic, adrenergic and sensory fibres. In the walls of the proximal branches of the pulmonary artery were fibres containing large dense-cored vesicles. These profiles, which were associated with the vasa vasorum, were similar to neurosecretory fibres. After denervation all neural profiles associated with the vasculature had degenerated. The observations suggest that vagal vasodepressor effects in the toad lung are mediated indirectly through relaxation of visceral muscle strands which in their contracted state compress vascular channels.

Adrenergic Fibers↗
PubMed1984

Localization of proteoheparan sulfate in rat aorta.

This study describes the distribution of heparan sulfate proteoglycan ( HSPG ) within the rat aorta using immunocytochemical (biotin-avidin-peroxidase) and immuno-electron microscopy (125I-autoradiography). Heparan sulfate proteoglycan was isolated from a basement membrane producing mouse EHS sarcoma ( Hassell et al. 1980) and used to generate antisera in rabbits. Light microscopic observations revealed intense immunostaining of the intima and media of normal aorta, adventitial vasa vasorum, and aortic intimal fibromuscular thickenings induced by experimental injury (balloon de-endothelialization). Immunoelectron microscopy using 125I labeled antibodies to HSPG revealed that proteoheparan sulfate was localized to the amorphous layer of basement membrane below aortic and capillary endothelium. In addition, labeled anti- HSPG could be localized to the external lamina surrounding the smooth muscle cells in the hyperplastic intima. These studies reveal that antibodies prepared against a proteoheparan sulfate isolated from a basement membrane producing EHS sarcoma cross react with basement membrane structures within the aortic wall. Furthermore, these results demonstrate that the basement membranes beneath aortic and capillary endothelium and the external lamina surrounding aortic smooth muscle cells contain a heparan sulfate proteoglycan that is antigenically similar.

Animals↗
PubMed1991

Acquired mural (dural) arteriovenous shunts of the vein of Galen. Report of 4 cases.

4 patients with acquired arteriovenous shunts located in the wall of an ectatic vein of Galen (VG) are reported. They represent so-called VG dural arterio-venous malformations (DAVM). These shunts involve the vasa vasorum normally present in the VG wall. Physiopathology, clinical signs and age groups are usually the same as those encountered in other DAVMs; conversely they are totally different from the other mural shunts of the VG, detected in the pediatric population (true VG arteriovenous malformations), and leading to different clinical symptoms. Venous approach in these VG DAVMs is almost always contraindicated unless secondary occlusion of VG afferent has spontaneously excluded the pouch from the cerebral venous circulation.

Adult↗
PubMed1982

Histological change in permanently clipped or ligated cerebral arterial wall. Part I. An experimental study in dogs.

In this paper, we discuss the results of a study by light microscope of the effect of permanent clipping or ligation on the intracranial arteries of 38 operation dogs and 7 control dogs. The findings obtained are: 1. In the cerebral arterial circle, necrosis could easily result from ordinary clipping or ligation because of scarce vasa vasorum. 2. As for the incidence of necrosis, the greatest was found in the case of the Yaşargil clip after electric coagulation, next came the Yaşargil clip alone, next ligation, and last the silver clip. The degree of necrosis correlated with the duration of clipping in the cases treated with a spring type clip, and was influenced more by the closing strength at the time of application in the cases with non-spring type clips or ligation. 3. In some of the cases ligated for long duration, recanalization was caused by the passage of the ligature through the vessel wall, suggesting that ligation is not a certain procedure if it is applied alone. 4. The granulation tissue round the clip and ligature began to grow after one month. As for its degree, the most marked granulation was that caused by the silver clip, next the ligature, than the Yaşargil clip after electric coagulation, and finally the Yaşargil clip used normally; in all of them the correlation with the passage of time was noted. 5. In the group of duration three months or more, concentric intimal proliferation was noted peripheral to the clip, and intimal proliferation was also noted exclusively localized to the side of a branch on the central or truncal side of a clip. This correlated in degree with the passage of time. 6. Clipping and ligation are liable to cause necrosis and fragmentation, but on the other hand it was considered that rupture of the vessel wall did not result because of the reinforcing and reparative effect of the reactive granulation tissue and the intimal proliferation which developed in such a manner as to strengthen the area involved.

Animals↗
PubMed1978

Histological and ultrastructural study of intracranial saccular aneurysmal wall.

The material studied consists of 10 cases of intracranial saccular aneurysms. Four came from autopsies, and in each of the other six aneurysmal wall was obtained at surgery after clipping of the aneurysm. The most significant findings from this pathological study are the almost complete disappearance of the internal elastic lamina at the level of the aneurysmal neck, sclerosis of the muscle coat, and in satellite vessels and vasa vasorum disruption of the internal elastic lamina and partial luminal occlusion. The importance of ischaemic changes in the aneurysmal wall is discussed. Rupture of the aneurysm at the distal extremity of the sac depends probably on the progressive brittleness of its wall which becomes sclerotic and less resistant to the blood pressure within. Splitting or rupture of the aneurysm appears to be dependent on degenerative ischaemic alterations in its wall.

Adult↗
PubMed1992

Pathological studies on Takayasu arteritis.

Takayasu arteritis is a primary inflammatory disease of elastic arteries such as the aorta, its larger branches and the pulmonary artery trunk. According to our recent statistical survey of autopsy cases in Japan, the frequency of the disease in all autopsy cases was approximately 0.033% and the sex ratio was 1:4.5. The most frequent ages of the onset were 20-30 years, those of the death were 40-50 years. The latter was delayed about 20 years in comparison with a previous report. In the recent cases, the vascular lesions widely expanded. Luminal dilatation and aneurysm formation also increased in frequency, their ratio being approximately 57%. In the autopsy cases, the following active lesions were observed: (1) acute exudative inflammation (including suppuration), (2) chronic non-specific productive inflammation and (3) various types of granulomatous inflammation. These findings suggest that many triggers may play a role in the morphogenesis of Takayasu arteritis. The inflammatory lesions are produced in the media and adventitia through the vasa vasorum, and terminate in a diffuse or nodular fibrosis. New active lesions are often observed near the old fibrotic ones. This suggests that Takayasu arteritis may be a progressive disease. Intimal thickening of the peripheral branches from the affected arteries is very often observed. In consequence, secondary ischemic lesions are formed in various organs, especially the heart, brain and kidneys.

Adolescent↗
PubMed1986

Immunohistochemical evidence for mast cells containing 5-hydroxytryptamine in rat portal vein.

Serotonin was localized to mast cells in the adventitia of the rat portal vein by indirect immunohistochemistry. The mastocytes where preferentially localized to a region delimited by the pyloric and splenic veins. Since neither 48/80 nor reaginic antibody induced a significant change in the intrinsic spontaneous activity of the portal vein it would appear that the mast cells are not involved in a direct vasomotor function. It is suggested that amines released from the mastocytes could regulate blood flow in the vasa vasorum and/or have a role associated with the sensory functions displayed by this vein.

Animals↗
PubMed1992

Atraumatic vascular anastomoses using a tourniquet.

Because of the occurrence of stenoses just beyond the distal anastomosis, lower leg exsanguination and the use of a mid-thigh tourniquet was adapted. From July 1, 1988 until June 30, 1990, 75 primary operations and 18 secondary operations on failing bypasses were performed using this technique. The primary operations were to the below-knee popliteal (4), anterior tibial (19), posterior tibial (16), peroneal (26), and inframalleolar arteries (10). The proximal anastomoses were also done while the tourniquet was inflated in 11 cases (three tibio-tibial and eight from the popliteal below the knee). Of the secondary procedures, 15 were patch angioplasties and three were distal extensions. The cuff was inflated to 400 mmHg from 22 to 73 minutes. This technique offers numerous advantages: only enough arterial surface is dissected for the anastomoses to be performed. Veins and arterial branches are left intact, thus decreasing the risk of bleeding. The artery is left in its bed to preserve its vasa vasorum. The lumen is not obliterated by clamps assuring the best anastomosis. Since there are no clamps in the field, suturing is less difficult. The tourniquet facilitates a faster, drier operation. No stenoses have been noted in the arteries just distal to the anastomoses on follow-up showing the value of atraumatic occlusion, especially on small vessels. No inflow stenoses occurred in the area under the tourniquet if the artery was patent at the time of operation.

Arteriovenous Shunt, Surgical↗
PubMed1980

Comparative study on the fibrinolytic activity of pseudointima in varying types of autovein grafting.

Three types of autovein grafting procedures have been commonly employed for peripheral arterial reconstruction, that is, non-reversed, reversed and in-situ autovein grafting, and these procedures were comparatively studied in dogs to assess the best one for grafting. In the fibrinolytic activity of the internal surface of the grafts, as measured by standard fibrin plate method and Todd's fibrin slide technique, the in-situ autovein graft showed the highest activity, 139.5% in the mean, followed by 18% (mean) in the reversed autovein graft and 5.2% (mean) in the nonreversed autovein graft. The extent of fibrous proliferation of the pseudointima was least in the in-situ graft followed by the reversed and the non-reversed graft. These results suggest that preservation of the vasa vasorum is the most important factor to minimize fibrous proliferation of the graft pseudointima and to maintain high fibrinolytic activity on the internal surface of the graft. Consequently, the in-situ autovein grafting appears to be the most suitable method to ensure peripheral arterial continuity following surgical reconstruction.

Animals↗
PubMed1986

Percutaneous laser treatment of atherosclerosis: an overview of emerging techniques.

In recent years, rapid progress in the application of lasers to the percutaneous treatment of atherosclerosis has been made. An overview of this progress is provided herein in terms of a description of promising laser approaches and problems to be solved. Direct vaporization of obstructing atheroma with fiberoptic delivery of laser energy has been associated with a high incidence of mural perforation, but each of a variety of techniques, including those for improved energy delivery, plaque recognition, alignment of the fiberoptic, and, perhaps, reduction of unnecessary thermal injury, has shown promise for reducing this complication. Nonablation applications of laser energy may also have a role in the treatment of atherosclerosis. During laser balloon angioplasty, the tissue coagulation effects of laser-thermal energy may be used during balloon inflation to eliminate arterial dissections and to reduce elastic recoil, thereby potentially eliminating abrupt reclosure and, perhaps, reducing the incidence of restenosis associated with conventional balloon angioplasty. Photochemical destruction of viable plaque tissue and vasa vasorum with porphyrins and intraarterial light represents a nonthermal, laser-based approach that could have a prophylactic role in slowing progression of diffuse atherosclerotic disease. The remarkable versatility of lasers is responsible for the multiplicity of approaches being investigated and for the current optimism that lasers will eventually play an important role in the percutaneous treatment of atherosclerosis.

Angioplasty, Balloon↗
PubMed2001

[Aortic rupture in Behçet's disease].

Behçet's disease is a vasculitis of unknown aetiology, which becomes apparent by ocular and mucocutaneous symptoms. In rare cases, owing to vasculitis of the vasa vasorum of large arteries, necrosis of the vascular wall and thus spurious aneurysms occur. The case of a 41-year-old patient is described who presented with a rupture of an infrarenal aortic aneurysm due to Behçet's disease. Therapy consisted of placement of an aortic-aortic Dacron prosthesis. On the basis of the case report, the diagnostic approach, the therapy and the value of secondary prophylaxis of Behçet's disease are discussed.

Adult↗