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PubMed2001

Influence of long-term experimental orthostatic body position on innervation density in extremity vessels.

The aim of this study was to quantitate the density of nerve terminals as well as their synaptic vesicle population in the adventitia of saphenous (SV and SA) and brachial veins and arteries (BV and BA) obtained from rats maintained in a horizontal control or a tilted position. Adult animals were kept individually in tube-like cages in a 45 degrees head-up position. After 2 wk, both tilted and control animals were anesthetized, and the whole body was perfused with fixative solution at physiological pressure. Vessels segments were then excised for electron microscopy and immunohistochemistry. The nerve terminal density (NTD) of SA was 8.20 +/- 1.46 nerve terminals/100 microm(2) cross section of adventitia and that of SV was 4.53 +/- 0.61 nerve terminals/100 microm(2) cross section of adventitia in control rats. Tilting caused a significant increase in NTD of both SA (70%) and SV (52%). The synaptic microvesicle density (SyVD) was larger in SA than SV in control rats (30.48 +/- 4.41 vs. 13.38 +/- 2.61 synaptic vesicles/10 terminal sections), but tilting resulted in more pronounced changes in SyVD of SV (95%) than SA (54%). No significant changes in NTD and SyVD of BA were found after tilt (-3.6% relative to 4.99 +/- 0.33 compared with 0.4% relative to 24.89 +/- 3.7, respectively). Whereas NTD of BV exhibited a tendency to increase (3.73 +/- 0.86 vs. 2.31 +/- 0.29 nerve terminals/100 microm(2) cross section of adventitia), SyVD did not change significantly (18.96 +/- 2.74 vs. 22.85 +/- 3.17 synaptic vesicles/10 terminal sections). A large number of nerve terminals of all vessels were tyrosine hydroxylase immunoreactive (containing norepinephrine). These findings support the hypothesis that long-term gravitational load causes adaptive morphological and functional remodeling of sympathetic innervation in blood vessels of the extremities.

Animals↗
PubMed2000

Rho-kinase is involved in macrophage-mediated formation of coronary vascular lesions in pigs in vivo.

We have previously shown that long-term treatment with an inflammatory cytokine from the adventitia causes the development of coronary vascular lesions, with the accumulation of macrophages. Recent studies in vitro have suggested that small G-protein Rho and its effector, Rho-kinase/ROK/ROCK, may be the key molecules for various cellular functions, including cell adhesion and movement. In this study, we examined whether adventitia-derived macrophages cause the formation of coronary vascular lesions in vivo and, if so, whether Rho-kinase is involved in the process. Porcine coronary segments from the adventitia were chronically treated with monocyte chemoattractant protein-1 alone, oxidized low density lipoprotein alone, or both. Vascular lesion formation (neointimal formation and development of vascular remodeling) was mostly enhanced at the coronary segment cotreated with monocyte chemoattractant protein-1 and oxidized low density lipoprotein, where the phosphorylation of myosin binding subunit of myosin phosphatase was increased, indicating an increased activity of Rho-kinase in vivo. Histological examination demonstrated that macrophages were accumulated at the adventitia and thereafter migrated into the vascular wall. Long-term oral treatment with fasudil, which is metabolized to a specific Rho-kinase inhibitor (hydroxyfasudil) after oral absorption, markedly inhibited the myosin binding subunit phosphorylation, the macrophage accumulation and migration, and the coronary lesion formation in vivo. These results indicate that Rho-kinase is involved in macrophage-mediated formation of coronary vascular lesions in our porcine model in vivo.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed2000

Hypercholesterolemia superimposed by experimental hypertension induces differential distribution of collagen and elastin.

We studied the mural distribution of collagen types I and III and tropoelastin in enhanced experimental atherogenesis induced in rabbits by hyperlipidemia superimposed by hypertension. Animals were fed a high-cholesterol diet for 5 weeks and also subjected to midthoracic aortic coarctation for 4 weeks. Serum cholesterol levels were increased and blood pressure was elevated proximal to the coarctation. Foam cell lesions developed in the aorta proximal to the coarctation. In situ hybridization and immunohistochemistry showed that gene expression of collagen types I and III and tropoelastin was upregulated, with a differential distribution across the arterial wall. New collagen type I was mainly distributed in the intima, the outer media, and the adventitia. New collagen type III was spread more uniformly across the wall, including the adventitia, whereas tropoelastin was mainly localized in intimal foam cell lesions. Morphometric data showed an increase in wall thickness. These results suggest that collagen types I and III play a role in remodeling of the aortic wall in response to hypertension. The remarkable involvement of the adventitia in this response indicates that the adventitia is an important component of the arterial wall. Tropoelastin is closely associated with foam cell lesion formation, suggesting a role for this component in atherogenesis as well.

Animals↗
PubMed2000

Adventitial mast cells connect with sensory nerve fibers in atherosclerotic coronary arteries.

BACKGROUND: The number of activated mast cells is increased in the adventitia of coronary segments with plaque rupture and in spastic atherosclerotic coronary segments. Neurogenic activation of mast cells has been demonstrated previously in other tissues. Here we identified and quantified contacts between mast cells and nerves in the adventitia of normal and atherosclerotic coronary segments. METHODS AND RESULTS: Normal (types 0 or I) and atherosclerotic (lesion types II, III, and IV) coronary segments from 22 unselected autopsy cases were stained for mast cells and sensory nerves by a histochemical double-labeling method. Contacts between mast cells and sensory nerves were quantified morphometrically and also identified by confocal microscopy. Coronary arteries obtained during heart transplantation were stained for the neuropeptides capable of stimulating mast cells, ie, substance P and calcitonin gene-related peptide. In the adventitia of atherosclerotic coronary segments with type IV lesions, the numbers of mast cells and mast cell-nerve contacts (104+/-15 mast cells/mm(2) and 30+/-5 nerve contacts/mm(2); mean+/-SEM) were significantly greater than in segments with type III lesions (79+/-12 [P<0.001] and 24+/-6 [P<0.001]), those with type II lesions (54+/-4 [P<0.001] and 12+/-2 [P<0.001]), or those with normal intima (31+/-3 [P<0.001] and 4+/-1 [P<0.001]). The nerve fibers connected with mast cells contained both substance P and calcitonin gene-related peptide, which identified them as sensory nerves. CONCLUSIONS: Neurogenic stimulation of mast cells in the adventitia of coronary arteries may release vasoactive compounds, such as histamine and leukotrienes, which can contribute to the complex neurohormonal response that leads to abnormal coronary vasoconstriction.

Calcitonin Gene-Related Peptide↗
PubMed1999

Paracrine role of adventitial superoxide anion in mediating spontaneous tone of the isolated rat aorta in angiotensin II-induced hypertension.

The relationship between vascular generation of superoxide anion and spontaneous tone observed in the isolated aorta was studied in hypertensive rats infused with angiotensin II. Aortic rings from hypertensive, but not from sham-operated rats, demonstrated oscillatory spontaneous tone that represented 52+/-5.6% of the maximal contraction to KCl. Spontaneous tone was prevented by calcium-free buffer or by blocking calcium influx through L-type calcium channels with nifedipine. The production of superoxide anion measured by lucigenin chemiluminescence was up to 15-fold higher than in sham-operated rat aorta. The adventitial site of production of superoxide anion was suggested by the fact that lucigenin chemiluminescence was 5.5-fold higher from the adventitia than from the intima. This was confirmed histochemically by demonstrating that the adventitia was the site of reduction of nitroblue tetrazolium as well as immunohistochemical staining of NAD(P)H oxidase subunit proteins. A causal link between superoxide anion production by NAD(P)H oxidase and the spontaneous tone is suggested by the fact that superoxide dismutase or the inhibitor of NAD(P)H oxidase, diphenylene iodonium, decreased both superoxide anion production and spontaneous tone. L-NAME or removal of the endothelium from the aorta had no significant effect on superoxide anion levels or spontaneous tone. However, although superoxide dismutase decreased superoxide anion levels in the presence of L-NAME or in endothelium-denuded rings, it no longer inhibited the tone. This suggests that the effect on tone of superoxide anion originating in the adventitia is mediated by inactivating endothelium-derived nitric oxide, which promotes smooth muscle calcium influx and spontaneous tone. The adventitia is not a passive bystander during the development of hypertension, but rather it may have an important role in the regulation of smooth muscle tone.

Acridines↗
PubMed1980

Morphological study on experimental cerebral vasospasm. II. Fluorescence microscopic examination on experimental cerebral vasospasm.

Basilar arteries with experimental vasospasm were studies histochemically using a catecholamine fluorescence technique in 15 cats. Fluorescence microscopy of normal vessels revealed abundant catecholamine fluorescence in the adventitia and in close contact with the media, but none within the media. Experimental subarachnoid hemorrhage resulted in depletion of catecholamine fluorescence in the adventitia and in its appearance in the media. In vessels with vasospasm which lasted for 2 or 5 h and responded to vasodilators, fluorescence was scarce in the adventitia, but abundant in the media. In vessels with vasospasm unresponsive to spasmolytic agents, fluorescence was observed neither in the adventitia nor in the media. The results suggest that noradrenaline in the media of spastic arteries plays an important role in the development of cerebral vasospams.

Animals↗
PubMedDate not supplied

Investigation about origin and spreading of neoendothelium in autologous arterial vessel replacement.

INTRODUCTION: In many fields of surgery an autologous arterial vessel replacement is used. Because of trauma and insufficient nutrition, a loss of complete endothelium in the replaced vessel segment and at the anastomoses can be observed within a few hours. The origin and the spread of the neoendothelium are unknown. Our study uses Von-Willebrand-protein, a product of endothelium cells, as a marker to obtain new information about the origin and spread of the new endothelial cells. MATERIALS AND METHODS: Seventy Wistar rats, seven groups of 10 animals each, were operated. A four-millimetre-long segment of the common carotid artery was isolated and reinserted. After a varying length of time (between directly after the operation and six months after), the common carotid artery including bifurcation was isolated after cardioperfusion. Carotid arteries were embedded and cross-sections were stained with hematoxylineosin, Verhoeff's tissue elastin stain and immunohistochemical anti-Von-Willebrand-factor-antibody. The complete vessel was divided into nine points of measurement on each side, three points at each anastomosis and three points in transplanted segment. There the number of positive endothelial cells was rated. RESULTS: Twenty-four hours after the operation no further endothelium was detectable in autologous transplant. Stainings eight days after operation contained Von-Willebrand-factor-positive cells in luminal cell layers. Near to the anastomosis excessive myointimal hyperplasia was detectable. Also, eight days after operation, some positive endothelial cells in adventitia were seen near to the anastomosis in small vessel lumina. Four weeks after operation, the luminal endothelium was completely regenerated and the luminal endothelial layer was confluent. Eight days after the operation regeneration in lateral regions was faster than in the region of the transplant. CONCLUSION: In our experiment regeneration in lateral regions was faster than in the region of the transplant. Early staining in adventitia and proof of newly formed vasa vasora in adventitia may be a sign of a possible migration from adventitia to luminal area.

Anastomosis, Surgical↗
PubMed2004

[Effect of castration on restenosis after precutaneous transluminal angioplasty in male rats].

OBJECTIVE: To observe the developing changes of adventitia in restenosis after precutaneous transluminal angioplasty(PTA), and investigate the effect of androgen on restenosis through contrasting the castrated male rat models and its mechanism. METHODS: Models were constructed of castrated male rats and restenosis of the common carotid artery, and specimens were collected at the 3rd, 7th, 14th and 28th day respectively after modeling. Hematoxylin and eosin staining, immunohistochemical staining, and electronic microscopy were performed to observe the condition of restenosis. RESULTS: Proliferating cells occurred in adventitia first and phenotype of adventitial cells was changed at the 3rd day after PTA. The adventitial proliferating index was the highest at the 7th day after PTA, and proliferating migration towards intimal was observed. The proliferating cells mostly occurred in the middle layer and neointima at the 14th day after PTA. The areas of adventitia and neointima were larger and the degrees of restenosis were higher in the castrated rats than in the non-castrated ones at different time points. Take the 14 d group, the adventitial area was[(3,566 +/- 337) micron2 vs (2,751 +/- 401) micron2, P = 0.008], the neointimal area[(3,553 +/- 477) micron2 vs (2,757 +/- 435) micron2, P = 0.025], the restenosis rate[(76 +/- 2)% vs (60 +/- 8)%, P = 0.005], and the proliferating index [(29 +/- 2)% vs (13 +/- 1)%, P < 0.001]. CONCLUSION: Adventitial proliferation and migration contribute to restenosis after PTA; Androgen in rats can physiologically relieve restenosis, probably through intervening in the activation of adventitia.

Actins↗
PubMed1992

Electron microscopic observations of elastic fibres in the lung and aorta of tight-skin and beta-aminopropionitrile-fed mice.

The lung of the tight-skin (TSK) mouse was characterized by enlargement of the air spaces. Elastin in the alveolar walls of the TSK mouse exhibited fragmentation. The aorta of the TSK mouse was characterized by marked hyperplasia of loose connective tissue in the adventitia. Collagen fibres and ruthenium red-positive materials were markedly increased. Microfibrils surrounding elastin in the adventitia of the aorta were not clear in the TSK mouse. In the lung of the beta-aminopropionitrile (BAPN)-fed mouse, enlargement of the alveolar air spaces was not prominent compared with the TSK mouse. Elastic fibres in the alveolar walls did not show the fragmentation observed in the TSK mouse, and microfibrils surrounding elastin were clearly observed. However, elastic laminae in the media of the BAPN-fed mouse aorta were swollen and fragmented. Elastic fibres in the adventitia exhibited a normal appearance and microfibrils surrounding elastin in the adventitia were clearly observed. The results suggest that the mechanism of the connective tissue abnormality in the TSK mouse is different from that of BAPN, which inhibits the activity of lysyl oxidase. The abnormality of elastin and microfibrils surrounding elastin in the TSK mouse probably plays a role in the deformity or degradation of elastic fibres and the structural changes of the lung.

Aminopropionitrile↗
PubMed1990

Human abdominal aortic aneurysms. Immunophenotypic analysis suggesting an immune-mediated response.

Cellular immunity may play a role in the pathogenesis of atherosclerosis. In this report the potential role of these cells in the formation of abdominal aortic aneurysms by immunohistochemistry was investigated. Aortic tissues from 32 patients were examined: 4 normal aortas, 6 aortas with occlusive atherosclerotic disease, 17 abdominal aortic aneurysms, and 5 inflammatory abdominal aneurysms. Using monoclonal anti-CD3 (T cells), anti-CD19 (B cells), anti-CD11c (macrophages), anti-CD4 (T helper cells), and anti-CD8 (T suppressor cells), several distinctions among these groups were found. The amount of inflammatory cell infiltrate was as follows: inflammatory aneurysms more than abdominal aortic aneurysms more than occlusive aortas more than normal aortas. CD3-positive T lymphocytes rarely were found in the adventitia of normal or occlusive aortas. In contrast, abdominal aortic aneurysms and inflammatory aneurysms exhibited most of the CD3-positive infiltrates in the adventitia. CD19-positive B lymphocytes were present mainly in the adventitia of all pathologic tissues. The CD4-positive:CD8-positive ratio was greater in abdominal aortic aneurysms and inflammatory aneurysms than in the other groups, both in the adventitia and in the media of the aortas. CD11c-positive macrophages were present throughout the diseased tissues, often surrounded by lymphoid aggregates; the greatest numbers of macrophages were found in the inflammatory aneurysm group. Our data suggests that the aneurysmal disease may progress from occlusive disease and is accompanied by an increase in chronic inflammatory cells as well as a redistribution of these cell types. Therefore it is suggested that aneurysmal disease may represent an immune-mediated event.

Antibodies, Monoclonal↗
PubMed1990

[Pathological mechanism of spontaneous hemostasis in traumatic artery rupture].

In ruptures of arteries the spontaneous haemostasis was supposed to be induced by 'rolling' of the intima until now. Experiments with isolated arterial segments (human femoral artery) and in vivo with ovine femoral arteries could not show this mechanism as the reason for the spontaneous haemostasis. The structure of the adventitia and its typical behavior during rupture procedure explains better the 'sandglass formation' in arterial ruptures with fractures and dislocations. This is induced by a 'fingertrap'-mechanism of the adventitia. The adventitia is sealed by platelets, which show a direct interaction with the collagen fibers of the adventitia. The platelet thrombus is stabilized by fibrin.

Adult↗
PubMed1994

Recurrence of cystic adventitial disease in an interposed vein graft.

A case of cystic adventitial disease (CAD) of the popliteal artery with intermittent claudication in the left calf is reported. This patient was first treated by total excision of the cyst and the involved artery followed by graft interposition with an autogenous saphenous vein. Recurrence of CAD in the interposed vein graft was noted after 6 months, and excision of the cyst with the involved graft and graft interposition with an autogenous saphenous vein was again required. We consider that the definitive evidence from early recurrence in the interposed vein graft shown in this case will close the discussion of the cause of CAD. The cystic lesion is thought by some to originate from the adventitia; traumatic, embryologic, or systemic abnormality theories were proposed. We assume that the mucin-secreting synovial cells originating from the neighboring joint capsule, tendon sheath, or, in some cases, from the ganglion itself, directly invade the adventitia through any rough or injured crack caused by trauma to the adventitia or simply attach to and encircle the adventitia. Total resection of the lesion with grafting is the recommended treatment for CAD because of the excellent results. However, as shown in our case, complete removal of the synovial cells even by resection technique may be difficult; therefore intensive follow-up is fundamentally necessary in this disease.

Adult↗
PubMed1996

Differential expression of elastin and alpha 1(I) collagen mRNA in mice with bleomycin-induced pulmonary fibrosis.

Interstitial pulmonary fibrosis is characterized by increased production of connective tissue components, including collagen and elastin. The role of elastin turnover in pulmonary fibrosis is not clear, and it is not known whether elastin and collagen are regulated separately or together during the inflammatory process. Mice with bleomycin-induced pulmonary fibrosis were investigated to determine the temporal and spatial changes in localization of elastin mRNA expression, as well as to compare elastin mRNA expression with that of alpha 1(I) collagen mRNA expression. In control (saline-treated) lungs, elastin mRNA was detected by in situ hybridization in arterial walls. No signal was found in alveolar or airway walls or in pleura; alpha 1(I) collagen mRNA was detected in the tissue underlying the airway epithelium. An increase in elastin mRNA expression in muscular arteries was observed 3 days after bleomycin instillation. Expression was also seen in the adventitia of terminal airways and adjacent small blood vessels. Expression of alpha 1(I) collagen mRNA increased in the tissue underlying the airway epithelium. In the pleura, alpha 1(I) collagen mRNA expression was found, although no pleural thickening was evident. The alpha 1(I) collagen mRNA expression was particularly increased in the adventitia of terminal airways and in associated small blood vessels. Obvious in areas of fibrosis, elastin mRNA expression was occasionally increased in the pleura and airway wall 7 days after bleomycin treatment; alpha 1(I) collagen mRNA expression was generally stronger than elastin mRNA expression in areas of fibrosis and was frequently intense in the adventitia of airways and associated blood vessels. The fibrotic areas showed increased elastin mRNA expression 14 and 30 days after bleomycin treatment. The arteries in fibrotic areas showed normal elastin mRNA levels. In the areas of fibrosis and in the adventitia of airways and adjacent blood vessels, alpha 1(I) collagen mRNA expression was very high. In conclusion, lung elastin biosynthesis is markedly altered by bleomycin treatment. The localization and intensity of elastin mRNA expression is different from the expression of alpha 1(I) collagen mRNA.

Animals↗
PubMed1997

Why the internal mammary artery is an ideal graft for myocardial revascularisation? (an experimental model with omentoplasty).

Ten dogs underwent coronary artery bypass grafting through a right thoracotomy. Free internal mammary artery grafts (IMA) was used for aortocoronary bypass to right coronary artery (RCA) without temporary cardiopulmonary bypass. In upper median laparotomy approach, mobilization and lengthening of the omentum was performed through the retrosternal part of the diaphragm. An epiploic muff was effectuated surrounding the IMA graft. After three months the animals were sacrificed and the grafts folded by omentum were used for microscopical study. The histological evaluation has shown that the omentum has formed a new adventitia around the graft. In the new-formed adventitia, newly formed vessels can be found and these are grouped around the adventitia-media border zone, very rarely penetrating into the external layer of the media. This graft-omentoplasty offer a good experimental model which facilitates to investigate in vivo the blood supply needed by free IMA grafts through the adventitia in experimental conditions. The biological mechanism of angiogenesis in graft wall can be investigate as well.

Animals↗
PubMed1998

Morphological and quantitative study of the intrinsic nerve plexuses of the canine trachea as revealed by immunohistochemical staining of protein gene product 9.5.

BACKGROUND: The ganglionated nervous plexuses in the trachea play an important role in the regulation of respiration. Although the tracheal tissue of the dog has frequently been used in physiological and pharmacological studies, little is known about the morphology of the intrinsic nervous plexuses in the dog trachea and quantitative data about the ganglia and nerve cell bodies are lacking. The structure of the nervous plexuses and detailed morphometric data about the intrinsic neurons of the dog have not previously been reported. METHODS: The structure of the intrinsic nerves in the dog trachea was examined by a combination method of digestion with KOH and immunohistochemical attaining of protein gene product 9.5. In addition, areas of nerve cell profiles, numbers of nerve cell bodies per ganglion and densities of nerve cell bodies per ganglion were estimated in preparations from five dogs. RESULTS: In the dog trachea, the peritracheal plexus, outer submucosal plexus, inner submucosal plexus, and mucosal plexus were identified from adventitia to epithelium in that order. The peritracheal plexus, situated in the lamina adventitia of the trachea, consisted of thick nerve bundles that were densely distributed in the membranous wall. The peritracheal plexus contained ganglia with round or oval nerve cell bodies. In the trachealis muscle, the intramuscular plexus, which was a well-developed, three-dimensional nervous network, was observed. It did not include ganglia and consisted of inter- and intrafascicular networks. The outer submucosal plexus was observed as small clusters in the inside of the trachealis muscle. A few round nerve cells were observed in the outer submucosal plexus as small clusters. The ganglionated inner submucosal plexus was identified in the superficial layer of the submucosal layer. A finer meshwork, namely, the mucosal plexus, was observed in the lamina propria. Among the entire length of the trachea, we counted 2,134-2,873 ganglia (average, 2,389) and 13,902-24,232 nerve cell bodies (average,18,461) were counted in the peritracheal plexuses of five dogs. The densities of ganglia and nerve cell bodies were high near the carina and low near the thoracic inlet. The number of nerve cell bodies per ganglion was estimated as 6.5-8.8 (average, 7.7). The average maximum area of nerve cell profiles was 522 +/- 223 microm2. CONCLUSIONS: The structure of the tracheal plexuses in the dog is more complex than those in other smaller animals. The constitution of the plexuses seems to be that of the intestine. The numerous nerve cells in the peritracheal plexus in the adventitia can be expected to play important roles in airway regulation and in the pathogenesis of tracheal collapse.

Animals↗
PubMed1995

Elastin and mechanoreceptor mechanisms with special reference to the mammalian carotid sinus.

Light microscopic studies reveal that the carotid baroreceptor region in mammals, located at the origin of the internal carotid artery, has a preponderantly elastic structure and a thick tunica adventitia. Electron microscopy discloses the presence of sensory nerve endings within the parts of the tunica adventitia adjoining the preponderantly elastic zone of the internal carotid artery. Bundles of collagen fibres in the tunica adventitia form convolutions or whorls around the nerve terminals and often terminate on the surface of the elastic fibres or into the basement membranes of the neuronal profiles. It is concluded that the large content of elastic tissue in the tunica media of the baroreceptor region renders the vessel wall highly distensible to intraluminal pressure changes, and thereby facilitates transmission of the stimulus intensity to sensory nerve terminals. However, a change in the geometrical configuration of the bundles of collagen under the influence of elastic fibres may provide a better insight into the mechanisms of distortion of the baroreceptors related to and/or in contact with collagen fibres. In support of this is the demonstration of contact sites between collagen and elastic fibres.

Animals↗
PubMed1985

Occurrence of cardiac muscle in the hepatic portal vein wall of the mouse and rat.

Cardiac myocytes have been shown to occur in the tunica media and adventitia at the region near the hepatic end of the portal vein of the mouse and rat, and have been studied by electron microscopy in the mouse portal vein. They measured 3-10 microns in breadth at their nuclear level, possessed centrally located nuclei, and were connected with each other by the intercalated disk. In these myocytes in the mouse portal vein, sarcoplasmic reticulum was represented by a rather simple and loose network of the anastomosing tubules. The membrane-bound granules, which closely resemble the atrial specific granules, were found in many of the mouse portal vein myocytes. Transverse tubules, 40-200 nm in diameter, were sometimes detectable at the Z line level. The nexus occupied about 3-5% of the whole junctional area between cardiac myocytes in the tunica media, whereas in the tunica adventitia the corresponding value was about 17%. Blood capillaries with fenestrated endothelium supplied the cardiac myocytes in the adventitia of mouse portal vein. The closest relationship between the adrenergic axon and portal vein cardiac myocytes was observed to be ca. 0.3 micron apart. The significance of these findings is discussed in relation to pulsations of the portal vein.

Animals↗
PubMed1986

Dynamic features of duct epithelial cells in the mouse pancreas as shown by radioautography following continuous 3H-thymidine infusion.

The possibility of turnover of the epithelial duct cells was examined in the adult mouse pancreas by radioautography following continuous administration of 3H-thymidine for periods varying from 1 h to 60 days. One hour after an injection of 3H-thymidine, the label observed in small and large ducts was low but increased with the duration of the continuous infusion of 3H-thymidine and reached a level of about 67% cells labeled after 60 days. The rate of duct cell labeling was estimated from the regression line of the labeling index vs. time in four types of ducts classified according to their inner diameter and the presence of the adventitia and was given as 0.60% cells per day in small (adventitia-free) ducts (phi 4-12 micron), 0.89%, 1.02%, and 1.23% cells per day in large (adventitia-including) ducts (phi 15-29, 30-49, and 50-160 micron respectively). In contrast, the labeling index of aciner cells after a 60-day infusion indicated an addition of only 0.02-0.07% per day, and that of islet cells 0.14-0.22% per day. It is known that most parenchymal cells belong to either expanding or renewing cell populations. The acinar cells of the pancreas have been shown to constitute an expanding population, a conclusion confirmed by the low addition of cells observed in the present work. However, the relatively high rate of cell addition in the duct epithelia indicates that they may turn over in a period of 2.7 months in the case of large ducts and 5.6 months in the case of small ducts.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗