Heterogeneity of myosin antigenic expression in vascular smooth muscle in vivo

Rabbit antisera elicited against purified human nonmuscle (platelet) and smooth muscle (uterine myometrium) myosins identified distinct species of myosin when frozen sections of a variety of mammalian tissues were examined by immunofluorescence microscopy. Antiplatelet myosin antiserum specifically stained several nonmuscle cell types including epithelial, some connective tissue, and all vascular endothelial (arterial, venous, capillary) cells. Antismooth muscle myosin antiserum stained only smooth muscle and no other cell types. Neither antiserum reacted with rat cardiac (ventricular) or skeletal muscle cells. Antismooth muscle myosin antiserum staining was detectable in medial vascular smooth muscle in all vessels examined from rat, bovine, human, and guinea pig sources (including elastic and muscular arteries, arterioles, venules, and veins). Although antiplatelet myosin antiserum did not stain nonvascular smooth muscle or vascular smooth muscle in muscular arteries, arterioles, venules, or veins, it did uniformly and specifically stain medial vascular smooth muscle in elastic arteries. This staining of elastic arteries was abolished by absorption of antiplatelet myosin antiserum with purified platelet myosin but not uterine myosin. Similarly, the reactivity of antismooth muscle myosin antiserum was abolished by incubation with uterine but not platelet myosin. The differences in staining patterns observed with antiplatelet myosin antiserum and antismooth muscle myosin antiserum in elastic arteries versus other blood vessels suggests a heterogeneity of antigenic expression in vascular smooth muscle myosin. The most likely explanations for this heterogeneity are the presence of different gene products (myosin isozymes) or a posttranslational alteration (possibly conformational) of a single myosin species. Heterogeneity in this important component of the contractile apparatus of vascular smooth muscle may have significant implications for the physiology and pathophysiology of the vessel wall.     

Remodelling of the pulmonary arteries during recovery from pulmonary hypertension induced by neonatal hypoxia

Little is understood of the mechanisms involved in reducing pulmonary arterial wall thickness on recovery from pulmonary hypertension and the present study sought to clarify the events that occur. Piglets were exposed to hypobaric hypoxia for 3 days, either from birth or from 3 days of age, and others were exposed for 11 days starting at 3 days. All recovered in room air for up to 6 days. Using light and electron microscopy, the pulmonary artery wall thickness, the relative contribution of smooth muscle and matrix, smooth muscle cell replication, and apoptosis were assessed after hypoxic exposure and during recovery from hypoxic exposure. In elastic arteries, after 6 days' recovery in room air, a reduction in wall thickness to normal was associated with a similar reduction in proportional area of smooth muscle cells and matrix (p < 0.05), increased apoptosis (p < 0.05), and an abnormally low replication rate (p < 0.05). In peripheral muscular arteries, an increase in external diameter, and wall thinning on recovery, was achieved by smooth muscle cell remodelling and a reduction in cell replication (p < 0.05). Apoptosis did not contribute. Thus, different mechanisms are involved in recovery from hypoxia-induced pulmonary hypertension in elastic and muscular pulmonary arteries. Recovery is slower in animals exposed from birth rather than from 3 days of age.     

Normal adaptation of pulmonary arterial intima to extrauterine life in the pig: ultrastructural studies

Adaptation of the pulmonary arterial intima was studied in injected lung specimens of 34 Large White pigs. Each type of pre- and intra-acinar artery was studied separately using transmission and scanning electron microscopy. Determination of the endothelial surface/volume ratio and volume densities of (1) endothelium and subendothelium, (2) endothelial cytoplasmic organelles and (3) subendothelial connective tissue elements yielded 6832 measurements which comprised a computerized database. At birth, endothelial cell morphology changed more rapidly and to a greater extent in peripheral than in proximal arteries. Endothelial surface/volume ratio increased (p less than 0.0001). Fetal surface projections, junctional interdigitations and overlap became less evident. Adaptational changes were complete in three weeks. Between three weeks and adulthood a reduction in endothelial surface/volume ratio suggested cell growth. In the subendothelium the volume density of collagen and basement membrane and elastin increased (p less than 0.001). The internal elastic lamina, immature in all arteries at birth increased in thickness and integrity until in the adult, only in small muscular arteries did gaps between elastin profiles ensure frequent contact between endothelial and smooth muscle cells. At all ages regional differences in endothelial cell morphology were evident.     

Structural organization of pulmonary arteries in the rat lung

The structure of the normal pulmonary arteries in the rat was studied with light and electron microscopy after use of a newly devised technique of perfusion fixation and tissue preparation. We distinguished two main types of artery in the rat lung on the basis of the structure of the media, an elastic artery and a muscular artery. The elastic artery was characterized by an abundance of extracellular matrix in the media and by an oblique arrangement of smooth muscle cells to connect neighboring elastic laminae. It was subdivided into two segments, a classical elastic and a transitional elastic segment. The muscular artery was distinguished by a paucity of extracellular matrix in the media and by a circumferential arrangement of smooth muscle cells (or pericytes) enclosing the lumina, and was subdivided into four segments, a thick muscular, an ordinary muscular, a partially muscular and a nonmuscular segment. The smooth muscle cells in the muscular artery contained well-developed microfilament bundles compared with those in the elastic artery. Structural differences in smooth muscle cells and in extracellular matrix in the media between the elastic and muscular arteries may reflect the functional heterogeneity of pulmonary arteries in response to hypoxic pulmonary vasoconstriction and to vasoactive substances such as endothelium-derived relaxing and hyperpolarizing factors, and endothelin.     

Rat pulmonary artery wall injury by chronic intermittent infusions of Escherichia coli endotoxin. Obliterative vasculitis and vascular occlusion

To examine the effect of intermittent endotoxemia on rat pulmonary artery structure and hemodynamic function we infused purified Escherichia coli endotoxin on four occasions over 3 weeks (at 7-day intervals), through an indwelling catheter placed in the external jugular vein. The fourth infusion of endotoxin was associated with widespread but focal alveolar consolidation, reduced perfusion of small pulmonary arteries by lumen occlusion and obliteration, pulmonary vascular wall injury, and a peripheral leukocytosis (mean +/- SEM total leukocytes, endotoxin 133.5 +/- 23 X 10 mm3, control 12.2 +/- 1.2 X 10 mm3, p less than 0.001) in which polymorphonuclear (PMN) leukocytes predominated at the expense of lymphocytes (p2x less than 0.01). The alveolar wall was thickened and the alveolar space was consolidated by degenerating polymorphonuclear leukocytes, mononuclear cells, lipid laden alveolar macrophages, erythrocytes, fibrin, and cell debris. In regions of alveolar consolidation vessel lumens were either narrowed by subendothelial cell collections that consisted either of mononuclear cells or degenerating mural and inflammatory cells, or they were occluded by degenerating inflammatory cells and cell debris. The walls of occluded vessels were evident only by their residual elastic laminae: remnants of lysed endothelial cells lined the intima and the media consisted of degenerating mural and inflammatory cells. Capillary endothelial cells showed extensive hydropic degeneration and lysis of cell contents. Intimal precursor smooth muscle cells were hypertrophied but were not associated with the appearance of mature smooth muscle cells in the walls of small pulmonary arteries. In regions of less severe alveolar consolidation by inflammatory cells, vessel wall injury was still evident but less marked; precursor smooth muscle cells were hypertrophied; subepithelial and subendothelial collections of fluid and fibrin were present; and plasma membranes of endothelial cells were disrupted. Despite extensive pulmonary vascular injury, chronic intermittent endotoxemia did not produce the structural changes associated with pulmonary hypertension (medial thickening and appearance of medial muscle in previously nonmuscular arteries) nor a significant change in pulmonary artery pressure.     

Thinning of fetal pulmonary arterial wall and postnatal remodelling: Ultrastructural studies on the respiratory unit arteries of the pig

Summary Adaptation to extra-uterine life and postnatal remodelling of intra-acinar arteries was followed in 34 Large White pigs, from birth to adult life, applying morphometry to light and electronmicroscopic studies. After birth, percentage wall thickness decreased rapidly due to a reduction in overlap of adjacent smooth muscle cells and an increase in smooth muscle cell surface area/volume ratio, (p<0.01 at 12 h), without a reduction in the volume density of smooth muscle cells. Smooth muscle cells appeared immature at birth and synthetic rather than contractile organelles predominated. Between 3 weeks and 6 months myofilament volume density doubled (p< 0.0001). At all ages, pericytes, intermediate and smooth muscle cells showed similar volume densities of contractile and synthetic organelles. Thus, the high fetal pulmonary vascular resistance appeared to be due to the shape and arrangement of smooth muscle and other contractile cells within the vessel wall, rather than an excessive contractility of these cells. After birth rapid remodelling of arterial wall structure achieved a reduction in wall thickness by 30 min, continuing during the first week of life. After 3 weeks, remodelling involved an increase in wall thickness, connective tissue deposition with more collagen than elastin (p<0.0001), and smooth muscle cell differentiation.     

Arteries and veins of the normal dog lung: Qualitative and quantitative structural differences

As a necessary preliminary step to the study of pulmonary hypertension and edema, the structure of the pulmonary vasculature of seven normal dogs was examined in detail to distinguish arteries and veins. For light microscopy and morphometry, the left lung was injected from the arterial and venous sides with pigmented gelatin masses of different colors. The right lung was fixed for electron microscopy. The percentage of medial muscle thickness of arteries was greater (P < 0.05) than that of veins, for vessels over 200 μm diameter. Smooth muscle cells extended more peripherally into arteries (including in vessels less than 50 μm) than into veins. The larger arteries were elastic or transitional in type, whereas larger veins were muscular. The arteries branched with the airways. Fifty percent of arteries under 50 μm and more than 50% of veins under 200 μm were surrounded by alveoli. Muscular arteries had a thick media between distinct internal and external elastic laminae, whereas veins had no internal lamina but had a thin media separated from a thick adventitia by an external elastic lamina. By electron microscopy, the muscular arteries had tightly packed smooth muscle cells with few myoendothelial junctions; the venous smooth muscle cells were arranged loosely, and more numerous myoendothelial junctions were seen. No definite differences were noted between nonmuscular arteries and veins. The functional implications of these morphological findings (differential reactions to pharmacological agents, distensibility of pulmonary arteries and veins, and responses of small vessels to alveolar pressure) are discussed.     

Segmentation features and structural organization of the intrapulmonary artery of the yak

This study aims to systematically investigate intrapulmonary artery segmentation, blood vessel wall characteristics and structure organization, and the interrelation between intrapulmonary artery structure and plateau hypoxia adaptation in yak. The normal intrapulmonary artery structure of the yak had been studied using histological methods and transmission electron microscopy. The intrapulmonary artery of the yak was also examined using morphometric analysis and angiography. Results showed that the elastic intrapulmonary artery is divided into two types, namely, classical and transitional elastic segments. The muscular intrapulmonary artery is divided into three types, namely, transitional, classical muscular, and muscular arteriole segments. In the transitional elastic artery, elastic fibers and smooth muscles are linked through three models of ends, lateral branches, and branch tops. Two phenomena are possible for the transition from the elastic intrapulmonary artery to the muscular artery. One phenomenon postulates that a less elastic membrane is first increased and then suddenly decreased, and another supposes that the elastic membrane is gradually reduced and assembled in one to two layers before entering the transitional muscular artery. The smooth muscle of the intrapulmonary artery tunica media had more apophysis; it was physically connected with elastic membrane or fiber and composed of functionally resilient unit of the intrapulmonary arterial wall. Glycogenosomes increased in the muscular intrapulmonary artery smooth muscle cells. It exist one to two layers intact smooth muscle in intrapulmonary arteriole, the presence of intact smooth muscle in the intrapulmonary arteriole of the yak is a kind of structure adaptation to low‐oxygen environment. Anat Rec, 296:1775–1788, 2013. © 2013 Wiley Periodicals, Inc.     

Impaired adaptation of pulmonary circulation to extrauterine life in newborn pigs exposed to hypoxia: an ultrastructural study

Twelve Large White pigs aged less than 1 min, and 3, 5.5, and 14 days were exposed to hypoxia (380 torr) for 2.5-3 days. The wall structure of terminal bronchiolar (resistance arteries) and elastic arteries was assessed by light and electron microscopy using quantitative morphometric techniques. In animals exposed from birth, mean terminal bronchiolar arterial medial thickness was increased (p less than 0.05) because endothelial and smooth muscle cells (SMCs) retained their fetal shape, position, overlap, interdigitation and the low surface/volume ratio characteristic of fetal life. In all older animals, the cells had a normal postnatal shape and surface/volume ratio. In the elastic vessels hypoxia did not prevent the normal postnatal reduction in mean SMC diameter of animals exposed from birth. SMC hypertrophy did not occur in any age group, but all animals save those first exposed at 14 days, showed an increase in SMC myofilament volume density (p less than 0.01). Connective tissue volume density also increased (p less than 0.01), mainly due to an increase in elastin and ground substance. Thus a short period of neonatal hypoxia impaired adaptation and appeared to potentiate contractile capacity in stiff-walled arteries but elicited a less marked response from animals first exposed at 14 days.     

An electron microscopic study of intimal cushions in intracranial arteries of the cat

Subendothelial protuberances associated with the tunica intima have been described by light microscopy at branching sites of arteries in various animal species. These structures are termed intimal cushions or intimal pads. Some investigators regard them as being pathologic, preceding the appearance of atherosclerosis in the vessel wall. This fine structural study was done because of the possible role of intimal cushions in the regulation of cerebral blood flow at branching sites of intracranial arteries. The internal elastic lamina is split at the margins of a cushion to enclose irregularly arranged bundles of smooth muscle cells and collagenous fibrils. These smooth muscle cells are generally arranged at a right angle to smooth muscle cells in the underlying media. The outermost layer of the internal elastic lamina forms a boundary between the body of the cushion and the media; however, areas of discontinuity cause this border to be poorly defined in some instances. Perivascular autonomic nerves do not extend into either media or intimal cushions. Intercellular contacts between smooth muscle cells are observed within cushions as well as in the media, suggesting that cushions may be contractile and capable of modifying cerebral blood flow.     

Oxygen toxicity and restructuring of pulmonary arteries--a morphometric study. The response to 4 weeks'' exposure to hyperoxia and return to breathing air.

This study describes the pulmonary vascular lesions in rat pulmonary arteries and altered right ventricular weight after 1) prolonged exposure to hyperoxia (87% O2 for 4 weeks) at ambient pressure, 2) weaning from hyperoxia to air over 7 days, and 3) return to breathing air for 2, 4, or 8 weeks. Hyperoxia for 28 days narrows the lumen of intraacinar and preacinar arteries, increasing the percent medial thickness (%MT) by reducing the external diameter and thickening medial muscle. The ratio of patent intraacinar arteries to alveoli is significantly reduced, and pulmonary vascular obstruction and obliteration is evident by electron microscopy. A higher proportion of intraacinar and preacinar arteries have muscle in their wall than in the normal lung: in alveolar wall and duct regions, the proportion of partially muscular and muscular intraacinar arteries increases at the expense of nonmuscular ones (for both regions P chi 2 less than or equal to 0.001); and in arteries associated with terminal bronchioli and bronchioli the proportion of muscular arteries increases at the expense of partially muscular ones (for both regions P chi 2 less than or equal to 0.001). Both after weaning and after return to breathing air lumen size increases; but, even after 8 weeks, the %MT remains significantly increased, and the ratio of intraacinar arteries to alveoli is less than normal. After weaning, the proportion of muscularized intraacinar and preacinar arteries is similar to that after hyperoxia. Two weeks after return to breathing air, the proportion of muscularized alveolar wall and duct arteries is greater (for both regions P chi 2 less than or equal to 0.001). Even 8 weeks after return to breathing air more arteries are muscularized than normal (for both alveolar wall and duct regions P chi 2 less than or equal to 0.001), and within the alveolar wall still more are muscularized than after hyperoxia (P chi 2 less than or equal to 0.001). Hyperoxia causes right ventricular hypertrophy, reducing the ratio of the weight of the left ventricle and septum to that of the right ventricle (P chi 2 less than or equal to 0.001). Weaning further increases the hypertrophy, the ratio being further reduced (P chi 2 less than or equal to 0.001, compared with both hyperoxia and control values). On return to breathing air the degree of hypertrophy is less, but it persists, and even after 8 weeks the ratio is still less than normal (P chi 2 less than or equal to 0.01).     

Transitions in cell organization and in expression of contractile and extracellular matrix proteins during development of chicken aortic smooth muscle: evidence for a complex spatial and temporal differentiationprogram

 Whereas the understanding of the mechanisms underlying skeletal and cardiac muscle development has been increased dramatically in recent years, the understanding of smooth muscle development is still in its infancy. This paper summarizes studies on the ontogeny of chicken smooth muscle cells in the wall of the aorta and aortic arch-derived arteries. Employing immunocytochemistry with antibodies against smooth muscle contractile and extracellular matrix proteins we trace smooth muscle cell patterning from early development throughout adulthood. Comparing late stage embryos to young and adult chickens we demonstrate, for all the stages analyzed, that the cells in the media of aortic arch-derived arteries and of the thoracic aorta are organized in alternating lamellae. The lamellar cells, but not the interlamellar cells, express smooth muscle specific contractile proteins and are surrounded by basement membrane proteins. This smooth muscle cell organization of lamellar and interlamellar cells is fully acquired by embryonic day 11 (ED11). We further show that, during earlier stages of embryogenesis (ED3 through ED7), cells expressing smooth muscle proteins appear only in the peri-endothelial region of the aortic and aortic arch wall and are organized as a narrow band of cells that does not demonstrate the lamellar-interlamellar pattern. On ED9, infrequent cells organized in lamellar-interlamellar organization can be detected and their frequency increases by ED10. In addition to changes in cell organization, we show that there is a characteristic sequence of contractile and extracellular matrix protein expression during development of the aortic wall. At ED3 the peri-endothelial band of differentiated smooth muscle cells is already positive for smooth muscle alpha actin (αSM-actin) and fibronectin. By the next embryonic day the peri-endothelial cell layer is also positive for smooth muscle myosin light chain kinase (SM-MLCK). Subsequently, by ED5 this peri-endothelial band of differentiated smooth muscle cells is positive for αSM-actin, SM-MLCK, SM-calponin, fibronectin, and collagen type IV. However, laminin and desmin (characteristic basement membrane and contractile proteins of smooth muscle) are first seen only at the onset of the lamellar-interlamellar cell organization (ED9 to ED10). We conclude that the development of chicken aortic smooth muscle involves transitions in cell organization and in expression of smooth muscle proteins until the adult-like phenotype is achieved by mid-embryogenesis. This detailed analysis of the ontogeny of chick aortic smooth muscle should provide a sound basis for future studies on the regulatory mechanisms underlying vascular smooth muscle development. Accepted: 17 December 1997     

Ultrastructure of intramural coronary arteries in pigs with hypertrophic cardiomyopathy.

Pigs with hypertrophic cardiomyopathy diagnosed by echocardiographic examination were selected for study from a genetic breeding herd. Under dissecting microscopic examination, intramural coronary arteries in the septum and left ventricular free wall of euthanized pigs were collected for ultrastructural study. The major lesions of wall thickening included degeneration or denudation of endothelium, subendothelial edema, proliferation of collagen fiber, and hyperplasia of smooth muscle cells. Smooth muscle cells proliferated and migrated through the internal elastic lamella into the intima, which caused the early lesion of wall thickening of the intramural coronary arteries. The extent of smooth muscle cell proliferation was related to the severity of endothelial damage. The smooth muscle cells in the intima were identified by immunohistochemical staining (i.e., smooth muscle actin [SMA] stain). Three major types of severe wall thickening with narrow lumen were observed in the intramural coronary arteries. Edema in the intima caused the major lesion of Type I wall thickening. The internal elastic lamella was broken into small interrupted fragments, and fine fragments of elastic fibers surrounded by the cellular processes of smooth muscle were observed in Type I lesions. Many smooth muscle cells proliferated in the intima and media, which constituted the major lesion of Type II wall thickening of the intramural coronary arteries. Many vacuolized, degenerated smooth muscle cells with fewer sarcoplasmic myofilaments could be clearly observed in the Type II lesions. In advanced cases, severe vacuolization and degeneration of smooth muscle cells with the presence of many bizarrely shaped smooth muscle cells in the walls of the intramural coronary arteries could be observed, which caused the major lesion of Type III wall thickening. Pigs with hypertrophic cardiomyopathy, characterized by spontaneously occurring lesions in intramural coronary arteries, may prove a valuable animal model for human disease.     

Cellular breakdown within muscular arteries in hypercholesterolemic rats

Adult male rats were fed a high-fat cholesterol, thyroid-suppressive diet for three months, after which the structure of the muscular arteries (coronary and tarsal pedis) was examined by transmission electron microscopy. The plasma cholesterol concentration was elevated when the animals were killed and a distinct ultrastructural finding was the presence of necrotic cells in the media of both the coronary and the tarsal pedis arteries. Medial smooth muscle cells contained multivesicular membranous bodies, and membranous material accumulated in the intercellular space of the arterial media. It is proposed that the membrane changes and cellular death within muscular arteries may primarily be due to the increased membrane cholesterol concentration of smooth muscle cells during hypercholesterolemia. Dietary saturated fatty acids may have a contributing effect on smooth muscle cell injury in the hypercholesterolemic state.     

Structural identification and characterization of arteries and veins in the placental stem villi

The vascular wall structure in the human full-term placental villi of normal pregnancy was studied by means of light and electron microscopy with an improved technique of perfusion fixation and tissue preparation. We observed 81 sections of stem villi that showed cross-sectional profiles of paired vessels in their center. Both vascular walls contained a large amount of extracellular matrix and no elastic lamina between smooth muscle cells of the media, making identification of the artery and the vein quite difficult at first sight. We then noted that the density of the smooth muscle cell population was always considerably higher in one than the other, and identified the former as artery and the latter as vein on the basis of their connection with larger arteries and veins running on the chorionic plate. Between the paired vessels, the artery had a smaller caliber than the vein, and the ratio of venous to arterial caliber was distributed from 1.0 to 2.5. The thickness of media was usually thicker in the vein than in the artery. Clusters of elastic fibers were found occasionally in the media of arteries and veins, and basement membrane-like materials were associated frequently with the elastic fibers and were distributed widely in the media as well as in the adventitia. In the veins, the smooth muscle cells of the most superficial part of the media contained well-developed rough endoplasmic reticulum and Golgi apparatus, indicating differentiation to secrete extracellular matrices. The present study revealed the difference of wall structure between arteries and veins in the placental stem villi for the first time at the ultrastructural level, and suggested differentiation of venous smooth muscle cells, possibly by some influence from the luminal side.     

Intermediate filament proteins in developing human arteries

 The distribution of intermediate filament proteins in adult human blood vessels and in human fetal elastic arteries is relatively well-known. However, the distribution of these proteins in the course from neonate to adult has not been established. In this investigation, human postnatal arteries were studied with immunohistochemistry, using antibodies targeted on the intermediate filament proteins desmin, vimentin and cytokeratins 8, 18 and 19. Vimentin was present in most smooth muscle cells in all vessels and at all ages. The proportions of desmin-expressing cells increased in the elastic arteries during the first year of life and was higher in the pulmonary trunk than in the aorta. In the muscular arteries, the proportion of desmin-labelled cells increased in the coronary and the deep femoral arteries, but remained constant in the renal and the cerebral arteries. Cytokeratins were detected in the pulmonary trunk earlier than in the aorta. Cytokeratins were present throughout the wall of the ductus arteriosus, but desmin was present only in some cells. Thus, there are postnatal changes in the distribution of intermediate filament proteins in the elastic arteries and in some muscular arteries, whereas the intermediate filament pattern remains unchanged in other muscular arteries. Accepted: 31 July 1998     

Longitudinally orientated smooth muscle cells in rabbit arteries

Intima formation in vessels, spontaneous or experimentally induced, is generally characterized by the presence of longitudinally orientated smooth muscle cells (LSMC). During an experiment of neo-intima induction in carotid arteries in rabbits, by application of a nonconstrictive silastic cuff, a study was performed to investigate the presence of LSMC in the systemic and pulmonary circulations, in both elastic and muscular arteries. Three patterns could be distinguished: intimai cushions in muscular arteries, single or small groups of LSMC in the intima in elastic and larger muscular arteries, and intra-medially located layers or columns of LSMC in the aorta, the pulmonary artery, at the bifurcation of the aorta and around orifices of branches. In order to understand this peculiar orientation a biomechanical approach was used: this showed that near the lumen the circumferential stress is 4.5 times higher than the longitudinal. Because the cell surface of the smooth muscle cells exposed to this stress per unit vessel length is much less in the longitudinal than in the circular direction we conclude that the LSMC align in the direction which allows them to cope most effectively with the mechanical stresses.     

Structural organization of the vertebral artery in the giraffe (Giraffa camelopardalis)

Vertebral arteries in the giraffe were removed and their structural organization was studied with light microscopy. It has been shown that the caudal segment of the vertebral artery extending to the level of the seventh cervical vertebra has a largely elastic structure, while the cranial segment has a muscular structure. The transition of the arterial wall normally occurs between the seventh and fifth cervical vertebral levels, and involves diminution of elastic tissue in the luminal portion of the tunica media and simultaneous increase of the smooth muscle content. The smooth muscle cells in the cranial portion show a clustered arrangement consisting of several smooth muscle fibres. The individual clusters are separated by connective tissue septa from which finer strands extend to surround individual muscle fibres. It is suggested that the vertebral and carotid arteries though found in the neck have a different structural organization, which, in turn, may imply that the two blood vessels are subjected to different haemodynamic demands. The findings of this study therefore render further support to the statement that the largely muscular structure of the common carotid artery in the giraffe may be related to the unique cerebral haemodynamics of this animal, rather than being a common feature of the blood vessels situated in the neck. A corollary to this suggestion is the fact that, in the giraffe, as in most other Artiodactyls, the vertebral blood does not participate in the supply of cephalic structures because it is confined to the cervical region by the pressure barrier in the carotid-vertebral anastomosis.     

血管周肾上腺素能神经密度与管壁组成成分的关系

本文应用组织化学技术和电镜方法对家兔、豚鼠和大鼠血管周的肾上腺素能神经密度与管壁组成成分的关系进行了观察。实验结果证明,血管周神经分布于外膜层,中膜内未见有神经分布,肌性动脉(以肠系膜动脉为代表)较弹性动脉(以颈总动脉为代表)的血管周神经密度和含膨体数都较高。神经肌肉间隔近(0.05—3微米),最近者神经与肌肉间除基板外无其它组织成分。弹性动脉神经肌肉间隔较远(1—12微米),神经肌肉间隔以外弹力膜、成纤维细胞和板层状的结缔组织。股动脉和肾动脉周的神经分布特点介于上二者之间。静脉较相应动脉神经分布稀疏。但也存在部位的特殊性和种属差异性。如脐动脉虽属肌性动脉,但动脉周并无神经分布,豚鼠肾动脉周的神经密度远较兔及大鼠稀疏。作者认为血管周的神经密度与血管壁中平滑肌的含量有关。本文并对肌性动脉周神经分布致密的原因,不同类型动脉的神经分布特点与生理功能的关系进行了讨论。     

人胚胎冠状动脉组织发生的光镜研究

本文用Van Gieson-orcein染色法对35例(第5周至第10个月)人胚胎冠状动脉的组织发生作了光镜观察.结果显示第5周心外膜内的间充质细胞形成了血管壁.第6周冠状动脉初步形成,内皮直接贴附于内弹性膜,中膜为1～2层平滑肌细胞,外弹性膜为2层弹性纤维组成,外膜厚于中膜.内皮下层第6个月可辨认出来.内弹性膜、中膜、外膜的厚度及管径均随胎龄而增加.内弹性膜厚度随胎龄呈直线上升,中膜和外膜厚度随胎龄呈指数曲线上升.内径和外径的比值在各期胎龄保持相对衡定.