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.     

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.     

Arteries and veins formed within renal vessels: a previously neglected observation

Summary An abnormality of blood vessels was noted in a biopsy of a renal transplant. This took the form of apparent development of a new artery inside and concentric with the old, with elastic laminae and a muscular media, separated from the old internal elastic lamina by poorly cellular tissue. In a systematic study of material from another 119 renal transplants, 13 nephrectomy specimens for chronic pyelonephritis and hydronephrosis, 28 renal biopsies showing interstitial nephritis, and 18 renal biopsies showing small vessel vasculopathy of accelerated hypertensive type, similar arterial changes were seen in another 10 renal transplants that showed chronic vascular rejection, 1 case of chronic interstitial nephritis, and 3 cases of vasculopathy, 2 with accelerated hypertension and 1 with systemic sclerosis. One renal transplant also showed apparent development of new muscular veins inside old veins. Immunohistological study for smooth muscle actin confirmed that the apparently new arterial and venous structures contained smooth muscle cells. The arterial abnormality may be called arterialisation of intrarenal arteries. This change appears to be not rare, is distinctive, and has scarcely been previously recognised or reported as a response of intrarenal blood vessels to damage.     

The vascular anatomy of the liver of the monitor lizard (genus varanus)

The gross and microscopic anatomy of the vasculature of the monitor lizard liver was studied. The portal vein has a peculiar arrangement of smooth muscle. The tunical media of the entering portal vein has bundles of smooth muscle cells separated by large numbers of collagenous fibers. The amount of smooth muscle decreases as the vessel decreases in diameter and soon one finds intermittent broad, thin bands of smooth muscle. As the caliber of the vessels continues to decrease, the smooth muscle bands become narrower and thicker so that they appear as doughnut-shaped sphincters. The sphincters are usually found at the beginning of each branch of the portal vein as well as along the course of veins between areas of branching. Some sphincters are found in direct contact with the outer capsule of the liver. Sphincters occur in the terminal branches of the portal vein just proximal to the sinusoids. Small numbers of scattered smooth muscle cells were seen arranged longitudinally, obliquely, or circularly in the smaller hepatic veins. Even the large hepatic veins had only small amounts of smooth muscle. At no place along the course of hepatic veins could smooth muscle sphincters equivalent to those seen around portal veins be found. The monitor lizard should be an excellent subject for physiological and pharmacological studies of regulation of intrahepatic portal vein blood flow.     

The vasculature of the rat penis: A scanning electron microscopic and histologic study

As a basis for understanding the mechanism of erection in an animal model frequently used in research in reproductive biology, the angioarchitecture of the penis of the rat has been described using scanning electron microscopy. Study of the penile vasculature of the rat indicates that the corpora cavernosa penis and the corpus spongiosum are independent erectile tissues, each with its own arterial and venous vessels. The large vascular spaces and abundant smooth muscle of the penile crura are compatible with its role in regulating blood flow to more distal penile tissues. Helicine arteries of the crura, but not the parent deep penile artery or arteries elsewhere, have muscular cushions in their walls. The venous drainage of the penile crura is via subtunical veins which are thought to be compressed during erection to elevate pressure within the penis. Large, paired cavernous veins drain the shaft of the penis. A unique method for inhibiting blood flow from the penis is indicated by the division of the cavernous veins into smaller channels prior to joining the subtunical venous plexus. Erectile tissue in the bifid origins of the corpus spongiosum has abundant cavernous muscle, while in the remainder of the corpus spongiosum little smooth muscle lines the cavernous spaces. The cavernous spaces on either side of the urethra coalesce to form vessels, each of which communicates with cavernous spaces in the glans. In addition, a bypass of the glans is effected by communication of these vessels directly with the deep dorsal vein. The apparent absence of muscular pads in vessels of the spongiosum, the relative paucity of cavernous smooth muscle, and the ample venous drainage provided by the deep dorsal vein may account for the lack of a venous occlusive mechanism similar to that of the corpora cavernosa penis.     

Scanning electron microscopy of an elastic fiber network which forms the internal elastic lamina in canine saphenous vein

Scanning electron microscopy (SEM) was used to study the arrangement of elastic fibers in the canine saphenous vein as the basis for further studies of veins used in by-pass grafting operations. The elastic fiber arrangement in distended and non-distended veins was examined in both immersion-fixed and perfusion-fixed vessels. Transmission electron microscope (TEM) observation of the SEM samples confirmed the identity of these fibrillar structures as elastic fibers. In addition, specific stains for elastic fibers (Verhoeff's iron hematoxylin and orcein) were used. The elastic fibers forming the internal elastic lamina were arranged in a fishnet-like pattern. Large-diameter fibers, running longitudinally along the vascular wall, were interconnected by smaller oblique fibers. Together the fibers formed an elastic cylindrical network between the endothelium and the smooth muscle cells. The thicker longitudinal fibers were the same diameter in distended and non-distended veins. By contrast, the oblique fibers were thinner and more complexly branched in distended veins. The architecture of the elastic fiber network contributes to vascular flexibility and allows circumferential distension. The interconnecting oblique fibers presumably serve to distribute internal pressure equally around the venous wall.     

小口径组织工程血管在羊体内的远期结果

背景：对小口径组织工程血管的研究至今仍主要集中于体外构建上,体内远期结果的研究少有报道。 目的：观察脱细胞猪股动脉支架和绵羊骨髓间质干细胞体外构建的小口径组织工程血管间置于骨髓间质干细胞供体绵羊体内12个月后组织学改变。 方法：将12只成年绵羊随机分为支架组和再细胞化组,支架组将猪股动脉脱细胞后间置于绵羊右侧股动脉;再细胞化组将体外诱导培养的绵羊骨髓间质干细胞种植于脱细胞猪股动脉支架中,经过体外预适应所构建的小口径组织工程血管(直径< 6 mm)间置于骨髓间质干细胞供体绵羊左侧股动脉;将12只绵羊的自体股动脉设为对照组。12个月后切取支架组和再细胞化组的植入物及邻近受体股动脉,行苏木精-伊红染色和扫描电镜检查,观察植入物和对照组股动脉内皮细胞及中层平滑肌细胞密度,采用邻甲酚酞络合酮法测定2组植入小口径组织工程血管和受体股动脉组织的钙含量。 结果与结论：支架组和再细胞化组植入后12个月内管腔均通畅,无明显管道扩张与狭窄,无腔内血栓形成,无管壁明显增厚等改变,管道内表面均已内皮化。但2组植入物管壁均有僵硬和搏动性减弱,尤以支架组植入物管壁僵硬更明显;支架组植入物管道组织钙含量最高(P < 0.01);支架组和再细胞化组管道中层平滑肌细胞密度均低于对照组(P < 0.01)。与支架组植入物相比,再细胞化组植入物组织钙含量较低(P < 0.05),中层平滑肌细胞密度较高(P < 0.01)。说明利用脱细胞猪股动脉支架体外构建小口径组织工程血管时,提高中层平滑肌细胞密度有助于改善小口径组织工程血管的远期功能。     

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.     

Scanning electron microscopic studies of the vascular smooth muscle cells and pericytes in the rat heart

The cytoarchitecture of smooth muscle cells and pericytes in the rat cardiac vessels was studied by scanning electron microscopy after the removal of connective tissue matrices using a modified KOH-collagenase digestion method. The initial stem of the coronary arteries had groups of smooth muscle cells which ran in various directions on the outermost layer of the media. Although smooth muscle cells in coronary arteries of more than 100 microm in the outer diameter were arranged in a rough circle around the vessel axis, oblique and/or longitudinal muscle bundles were often present in the medio-adventitial border of the vessels. The presence of irregularly oriented muscular bundles is probably connected with resistance against the stretching force induced by the beating of the heart. As the vessel size decreased toward the periphery, almost all of the smooth muscle cells became spindle-shaped with several tiny processes and ran circularly or helicaly to the vessel axis. In the precapillary arterioles (6-12 microm), smooth muscle cells acquired various cytoplasmic processes which helicaly surrounded endothelial cells. Unmyelinated nerves were often associated with arterioles. Blood capillaries were morphologically divided into three segments: arterial capillaries which had pericytes with wide and circularly oriented processes, true capillaries whose pericytes extended long and thin primary processes bilaterally along the vessel axis, and venous capillaries surrounded irregularly and loosely by wide pericytic processes. The stellate pericytes in the postcapillary venules (10-30 microm) gradually changed into flat tape-like smooth muscle cells, which ran circularly in the collecting venules and veins (30-200 microm). The large collecting veins were finally overwhelmed by superficial thin layer of the myocardium, their own smooth muscle cells being very sparse. This suggests that large veins have poor ability to contract by themselves but are influenced by the surrounding myocardial cells.     

Oxygen modifies artery differentiation and network morphogenesis in the retinal vasculature.

The mechanisms that control differentiation of immature blood vessels into either arteries or veins are not well understood. Because oxygen tension in arteries is higher than in veins, oxygen has the potential to be an instructive signal for artery/vein (AV) differentiation. We test this hypothesis by exposing newborn mice to moderate hypoxia (10% atmospheric oxygen) and studying AV differentiation in the developing retinal vasculature. Forming retinal arteries fail to express the artery-specific markers Delta-like 4 (Dll4) and EphrinB2 during hypoxia. However, other aspects of AV differentiation are retained such as high levels of alpha smooth muscle actin in arterial mural cells and vein-specific expression of the msr/apj gene. The capillary network between arteries and veins is denser, and capillaries expressing the venous marker msr/apj are found in territories normally occupied by arterial capillaries. Thus, it appears that high oxygen in arterial blood is required for arterial expression of Dll4 and EphrinB2, which could be involved in cell-cell repulsion pathways that dictate the normal segregation of arteries and veins.     

Segmental arterial mediolysis of the middle colic artery: report of a case with special reference to lesions of small arteries and veins

We report a case of segmental arterial mediolysis (SAM) that involved the middle colic artery, and present some pathologic alterations found in mesenteric small arteries and veins. The patient, a 52-year-old woman, underwent an emergency laparotomy for acute intra-abdominal hemorrhage, and a segment of the transverse colon with hemorrhagic mesocolon was excised. Microscopic examination demonstrated two separate lesions of SAM in the middle colic artery. The involved arterial segments showed a partial to circumferential loss of the media (mediolysis) and intima associated with the formation of a pseudoaneurysm. Smooth muscle cells adjacent to the mediolysis showed various degenerative changes. In addition, we found multiple, tiny foci of degenerative lesions affecting the outer media in the wall of small arteries. Subendothelial vacuoles and nodular intimal proliferation were also noted in small veins. Whereas SAM chiefly affects large or medium-sized arteries, small blood vessels, including veins, are also affected. The present case is unusual in that degeneration of medial smooth muscle cells was clearly observed in the arterial walls, and the small veins were affected by lesions similar to those in arteries. We suspect that a phenotypic modulation of vascular smooth muscle cells induced by some genetic vulnerability plays a role in the pathogenesis of SAM.     

Differential lectin binding on walls of thoraco-cervical blood vessels and lymphatics in rats.

Lectin binding in the walls of large to medium-sized blood vessels and lymphatics in the rat thoraco-cervical region was examined histochemically. The tunica intima of the aorta and superficial cervical artery showed positive reactions with wheat germ agglutinin (WGA) and Concanavalin A (ConA) but not with Dolichus biflorus agglutinin (DBA). The tunica media of the aorta exhibited intense WGA binding, especially on the smooth muscle cells, but the tunica media of the superficial cervical artery did not react with the lectin. Neither ConA nor DBA bound to the tunica media of the aorta and superficial cervical artery. The tunica adventitia of both arteries contained sites binding the three lectins, although DBA reactivity declined as the vascular diameter decreased. The tunica intima of the superior vena cava and azygos vein exhibited positive WGA and ConA binding, whereas DBA binding was noted on only part of the tunica intima of the superior vena cava and not on that of the azygos vein. The tunica media and tunica adventitia were reactive for all three lectins. The WGA and ConA binding sites in the tunica adventitia showed loose networks, suggesting lectin binding on connective tissue elements interlacing among smooth muscle bundles. Lectin binding sites in the walls of lymphatics exhibited an arrangement similar to those in the walls of the veins. Moreover valves protruding into the lumen showed intense WGA and ConA binding and scattered DBA binding. Three other lectins (Ulex europaeus agglutinin, peanut agglutinin, Maclura pomifera) were examined, but they showed no reactions with the vessels. Thus, the differential binding of lectins on the walls of blood vessels and lymphatics of various sizes suggests the functional complexity of monosaccharide residues in the vascular walls.     

The vertebral venous plexuses: the internal veins are muscular and external veins have valves

The internal and external vertebral venous plexuses (VVP) extend the length of the vertebral column. Authoritative sources state that these veins are devoid of valves, permitting bidirectional blood flow and facilitating the hematogenous spread of malignant tumors that have venous connections with these plexuses. The aim of this investigation was to identify morphologic features that might influence blood flow in the VVP. The VVP of 12 adult cadavers (seven female, mean age 79.5 years) were examined by macro- and micro-dissection and representative veins removed for histology and immunohistochemistry (smooth muscle antibody staining). A total of 26, mostly bicuspid, valves were identified in 19 of 56 veins (34%) from the external VVP, all orientated to promote blood flow towards the internal VVP. The internal VVP was characterized by four main longitudinal channels with transverse interconnections; the maximum caliber of the longitudinal anterior internal VVP veins was significantly greater than their posterior counterparts (P < 0.001). The luminal architecture of the internal VVP veins was striking, consisting of numerous bridging trabeculae (cords, thin membranes and thick bridges) predominantly within the longitudinal venous channels. Trabeculae were composed of collagen and smooth muscle and also contained numerous small arteries and nerve fibers. A similar internal venous trabecular meshwork is known to exist within the dural venous sinuses of the skull. It may serve to prevent venous overdistension or collapse, to regulate the direction and velocity of venous blood flow, or is possibly involved in thermoregulation or other homeostatic processes.     

Human diseased arteries contain cells expressing leukocytic and embryonic stem cell markers

Recent evidence suggests that smooth muscle cells within the intima of diseased human blood vessels of the elderly population contain the embryonic form of smooth muscle cells. We wanted to explore the idea that human diseased vessels may contain other primitive cell types, such as pluripotent embryonic stem cells and hematopoietic stem cells. Radial and internal mammary arteries were collected from patients undergoing coronary artery bypass surgery; and coronary arteries, from hearts at autopsy and transplant. Immunohistochemistry was used to identify the embryonic stem cell markers Octomer-4; stage-specific embryonic antigens 1, 3, and 4; TRA-1-60; and TRA-1-81, and the leukocytic markers CD34, CD14, CD133, and CD64 in all vessels. We found that diseased human radial arteries contained the highest numbers of cells in the media- and intima-expressing markers of embryonic and leukocytic origin compared with diseased human coronary arteries. In nondiseased human vessels (internal mammary arteries), such cells were rarely observed. Granulation tissue within the diseased human arteries contained similar cells, and the angiogenic vessel endothelial cell layer also expressed these markers. It is concluded that diseased human blood vessels contain cells that express markers from leukocytic and embryonic origin. These results suggest that cells within human arteries might be able to differentiate into various cell types and that blood vessels might be a reservoir for such cells.     

Mechanical Behavior of Vessel Wall: A Comparative Study of Aorta,Vena Cava,and Carotid Artery

We have used incremental stress-strain curves to study the mechanical behavior of porcine aorta, carotid artery, and vena cava. Elastic and viscous stress-strain curves are composed of low and high strain regions that are approximately linear. Analysis of the low strain behavior is consistent with previous studies that suggest that the behavior is dominated by the behavior of elastic fibers, and that the collagen and elastic fibers are in parallel networks. At high strain, the behavior is different than that of skin where it is dominated by the behavior of the collagen fibers. The high strain behavior is consistent with a series arrangement of the collagen and smooth muscle; however, the arrangement of smooth muscle and collagen may be different in aorta than in the other vessels studied. It is concluded that the mechanical behavior of the vessel wall differs from the behavior of other extracellular matrices that do not contain smooth muscle. Our results indicate that at least some of the collagen fibrils in the media are in series with smooth muscle cells and this collagen-smooth muscle network is in parallel with parallel networks of collagen and elastic tissue in aorta, carotid artery, and vena cava. It is concluded that the series arrangement of collagen and smooth muscle may be important in mechanochemical transduction in vessel walls and that the exact quantity and arrangement of these components may differ in different vessels. © 2003 Biomedical Engineering Society. PAC2003: 8719Rr, 8715La, 8719Uv, 8719Ff     

ULTRASTRUCTURAL STUDIES ON HUMAN ARTERIOSCLEROSIS-COMPARISON BETWEEN HYPERTENSIVE AND NORMOTENSIVE GROUPS

Systematic observation of arteriosclerosis by electron microscope was made on small arteries and arterioles of the stomach which were respected from 5 hypertensive cases and 6 normotensive cases who underwent surgery for gastric carcinoma or ulcer and which were fixed by perfusion with glutaraldehyde. Concurrently, three rabbits were used for animal experiments. Upon placing electrodes in the gastric wall of the rabbits, electric stimulation with 2.0 volt D.C. was repeated intermittently during the period of 5 to 12 days.
Repeated contraction of vessels resulted in crush-up effect of smooth muscle cells beneath the internal elastic lamina and in transition of irregularly minced cytoplasms into small osmophilic particles. At the same time dark cells appeared among the smooth muscle cells in the vicinity. The same findings were frequently noted in the lesions of gastric artery of man particularly in the hypertensive group. It was apparent that repeated angiospasm is an important factor for the histogenesis of sclerotic vascular lesion.
The cells proliferating beneath the endothelial cells in arteriosclerosis were smooth muscle cells, and the direction of the proliferated smooth muscle cell layers did not necessarily conform with that of the media. They originated in the media and penetrated through the fenestrae of the internal elastic lamina.
Fibrinoid necrosis and hyalinous thickening of arterioles were observed fairly frequently in the hypertensive group but always accompanied with intensive irregular atrophy or disappearance of the medial smooth muscle cells.
Vascular lesions with initial thickening showed formation of new elastic lamina most of which was elastic fibers consisting of microfibrillar components. The additional formation of elastic fibers was particularly strong in the hypertensive group as the whole.     

Regional heterogeneity of elastin and collagen gene expression in intralobar arteries in response to hypoxic pulmonary hypertension as demonstrated by in situ hybridization.

In situ hybridization was used to determine the morphologic distribution of tropoelastin and alpha 1(I) procollagen mRNA expression in elastic intralobar arteries from neonatal calves with hypoxic pulmonary hypertension induced by a 15-day exposure to a simulated altitude of 1500 m. In vessels from normotensive control animals, low levels of hybridizable tropoelastin mRNA were detected in smooth muscle cells (SMC) of the inner media associated with large elastic lamellae. Compared to control arteries, vessels from hypertensive animals demonstrated a markedly different pattern of hybridization. In these arteries, strong hybridization signals for tropoelastin mRNA were seen in SMC lying between the elastic lamellae of the outer media, and the density of labeling associated with these medial cells decreased progressively toward the lumen. Endothelial and adventitial cells in both control and hypertensive arteries were negative for tropoelastin mRNA. Type I procollagen mRNA was dispersed through the media of control arteries, and in hypertensive calves, the hybridization signal was more intense and was unevenly distributed through the media similarly to that for tropoelastin mRNA. Adventitial cells were strongly positive for procollagen mRNA, and the signal was equally intense for both control and hypertensive arteries. Cells that had no detectable tropoelastin mRNA were noted in the outer media of both control and hypertensive vessels. These cells occurred as broad circumferential bands in the normotensive artery and as nodular foci in the hypertensive artery. Immunocytochemical studies with antibodies to smooth muscle specific actin, desmin, and vimentin demonstrated that cells within these foci, as well as tropoelastin mRNA-positive cells, were SMC. These studies demonstrate that expression of tropoelastin and procollagen mRNA was differentially stimulated by pulmonary hypertension within specific regions and SMC populations of the vascular wall.     

Increase of segments of elastic-type blood vessel walls in fetal placental stem villi during pre-eclampsia at term

In recent studies we described the presence of elastic-type blood vessels within trunci and rami chorii of human placental stem villi. For systemic and pulmonary hypertension it is known that elastic fibres are enhanced in arteries. The aim of our study was, therefore, to examine whether pre-eclampsia may lead to an increase of elastic tissue fibres in blood vessel walls of placental stem villi and whether there are differences in the thickness of blood vessel walls within these villi when compared to normotensive pregnant women. Twenty-six women with uncomplicated pregnancies and 25 patients with pre-eclampsia were investigated. Unfixed cryostat serial sections were processed for conventional orcein staining and for the demonstration of alpha-actin-immunoreactivity. The intensity of orcein staining of stem villus blood vessel walls was evaluated by a semiquantitative score method. Significant higher intensities of orcein staining (P<0.00001) were calculated for blood vessel walls of placentae with pre-eclampsia. The amount of thick stem villus vessels (>41 microm) increased during pre-eclampsia from 39 gestational weeks onwards. Our study demonstrates that segments of thick blood vessel walls and elastic-type vessel walls are increased in placental stem villi of patients with pre-eclampsia. This reaction may protect the fetal placental vessels and avert an increase of the fetal hypertension.