Fine structure of the mouse portal vein in relation to its peristaltic movement

The hepatic portal vein has been known to make a spontaneous peristaltic movement in some mammals, including the mouse and rat. To investigate the fine structure of the portal vein in relation to its physiological characteristics, we observed the mouse portal vein by using various histological techniques including conventional light microscopy, videomicroscopy, transmission and scanning electron microscopy, and real-time confocal laser scanning microscopy. The mouse hepatic portal vein was provided with a spiral fold which was produced by the inner layer, i.e. the endothelium and smooth muscles of the wall protruding into the lumen. Longitudinal smooth muscle cells spanned the interval of the fold, like a spirally arranged palisade around the vessel wall. The longitudinal muscle fibers ended at the spiral fold, being partly connected with a network of irregularly shaped smooth muscle cells. This network, hitherto unknown, was recognized to be restricted to the fold in distribution and characterized by numerous gap junctions connecting the muscle cells. Real-time confocal laser scanning microscopy using a Ca2+ sensitive fluorescent dye revealed that a transient and periodic increase in Ca2+ concentration occurred in the longitudinal smooth muscle cells and was transmitted spirally from the intestinal to the hepatic side. These findings indicate that, during the peristaltic movement, the contraction of smooth muscle cells is transmitted along the longitudinal smooth muscles of the portal vein wall toward the liver, presumably controlled by the network of the irregularly-shaped smooth muscle cells in the fold of the portal vein. Light microscopic observation in some specimens indicated an occurrence of cardiac muscle cells outside the smooth muscle layer. Restricted to the site of the porta hepatis in distribution, their involvement in the peristaltic contraction of the portal vein seemed unlikely.     

Time course of the regression of intimal hyperplasia in experimental vein grafts.

A previous study in which vein grafts were removed from the arterial circulation and reimplanted into the venous circulation of the same animal demonstrated regression of vein graft intimal hyperplasia and medial thickening within 14 days. The present study was designed to characterize the kinetics of the morphological and ultrastructural changes over this 14-day period. Twenty-one male New Zealand White rabbits received a reversed vein interposition bypass graft of the right common carotid artery. Fourteen days after the procedure, 21 vein grafts were isolated, removed, and reimplanted into the contralateral external jugular venous system as veno-venous interposition bypass grafts (reversal grafts). The grafts were harvested at 60 minutes, 1 day, 3 days, 5 days, 7 days, and 14 days after reversal. Before insertion into the venous circulation, the vein graft had a confluent endothelial cell surface with multiple layers of smooth muscle cells representing intimal hyperplasia. After 1 hour, the reversal graft retained an intact endothelial cell layer with no evidence of tissue edema or cellular disruption. By 24 hours, there were a few blood cells on the endothelial cell surface. There was no inflammatory infiltrate seen in the subendothelium, and the smooth muscle cells were unaltered. At 3 days, the endothelial cell lining remained intact with no polymorphonucleocytes in the subendothelium or within the graft wall. Underlying smooth muscle cells at this time were noted to contain cytoplasmic vacuoles. At 5 days, there were no inflammatory cells seen on the surface or within the vein graft wall, but many of the underlying smooth muscle cells within the intimal hyperplasia were noted to be fragmented and to have clumping of chromatin. After 7 days, the endothelial cells remained intact and there was widespread evidence of apoptosis beneath the subendothelium with highly fragmented smooth muscle cells, some of which were histologically in the process of breaking up. At 14 days, the grafts retained uniform endothelial cell surfaces. Most of the smooth muscle cells that composed the intimal hyperplasia seen before implantation as a reversal graft were gone. Areas of newly laid down collagen could be observed. There were no acute inflammatory cells but for some mast cells seen in the graft wall. This study demonstrates that in this model, regression of intimal hyperplasia was associated with apoptosis of the smooth muscle cells and the deposition of collagen. There was no evidence that this process is mediated by an acute inflammatory response. Regression therefore appears to be due to induction of smooth muscle cell apoptosis by either a reduction in pressure or flow or a combination of both factors. The findings will enable a systematic cellular and molecular analysis of the biology of regression, which may afford clues to better understand the biology of the developing intimal hyperplasia.     

Reduction of smooth muscle hyperplasia in vein grafts in athymic rats

While developing an animal model of a vascular malformation, we found that two doses of cyclosporin A significantly reduced the smooth muscle cell hyperplasia observed in vein-arterial interposition grafts in Sprague-Dawley rats. Therefore, we hypothesized that T cells may either produce or augment a mitogen for vascular smooth muscle cells. To further investigate this, we quantitated the extent of smooth muscle cell hyperplasia in the vein grafts of athymic nude rats that lack mature, functioning T cells. Male Sprague-Dawley rats (275 to 350 gm) and athymic nude rats were anesthetized, and a segment of the superficial epigastric vein was placed into the transected femoral artery using microsurgical techniques. Sprague-Dawley rats (N = 9) and athymic nude rats (N = 5) undergoing vein grafting received 30 mg/kg cyclosporin A intraperitoneally, intraoperatively and 24 hours later. Sprague-Dawley rats (N = 7) and athymic nude rats (N = 6) that had vein grafts were not treated with cyclosporin A. Animals were killed at either 3 weeks or 6 weeks and histologic sections were taken from the middle of the graft to avoid clamp-induced trauma. At 3 weeks, untreated vein grafts in Sprague-Dawley rats exposed to arterial pressure exhibited a nine-fold increase in smooth muscle hyperplasia compared with the preoperative vein. Treatment of Sprague-Dawley rats with cyclosporin A resulted in a 57% reduction of smooth muscle hyperplasia (p less than 0.05). Vein grafts from athymic nude rats exhibited a 51% reduction in smooth muscle hyperplasia (p less than 0.05). Sprague-Dawley rats killed at 6 weeks revealed a recovery of smooth muscle hyperplasia equivalent to an untreated Sprague-Dawley vein graft at 3 weeks. Inhibition of smooth muscle hyperplasia persisted for 6 weeks in the athymic nude rats. Cyclosporin A administration or T cell deficiency in athymic nude rats decreases the smooth muscle hyperplasia observed in venous grafts exposed to arterial pressure. This finding provides evidence for a possible role of T cells in the regulation of cell growth in the vascular wall.     

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.     

Smooth muscle changes in the cephalic vein of renal failure patients before use as an arteriovenous fistula (AVF).

Complications in arteriovenous fistula (AVF) occur in up to 35% of renal failure patients on hemodialysis. The most frequent complication is thrombosis, usually from stenotic lesions in the venous outflow system. To study the pre-existing smooth muscle changes in the cephalic vein of these patients, we prospectively collected a total of 17 cephalic vein specimens from 3 normal controls and 14 renal failure patients undergoing primary AVF construction on the chosen limb. After preparation, ultrathin sections were stained with uranyl and lead acetate and were examined under the transmission electron microscope (TEM). Compared with the normal controls, abnormal fibrous infiltration of the intima and the media and varying degrees of smooth muscle degenerative changes were observed in all the cephalic vein sections of renal failure patients. Smooth muscle cells (SMCs) lost their normal fusiform shape and were widely separated by increased amount of irregularly disposed, extracellular collagen fibers. Other cellular abnormalities included irregular cell membrane, granular cytoplasm, Peri- and Paranuclear vacuoles and mega mitochondria. SMCs also showed morphological expression of phagocytosis of collagen and elastic fibers as a sign of remodeling of the vein wall. In conclusion, pre-existing wall and smooth muscle changes were observed in all the cephalic vein sections of renal failure patients, which may contribute to the later complications of AVFs.     

The modulation of smooth muscle cell phenotype is an early event in human aorto-coronary saphenous vein grafts

Summary The morphological changes in human vein grafts occurring in the first days after a coronary bypass operation (CBP) are rarely reported in the literature. Sections of aorto-coronary vein grafts from 11 patients who died during the first 10 days after a CBP were obtained at autopsy. The number of vein grafts per patient ranged from 1 to 4, yielding a total of 28 vein grafts. The early changes in the vein grafts have been studied by light microscopy, immunohistochemistry, transmission and scanning electron microscopy. The study demonstrates that soon after grafting, the vein wall is infiltrated by polymorphonuclear leucocytes (PMN). At 24 h the endothelium shows extensive desquamation. The massive migration of PMN through the venous wall occurs simultaneously with the endothelial damage. The circular layer of the media is severely damaged, resulting in a loss of smooth muscle cells (SMC). The remaining SMC in this layer show a change toward the synthetic phenotype and a reduced expression of α-smooth muscle actin. These early changes in the SMC function may initiate the process of fibrosis in the intima and the media of the vein grafts.     

Functional relationship of venous to metabolic vessels of muscles in experimental venous insufficiency]

Modelled venous insufficiency of the hind limbs of cats (ligation of the posterior vena cava for 4-6 weeks) led to structural reorganization of the venous walls of the gastrocnemius muscle, which was manifested by a sharp increase of stretchability of the venous bed of the muscle if the activity of the smooth muscles was removed by papaverine, and by significant loss of the sensitivity of the smooth muscles of the intramuscular veins to noradrenaline as regards function. The range of adrenergic changes of postcapillary resistance and capillary pressure was reduced sharply in animals with venous insufficiency. This may be among the causes of disorders of metabolic processes in the skeletal muscles in venous insufficiency.     

Histologic Fate of the Venous Coronary Artery Bypass in Dogs

The histologic fate of venous grafts used for coronary artery bypass has been observed with light and electron microscopy in dogs. Endothelial damage and thrombosis were chiefly limited to the first postoperative week. The muscular media uniformly suffered extensive necrosis and inflammatory cell infiltration during the first week. Its smooth muscle cells either hypertrophied, died or underwent apparent fibroblastic transformation, with eventual fibrous replacement, to a variable degree, of the vein wall. Vascular wall ischemia due to interruption of vasa vasorum during transplantation appears to initiate these medial changes. Much more slowly, intimal thickening by myointimal cells and collagen may reduce the graft lumen to a variable extent.     

Structural Organization of Hepatic Portal Vein in Rat with Special Reference to Musculature,Intimal Folds,and Endothelial Cell Alignment

Structural organization of hepatic portal vein (HPV) was examined in adult rats by means of light and electron microscopy. Three characteristic features were found in the wall structure of rat HPV. (1) Tunica media consisted of two kinds of smooth muscle. The inner circular smooth muscle (CSM) was composed with one or two layer of smooth muscle cells, and was found in the entire length of the HPV and its tributaries. The outer longitudinal smooth muscle (LSM) was limited to a specific region of HPV; in particular it was well‐developed at distal half of HPV. CSM counteracts luminal hydrostatic pressure to prevent circumferential hyperextension of venous wall, whereas LSM is likely to counteract a tractive force produced by gravity and movement of small intestine. (2) Intima of HPV showed a unique feature, intimal folds, which protruded into the lumen and were aligned almost circumferentially. Intimal folds were found only at the same region where the LSM was well‐developed. Thus, LSM is presumably involved in the formation of intimal folds. (3) The endothelial cells between intimal folds were circumferentially aligned along the folds, although those in the other regions of HPV were arrayed along the longitudinal axis of HPV or the direction of blood flow as reported in other kinds of blood vessel. This finding implied that the circumferential blood flow locally occurs on the surface of intima between the intimal folds. Anat Rec, 2010. © 2010 Wiley‐Liss, Inc.     

自体移植兔静脉细胞增殖与钙激活钾通道的变化

目的: 研究静脉移植后钙激活钾通道(K_Ca)的变化,并探讨其病理生理意义。方法: 将兔的双侧股静脉倒置移植于同侧股动脉缺损之间,采用离体血管灌流的方法,测定移植静脉环的张力。分别以图像分析和四唑盐(MTT)比色法检测移植静脉内膜增厚的程度以及K_Ca的阻断剂盐酸四乙胺(tetraethylammonium chloride, TEA)对培养的家兔股静脉血管平滑肌细胞(vascular smooth muscle cells, VSMCs)增殖的影响。进而采用膜片钳技术记录K_Ca电流。 结果: 移植后1 week, 静脉的收缩性和内膜相对厚度没有显著变化。静脉移植后2 weeks,收缩性和内膜相对厚度显著大于对照组(P＜0.05, n=8)。移植后4 weeks静脉的收缩性和内膜相对厚度进一步大于对照组(P＜0.01, n=8)。TEA(2-8 mmol/L)显著增加培养VSMCs的MTT吸光值,并且有剂量依赖性(P＜0.05, n=8)。膜片钳实验结果显示,指令电位在(30-60)mV时,移植(1-4) weeks静脉VSMCs的K_Ca 电流密度均显著低于对照组(P＜0.05, n=5),指令电位在20 mV时,只有移植4 weeks静脉VSMCs的K_Ca电流密度显著低于对照组(P＜0.05, n=5)。结论: 自体移植静脉VSMC的K_Ca受到抑制,可能是血管收缩性增强、VSMCs异常增殖的原因,从而导致自体移植静脉痉挛和狭窄。     

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.     

Some properties of the smooth muscle of rabbit portal vein

1. The morphology of the smooth muscle of the rabbit portal vein and its innervation were studied with fluorescence and electron microscopy. Two layers of smooth muscle were observed in the tunica media: an inner layer of circularly arranged muscle cells and an outer layer consisting of bundles of smooth muscle cells arranged in a near longitudinal direction. The membranes of neighbouring smooth muscle cells were occasionally fused to form ;tight junctions'.2. Bundles of non-myelinated nerve fibres were observed in the adventitia, and between bundles and layers of smooth muscle cells in the media. Studies on longitudinal sections with fluorescence microscopy revealed a network of varicose noradrenergic axons.3. Electrical and mechanical activity was recorded from longitudinal strips of smooth muscle from the media of the vein with a sucrose-gap apparatus.4. The preparation was spontaneously active under minimal resting tension (less than 150 mg) and at temperatures above 28 degrees C. Slow depolarizations led to a burst of spikes (multi-spike complexes), which corresponded to rhythmic contractions. In 10% of preparations, the interval between multi-spike complexes showed a slower depolarization, suggesting the record was from a pace-maker region.5. The frequency of spontaneous activity (3-27 beats/min) was very sensitive to changes in temperature and tension.6. Noradrenaline in low doses (0.01 mug) caused an increase in frequency of the multi-spike complexes. Higher doses (0.1-0.3 mug) initiated continuous high-frequency spiking, while very high doses (0.6-2.0 mug) caused maintained depolarization.7. Responses to repetitive electrical stimulation of the vein were qualitatively similar to those in response to exogenous noradrenaline. The relation between the mechanical response and the various parameters of stimulation was consistent with the stimulation of sympathetic nerve fibres in the wall of the vein.8. The actions of isoprenaline, phentolamine and propranolol indicated the presence of alpha ;excitatory' and beta ;inhibitory' adrenotrophic receptors on the smooth muscle.     

Immunocytochemical investigation of atherosclerotic changes observed in aortocoronary bypass vein grafts using monoclonal antibodies

The authors have performed immunocytochemical surveys on atherosclerotic changes observed in saphenous vein aortocoronary bypass grafts, comparing the changes occurring in coronary and aortic lesions. The two monoclonal antibodies used in this study were obtained by T. Tsukada. One of them, named HHF35, exhibited specificity to smooth muscle cells; the other, named HAM56, was specific to macrophages. These immunocytochemical studies clearly demonstrated that cells encountered within the fibrous intimal thickening in the vein graft were inevitably smooth muscle cell in origin. Macrophages were seldom seen in the grafts examined. In contrast to vein grafts, macrophages were noted within the intima of all specimens from arterial atherosclerotic lesions obtained from the same patients. These studies suggest a difference in the progression of intimal thickening between the venous graft and the arterial atherosclerotic lesions.     

In vitro and in vivo studies of ePTFE vascular grafts treated with P15 peptide

The purpose of this study is to evaluate the effectiveness of P15 cell-binding peptide treated ePTFE vascular grafts in vitro and in vivo. The P15 peptide was covalently immobilized onto ePTFE vascular grafts by an atmospheric plasma coating method. In vitro cell growth properties were studied using primary human umbilical vein endothelial cells (HUVECs) and primary human umbilical artery smooth muscle cells (HUASMCs). X-ray photoelectron spectroscopy and amino-acid analysis were used to analyze the surface characteristics of the peptide treated and untreated grafts. The cell growth study showed that the P15 peptide effectively promoted the adhesion and proliferation of endothelial cells. 700% more endothelial cells were proliferated on the P15-treated ePTFE grafts compared to the untreated ePTFE controls. In contrast, the P15 peptide was significantly less effective for promoting the adhesion and proliferation of smooth muscle cells than endothelial cells; only about 100% more smooth muscle cells proliferated on the P15-treated samples compared to the untreated control samples. The sheep model was used in the in vivo study. The amount of neointimal hyperplasia present at the arterial and venous sides of the anastomosis and the degree of endothelialization on the luminal surface of the grafts were assessed. Four P15-treated grafts and two control grafts were implanted as arteriovenous grafts between the femoral artery and vein or the carotid artery and jugular vein in two sheep (n = 6). The in vivo study showed that the thickness of the neointimal hyperplasia of untreated grafts was 3-times thicker than that of P15-treated grafts (P < 0.05) at the venous side of the anastomosis. P15-treated grafts also had a higher degree of endothelialization on the graft lumen.     

Immune-induced vascular connective tissue alterations in rabbits chronically immunized with bovine serum albumin: morphological and morphometric studies on normal and injured thoracic aorta

The effect of persistent immunostimulation on normal and mechanically injured thoracic aorta was investigated histologically, histochemically and morphometrically. In the uninjured vessel wall no alterations suggestive of acute inflammation were observed following immunization, in accordance with previous biochemical studies. When mechanically elicited vascular injury and repair processes were induced in chronic immunostimulated rabbits, the neo-intimal aortic smooth muscle cell nuclear volume fraction of the vessel wall was significantly repressed, indicating, that the proliferative response to injury was inhibited. Further, the neo-intimal volume fraction of the vessel wall was reduced, suggesting impaired matrix neoformation. A highly significant linear correlation existed between the biochemically estimated DNA concentration and the nuclear volume fraction of smooth muscle cells in the vessel wall (r = 0.6275, P = 5 X 10(-5). Thus, the present study confirms previous biochemical observations, that the early processes of vascular inflammation and repair, i.e. smooth muscle cell proliferation and matrix accumulation, is inhibited following persistent immunostimulation. In addition to describing the histological correlates to the biochemical findings, important regional differences were quantified.     

Immune-induced vascular connective tissue alterations in rabbits chronically immunized with bovine serum albumin: morphological and morphometric studies on normal and injured thoracic aorta.

The effect of persistent immunostimulation on normal and mechanically injured thoracic aorta was investigated histologically, histochemically and morphometrically. In the uninjured vessel wall no alterations suggestive of acute inflammation were observed following immunization, in accordance with previous biochemical studies. When mechanically elicited vascular injury and repair processes were induced in chronic immunostimulated rabbits, the neo-intimal aortic smooth muscle cell nuclear volume fraction of the vessel wall was significantly repressed, indicating, that the proliferative response to injury was inhibited. Further, the neo-intimal volume fraction of the vessel wall was reduced, suggesting impaired matrix neoformation. A highly significant linear correlation existed between the biochemically estimated DNA concentration and the nuclear volume fraction of smooth muscle cells in the vessel wall (r = 0.6275, P = 5 X 10(-5). Thus, the present study confirms previous biochemical observations, that the early processes of vascular inflammation and repair, i.e. smooth muscle cell proliferation and matrix accumulation, is inhibited following persistent immunostimulation. In addition to describing the histological correlates to the biochemical findings, important regional differences were quantified.     

Pathological anatomy of the post-thrombophlebitic syndrome

In the post-thrombophlebitis syndrome (PTPS) of the lower extremities pathomorphological changes develop in deep magistral venous trunks, communicating and surface veins, and microcirculation tracts. On the basis of the study on 90 cases of PTPS the following variants of morphological alterations in femoral veins as the most frequently affected segment in deep thrombophlebites were observed: complete restoration of the venous lumen but with the wall sclerosis muscle element atrophy, and loss of the valvular apparatus; partial restoration of the lumen on account of thrombus canalization; complete occlusion of the lumen on account of thrombosis and rethrombosis. Pathomorphological lesions of communicating ans surface veins and microcirculatory bed depend upon the features of lesions in magistral veins and result in the development of chronic venous insufficiency with the syndrome of regional capillary trophic changes leading to edema, dystrophic, necrobiotic, and sclerotic lesions.     

2型糖尿病小鼠移植静脉再狭窄的血管平滑肌分布和功能的初步研究

目的 在构建2型糖尿病小鼠下腔静脉移植模型的基础上,观察糖尿病对移植术后桥静脉再狭窄后血管平滑肌的影响.方法 取20只8周龄雄性自发2型糖尿病C57 BL/KsJ leprdb/db(db/db)小鼠和20只C57 BL/KsJ野生型小鼠,建立下腔静脉-颈总动脉旁路移植手术动物模型,通过超声评估移植后血管血流及血管直径...     

The effect of pressure on the morphology of superior mesenteric vein in rabbits]

The effect of pressure on the morphology of the superior mesenteric vein of rabbits (SMV) was researched with the method of constant pressure fixation. The results indicate the morphology of SMV is similar to human umbilical cord vein. It looks like the structure of femoral artery of vein in many ways. Under constant pressure fixation (4 kPa), the internal elastic membrane of SMV is straightened, and the wall of SMV becomes thin, with its media thinning from 51.680 microns to 32.3260 microns. The long diameter of nucleus of the smooth muscles decreases from 1.9146 microns to 3.4980 microns, the short diameter of nucleus of the smooth muscles becomes from 0.7884 micron to 0.5228 micron. The direction of the tension on the smooth muscles is mainly longitudinal.