RBC aggregation,deformation and adhesion to endothelium:Role of nitric oxide derived from L-Arginine and sodium nitroprusside

Red blood cells(RBCs)are the most abundant human blood cells.RBC aggregation and deformation strongly determine blood viscosity which impacts hemorheology and microcirculation.In turn,RBC properties depend on di®erent endogenous and exogenous factors.One such factor is nitric oxide(NO),which is mainly produced by endothelial cells(EC)from L-arginine amino acid in the circulatory system.Since the mechanisms of the RBC-endothelium interplay are not clear up to date and considering its possible clinical importance,the aims of this study are to investigate in vitro:(1)The effect of L-arginine induced NO on RBC aggregation and adhesion to endothelium;(2)the NO e®ect on RBC aggregation and deformation induced by L-arginine and sodium nitroprusside without the presence of endothelium in the samples.The RBC aggregation and adhesion to a monolayer of EC were studied using optical tweezers(OT).The RBC deformability and aggregation without endothelium in the samples were studied using the flow chamber method and Myrenne aggregometer.We confirmed that NO increases deformability and decreases aggregation of RBCs.We showed that the soluble guanylate cyclase pathway appears to be the only NO signaling pathway involved.In the samples with the endothelium,the "bell-shaped"dependence of RBC aggregation force on L-arginine concentration was observed,which improves our knowledge about the process of NO production by endothelium.Additionally,data related to L-arginine accumulation by endothelium were obtained:Necessity of the presence of extracellular L-arginine stated by other authors was put under question.In our study,NO decreased the RBC-endothelium adhesion,however,the tendency appeared to be weak and was not confirmed in another set of experiments.To our knowledge,this is the first attempt to measure the forces of RBC adhesion to endothelium monolayer with OT.

Effects of moxibustion at 46°C on blood lipids and related indicators of thoracic aortic endothelium in a hyperlipidemia rat model

Objective:To observe the effects of moxibustion at different temperatures(38℃,46℃)on blood lipids,endothelial morphology of the thoracic aorta,serum endothelin-1(ET-1),calcitonin gene-related peptide(CGRP),nitric oxide(NO),and endothelial NO synthase(eNOS)in hyperlipidemic rats.Methods:Using the random number table method,60 Sprague Dawley rats were randomly and evenly divided into blank,model,38℃-moxibustion,and 46℃-moxibustion groups.Rats in the 3 experimental groups were fed a high-fat feed to model hyperlipidemia in rats.Rats in the 38℃-moxibustion and 46℃-moxibustion groups were moxibustion on the Shenque and bilateral Zusanli acupoints for 10 minutes each,once every other day for 4 weeks,at temperatures of 38±1℃ and 46±1℃.After that,rat blood samples were collected to detect blood lipids and ET-1,CGRP,eNOS and NO.Take the endotheal tissue of the thoracic aorta to do HE staining.Results:(1)The serum total cholesterol,triglycerides,and low-density lipoprotein cholesterol of rats in the 46℃-moxibustion group were significantly lower than those in the model and 38℃-moxibustion groups.(2)Revealed by hematoxylin and eosin staining,showed necrosis in the local vascular endothelial cells and mild inflammatory cell infiltration in the tunica adventitia of the hyperlipidemic rats.These endothelial morphologies did not improve significantly after moxibustion at 38℃ but did improve at 46℃.(3)Compared with the blank group,serum ET-1 was significantly higher and serum CGRP,NO,eNOS were significantly lower in the model group.Compared with the model and the 38℃-moxibustion groups,serum ET-1 was significantly lower and serum CGRP,NO,eNOS were significantly higher in 46℃-moxibustion groups.Conclusion:Moxibustion at 46℃ effectively regulated blood lipids,improved the morphology of the vascular endothelium,and protected vascular endothelial function.

Endothelium-derived essential signals involved in pancreas organogenesis

Endothelial cells(ECs) are essential for pancreas differentiation, endocrine specification, and endocrine function. They are also involved in the physiopathology of type 1 and type 2 diabetes. During embryogenesis, aortic ECs provide specific factors that maintain the expression of key genes for pancreas development such as pancreatic and duodenal homeobox-1. Other unknown factors are also important for pancreatic endocrine specification and formation of insulin-producing beta cells. Endocrine precursors proliferate interspersed with ductal cells and exocrine precursors and, at some point of development, these endocrine precursors migrate to pancreatic mesenchyme and start forming the islets of Langerhans. By the end of the gestation and close to birth, these islets contain immature beta cells with the capacity to express vascular endothelial growth factor and therefore to recruit ECs from the surrounding microenvironment. ECs in turn produce factors that are essential to maintain insulin secretion in pancreatic beta cells. Once assembled, a cross talk between endocrine cells and ECs maintain the integrity of islets toward an adequate function during the whole life of the adult individual. This review will focus in the EC role in the differentiation and maturation of pancreatic beta cells during embryogenesis as well as the current knowledge about the involvement of endothelium to derive pancreatic beta cells in vitro from mouse or human pluripotent stem cells.

Changes in aortic endothelium ultrastructure in male rats following castration, replacement with testosterone and administration of 50α-reductase inhibitor

Aim： To investigate the relationship between low androgen level and ultrastructure of vascular endothelium. Methods： Forty-eight male Sprague-Dawley rats were randomly divided into four groups： group A, normal rats with sham castration; group B, castrated rats; group C, castrated rats given testosterone （T） undecanoate; and group D, intact rats treated with 5α-reductase inhibitor. After 10 weeks of treatment or castration, rats in different groups were killed and serum T, free T （FT） and dihydrotestosterone （DHT） were measured. The aortic endothelia were scanned under electron microcopy and the Vascular Endothelium Structure Score （VESS） was computed. Results： Serum T and FT concentrations of rats in group B were significantly lower than those of the other three groups （P 〈 0.01）; DHT concentrations of group D rats were significantly decreased （P 〈 0.01 ） when compared with those of groups A and C. Rats in groups B and D rats （with low androgen levels） had obvious damage to their endothelial surfaces, which appeared crimpled, rough, adhesive and ruptured, and had high destruction of VESS. Conclusion： These results suggest that low concentrations of T and DHT are associated with ultrastructural damage of the aortic endothelia in male rats.

Differences in energy and corneal endothelium between femtosecond laser-assisted and conventional cataract surgeries：prospective,intraindividual,randomized controlled trial

AIM： To compare intraoperative phacoemulsification parameters and its effect on the corneal endothelium of eyes undergoing femtosecond laser-assisted cataract surgery（FLACS） versus conventional phacoemulsification（CP） cataract surgery.METHODS： Two hundred eyes from one hundred patients were included in a prospective, non-blinded, randomized, controlled, intraindividual clinical study. One hundred eyes underwent FLACS while their one hundred fellow eyes underwent CP. All surgeries were performed using the Victus？ femtosecond laser platform and Infinity？ Vision System phacoemulsification machine. Primary outcome measure was endothelial cell density 6 mo after surgery. Secondary outcome measures included central corneal thickness（CCT）, average cell area, standard deviation, coefficient of variation and hexagonality before surgery and 6 mo after surgery and endothelial cell density loss during this period were also evaluated. Intraoperative efficiency parameters [cumulative dissipated energy（CDE）, total intraocular surgery time, total ultrasound time, total phacoemulsification time, total torsional energy time, total aspiration time, ultrasound energy, torsional amplitude and fluid required during surgery] were also collated. RESULTS： Data from these patients was not considered for analysis. Data from 92 patients were analysed. Postoperative endothelial cell density（cells/mm2） between groups（2211.88±392.49 CP; 2246.31±403.48 FLACS） was not statistically significant（P=0.869）. Total ultrasound time, torsional energy time, CDE and fluid requirements were significantly lower the FLACS group（P〈0.05）. Other parameters did not show statistically significant difference between FLACS and CP.CONCLUSION： FLACS displays significant improvements in phacoemulsification parameters in comparison to CP. There are no significant differences in corneal endothelium measures between FLACS and CP.

Effect of topical 0.05% cyclosporine A on corneal endothelium in patients with dry eye disease

· AIM: To determine the effect of topical 0.05% cyclosporine A (CsA) on corneal endothelium in patients with dry eye disease. · METHODS: Observational, prospective, case series study. Fifty-five eyes of 29 consecutive patients (9 males and 20 females; median age: 66.8 years, interquartile range: 61 -73.2 years) with moderate -severe dry eye disease were evaluated. All patients were treated with topical 0.05% CsA ophthalmic emulsion twice a day in addition to lubricant eyedrops 5 times a day. The follow- up period was 12 months. Before treatment and at 3 and 12 months post -treatment central corneal specular microscopy was performed. The endothelial cell density (ECD), coefficient of variation of cell size (CoV), and percentage of hexagonal cells (Hex %) were analyzed. ·RESULTS: The median ECDs pre-treatment and at 3 and 12 months post-treatment were 2 352.5/mm 2 (inter- quartile range, 2 178 -2548.5), 2 364/mm 2 (interquartile range, 2 174.25 -2 657.5), and 2 366 cells/mm 2 (inter - quartile range, 2 174.75-2 539.75), respectively (P=0.927, one way ANOVA). The median CoVs pre-treatment and at 3 and 12 months post -treatment were 34.5 (interquartile range, 30 -37), 35 (interquartile range, 30 -38), and 34 (interquartile range, 30.75-38.25), respectively (P=0.7193, one way ANOVA). The median Hex % values pre - treatment and at 3 and 12 months post -treatment were 53 (interquartile range, 47 -58), 54 (interquartile range, 45.75 -59), and 50.5 (interquartile range, 45.75 -58), respectively (P=0.824, one way ANOVA). · CONCLUSION: Treatment of patients with dry eye disease for 12 months with topical 0.05% CsA does not seem to cause substantial changes on corneal endothelium.

Relationship between vascular endothelium and periodontal disease in atherosclerotic lesions: Review article

Inflammation and endothelial dysfunction are linked to the pathogenesis of atherosclerotic disease. Recent studies suggest that periodontal infection and the ensuing increase in the levels of inflammatory markers may be associated with myocardial infarction, peripheral vascular disease and cerebrovascular disease. The present article aimed at reviewing contemporary data on the pathophysiology of vascular endothelium and its association with periodontitis in the scenario of cardiovascular disease.

VEGF Deficit is Involved in Endothelium Dysfunction in Preeclampsia

This study examined the association of expression of vascular endothelial growth factor(VEGF),a promoter of angiogenesis,with endothelium dysfunction in preeclampsia.The level of VEGF protein and mRNA in the placenta and peripheral blood samples of 30 preeclampsia patients and 30 normotensive pregnant women was measured by immunohistochemistry,real-time reverse transcriptase-polymerase chain reaction(RT-PCR) and enzyme-linked immunosorbent assay(ELISA),respectively.VEGF expression in the human umbilical vein endothelial cells(HUVECs) was blocked by small interfering RNAs(siRNAs).The monolayer barrier function of HUVECs was determined by measuring the fluorescence intensity of BSA that crossed the HUVEC monolayers.The cell proliferation and cell-secreted nitric oxide(NO) level were detected by MTT method and nitrate reductase assay,respectively.The results showed that VEGF was expressed in the syncytiotrophoblasts and endothelial cells of vessels and capillaries in the placenta tissue.The serum level of VEGF in the preeclampsia patients was significantly decreased as compared with that in normal pregnant subjects,although VEGF mRNA expression in the placenta tissue of preeclampsia patients remained still high.Moreover,VEGF deficit could lead to endothelium cell dysfunction,and the administration of VEGF could protect endothelium cells from injury.It was concluded that lack of VEGF contributes to endothelium dysfunction,which may lead to the occurrence and development of preeclampsia.

A multiscale model for analyzing the synergy of CS and WSS on the endothelium in straight arteries

A multiscale model was proposed to calculate the circumferential stress （CS） and wall shear stress （WSS） and analyze the effects of global and local factors on the CS, WSS and their synergy on the arterial endothelium in large straight arteries. A parameter pair [Zs, SPA] （defined as the ratio of CS amplitude to WSS amplitude and the phase angle between CS and WSS for different harmonic components, respectively） was proposed to characterize the synergy of CS and WSS. The results demonstrated that the CS or WSS in the large straight arteries is determined by the global factors, i.e. the preloads and the afterloads, and the local factors, i.e. the local mechanical properties and the zero-stress states of arterial walls, whereas the Zs and SPA are primarily determined by the local factors and the afterloads. Because the arterial input impedance has been shown to reflect the physiological and pathological states of whole downstream arterial beds, the stress amplitude ratio Zs and the stress phase difference SPA might be appropriate indices to reflect the influences of the states of whole downstream arterial beds on the local blood flow-dependent phenomena such as angiogenesis, vascular remodeling and atherosgenesis.

Androgen actions on endothelium functions and cardiovascular diseases

The roles of androgens on cardiovascular physiology and pathophysiology are controversial as both beneficial and detrimental effects have been reported. Although the reasons for this discrepancy are unclear, multiple factors such as genetic and epigenetic variation, sex-specificity, hormone interactions, drug preparation and route of administration may contribute. Recently, growing evidence suggests that androgens exhibit beneficial effects on cardiovascular function though the mechanism remains to be elucidated. Endothelial cells （ECs） which line the interior surface of blood vessels are distributed throughout the circulatory system, and play a crucial role in cardiovascular function. Endothelial progenitor cells （EPCs） are considered an indispensable element for the reconstitution and maintenance of an intact endothelial layer. Endothelial dysfunction is regarded as an initiating step in development of atherosclerosis and cardiovascular diseases. The modulation of endothelial functions by androgens through either genornic or nongenomic signal pathways is one possible mechanism by which androgens act on the cardiovascular system. Obtaining insight into the mechanisms by which androgens affect EC and EPC functions will allow us to determine whether androgens possess beneficial effects on the cardiovascular system. This in turn may be critical in the prevention and therapy of cardiovascular diseases. This article seeks to review recent progress in androgen regulation of endothelial function, the sex-specificity of androgen actions, and its clinical applications in the cardiovascular system.

Role of the endothelium in inflammatory bowel diseases

Inflammatory bowel diseases(IBD) are a complex group of diseases involving alterations in mucosal immunity and gastrointestinal physiology during both initiation and progressive phases of the disease.At the core of these alterations are endothelial cells,whose continual adjustments in structure and function coordinate vascular supply,immune cell emigration,and regulation of the tissue environment.Expansion of the endothelium in IBD(angiogenesis),mediated by inflammatory growth factors,cytokines and chemokines,is a hallmark of active gut disease and is closely related to disease severity.The endothelium in newly formed or inflamed vessels differs from that in normal vessels in the production of and response to inflammatory cytokines,growth factors,and adhesion molecules,altering coagulant capacity,barrier function and blood cell recruitment in injury.This review examines the roles of the endothelium in the initiation and propagation of IBD pathology and distinctive features of the intestinal endothelium contributing to these conditions.

Response of the xenograft endothelium in the concordant xenotransplantation

To investigate the response of the xenograft endothelium in the concordant hamster to rat cardiac xenotransplantation and the mechanism of acute vascular rejection. Methods： The animals were divided into 5 groups randomly： control group, CsA group, splenectomy group, DO splenectomy＋CsA group and D3 splenectomy＋CsA group. Hamster heart was heterotopicaly transplanted to rat abdominal cavity. The graft survival was monitored by palpation of the rat abdominal wall. The histological and ultrastructural changes of the xenogafts were investigated. NF-κB and P-selectin expression in the xenograft were detected. Heme Oxigenase-1 and Bcl-2 expression were also detected in the xenografts of different groups. Results： The mean survival time of the xenografts in control group, CsA group, splenectomy group, DO splenectomy＋CsA group and D3 splenectomy＋CsA group was 3.4±0.55, 3.8±0,45, 6.4± 1.52, 30 and 7.4 ±1.14 days. The rejected graft showed typical acute vascular rejection in control group, CsA group,splenectomy group and D3 splenectomy＋CsA group. Endothelial cells of the rejected xenograft showed dramatic assembly of ribosomes and expansion of the rough endoplasmic reticulum. However, the endothelium of the long-term survived grafts in DO splenectomy＋CsA group showed normal architecture. NF-κB and P-selectin expression were detected in the rejected xenografts. HO-1 expression was observed in the long-term survived xenografts in DO splenectomy＋CsA group. Conclusion： The endothelial cells of the xenograft might be activated during the acute vascular rejection. Expression of HO-1 might inhibit the upregulation of NF-κB and adhesion molecular which decreases the activation of the endotheliuna of the graft.

Two male study groups with adiposity and hypertriglyceridemia were at risk for hypertension and alcohol use declined renal endothelium

Men who attended a Bavarian General Medicine Practice were confidentially invented here. Two male study groups were enrolled to characterize adiposity or hypertriglyceridemia showing that these men were at baseline risk for hypertension [1]. Adverse alcohol consumption mediated dysfunction of renal endothelium as shown here and before [1]. This study found that alcohol use aggravated dyslipidemia, fatty liver disease and critical fasting blood glucose of obese men predicting then late hepatorenal disorders. Overall, two male study groups showed a relevant proportion of men who reported alcohol consumption showing then critical morning urines indicating dysfunction of renal endothelium. The present report looked also at healthy men who reported positive lifestyle behaviour and at men with nonalcohol adiposity and nonalcohol hypertriglyceridemia who then showed normal morning urines indicating functional renal endothelium. Relatively young men at risk were motivated to replace adverse alcohol use by healthy liquids without alcohol and by higher quality of food.

Scutellarin Reduces Cerebral Ischemia Reperfusion Injury Involving in Vascular Endothelium Protection and PKG Signal

Flavonoid glycoside scutellarin(SCU)has been widely applied in the treatment of cerebral ischemic diseases in China.In this article,we conducted research on the working mechanisms of SCU in hypoxia reoxygenation(HR)injury of isolated cerebral basilar artery(BA)and erebral ischemia reperfusion(CIR)injury in rat models.In isolated rat BA rings,HR causes endothelial dysfunction(ED)and acetylcholine(ACh)induces endothelium-dependent vasodilation.The myography result showed that SCU(100μM)was able to significantly improve the endothelium-dependent vasodilation induced by Ach.However,SCU did not affect the ACh-induced relaxation in normal BA.Further studies suggested that SCU(10-1000μM)dose-dependently induced relaxation in isolated BA rings which were significantly blocked by the cGMP dependent protein kinase(PKG)inhibitor Rp-8-Br-cGMPs(PKGI-rp,4μM).Pre-incubation with SCU(500μM)reversed the impairment of endothelium-dependent vasodilation induced by HR,but the reversing effect was blocked if PKGI-rp(4μM)was added.The brain slice staining test in rats’model of middle cerebral artery occlusion(MCAO)induced CIR proved that the administration of SCU(45,90 mg/kg,iv)significantly reduced the area of cerebral infarction.The Western blot assay result showed that SCU(45 mg/kg,iv)increased brain PKG activity and PKG protein level after CIR surgery.In conclusion,our findings suggested that SCU possesses the ability of protecting brain cells against CIR injury through vascular endothelium protection and PKG signal.

The Role of Endoplasmic Reticulum Stress-related Apoptosis in Vascular Endothelium Pathogenesis

Vascular endothelium refers to a single layer of endothelial cells that line the inner surface of blood vessels,serving as barriers and transducers between the circulating blood in the lumen and the rest of the vessel wall.Endothelial cells play essential roles in many aspects of vascular biology,such as barrier functions,thrombosis/fibrinolysis,inflammation,angiogenesis,vasoconstriction and vasodilation.

Transplanting embryonic stem cells onto damaged human corneal endothelium

AIM To investigate whether human embryonic stem cells(hESCs) could be made to attach, grow and differentiate on a human Descemet's membrane(DM).METHODS Spontaneously differentiated hESCs were transferred onto a human corneal button with the endothelial layer removed using ocular sticks. The cells were cultured on a DM for up to 15 d. The genetically engineered hESC line expressed green fluorescent protein, which facilitated identification during the culture experiments, tissue preparation, and analysis. To detect any differentiation into human corneal endothelial-like cells, we analysed the transplanted cells by immunohistochemistry using specific antibodies.RESULTS We found transplanted cells form a single layer of cells with a hexagonal shape in the periphery of the DM. The majority of the cells were negative for octamer-binding transcription factor 4 but positive for paired box 6 protein, sodium potassium adenosine triphosphatase(NaKATPase), and Zona Occludens protein 1. In four of the 18 trials, the transplanted cells were found to express CK3, which indicates that the stem cells differentiated into corneal epithelial cells in these cases. CONCLUSION It is possible to get cells originating from hESCs to become established on a human DM, where they grow and differentiate into corneal endothelial-like cells in vitro.

Expression of mucosal addressin cell adhesion molecule 1 on vascular endothelium of gastric mucosa in patients with nodular gastritis

AIM:The interaction of mucosal addressin cell adhesion molecule 1 (MAdCAM-1) with integrin α4β7 mediates lymphocyte recruitment into mucosa-associated lymphoid tissue (MALT).Nodular gastritis is characterized by a unique military pattern on endoscopy representing increased numbers of lymphoid follicles with germinal center,strongly associated with H pylori infection.The purpose of this study was to address the implication of the MAdCAM-1/integrin β7 pathway in NG. METHODS:We studied 17 patients with NG and H pylori infection and 19 H pylori-positive and 14 H pylori-negative controls.A biopsy sample was taken from the antrum and snap-frozen for immunohistochemical analysis of MAdCAM- 1 and integrin β7.In simultaneous viewing of serial sections, the percentage of MAdCAM-1-positive to von Willebrand factor-positive vessels was calculated.We also performed immunostaining with anti-CD20,CD4,CD8 and CD68 antibodies to determine the lymphocyte subsets co- expressing integrin β7. RESULTS:Vascular endothelial MAdCAM-1 expression was more enhanced in gastric mucosa with than without H pylori infection.Of note,the percentages of MAdCAM-1-positive vessels were significantly higher in the lamina propria of NG patients than in H pylori-positive controls.Strong expression of MAdCAM-1 was identified adjacent to lymphoid follicles and dense lymphoid aggregates.Integrin β7-expressing mononuclear cells,mainly composed of CD20 and CD4 lymphocytes,were associated with vessels lined with MAdCAM-1-expressing endothelium.CONCLUSION: Our results suggest that the MAdCAM一1/ integrin a4p7 homing system may participate in gastric inflammation in response to H py/o}i-infection and contributes to MALT formation, typically leading to the development of NG.

STUDY IN CYTOTOXICITY OF GENTAMYCIN TO CORNEAL EPITHELIUM AND ENDOTHELIUM IN TISSUE CULTURE

A study in cytotoxicity of gentamyein to tissue-cultured bovine corneal endothelial cells and rabbit corneal epithelial cells is reported. When the cultured cells reached confluence, they were exposed to tissue culture media containing gentamycin for 6 hours. We founl that 0.5% gentamycin caused significant damage to corneal epithelial cells---diffuse plasmolysis, with scattered cell necrosis and 5% loss.While corneal endothelial cells were exposed to 1.6 mg/ml gentamycin, extensive cell loss (approximate- ly 15%) was observed. The damaged cells recovered their normal morphology after 24 hours. When the concentration of gentamycin increased twice, serious damage to cells occured. The area of cell loss reached 40%, and the recovery of cellular morphology Was much slower. This study demonstrates that gentamycin potential cytotoxicity to corneal epithelium and endothelium, suggesting that gentamycin should be rationally used in the treatment of ocular diseases.

Combined antihypertensive effect of GSY and metoprolol,based on endothelium-dependent vasodilatation function

OBJECTIVE To investigate the synergistic effect on dilating blood vessels and anti-hypertension of GYS combined with metoprolol.METHODS ① Spontaneously hypertensive rats(SHR)were administered orally with the vehicle,GSY,metoprolol or GSY combined with metoprolol for 4weeks.Blood pressure,which included SBP,DBP and MBP was measured by a noninvasive method every week.At the end of4 weeks,blood was drawn from the ophthalmic venous plexus to determine blood fat levels(serum TC,TG,LDL-c,HDL-c),liver function(serum ALT,AST),and kidney function(serum BUN,UA and Cr)by the ACCUTE(TBA-40FR)automatic.② The aortae of normal SD rats were prepared and cleaned from periadventitial fat and surrounding connective tissue and cut transversely into 4-mm width rings.To observe different concentration of GYS,metoprolol or GSY combined with metoprolol causing relaxation of the isolated aortic rings precontracted until a stable plateau by noradrenaline(NA)directly or in the presence of eNOS inhibitor L-NAME and cyclooxygenase inhibitor indomethacin(INDO)respectively.③ The concentrations of plasma GSY was determined by the HPLC after rats administered orally with GSY or GSY combined with metoprolol for single-dose.DAS data processing software calculated the pharmacokinetic parameters of GSY.RESULTS There was a significant synergism between GYS and metoprolol in lowering blood pressure and the concentrations of serum TC and LDL-c of SHR.The relaxant effect of GYS combined with metoprolol on the aortic rings precontracted by NA could be attenuated by L-NAME or INDO.The AUC0-tof GSY significantly increased after in conjunction with metoprolol.CONCLUSION GYS combined with metoprolol increases the concentrations of plasma GSY and synergistically lowers blood pressure based on endothelium-dependent vasodilatation function(EDVF).

EXPERIMENTAL STUDY ON THE CORNEAL ENDOTHELIUM OF TRAUMATIC CATARACT

The cell morphology of corneal endothelium in 84 mice with experimental traumatic cataract was investigated with stained corneal buttons. In the experimental group, the boundaries between adjacent corneal endothelial cells were significantly distorted, some cell boundaries manifested degenerative changes that led to coalescence of the cells. The mean density and mean area of endothelial cells of the controls showed significant difference from those of the experimental group during the 12 weeks of observ...