Defective blood vessel development and pericyte/pvSMC distribution in alpha 4 integrin-deficient mouse embryos

Blood vessel development is in part regulated by pericytes/presumptive vascular smooth muscle cells (PC/pvSMCs). Here, we demonstrate that interactions between PC/pvSMCs and extracellular matrix play a critical role in this event. We show that the cranial vessels in alpha4 integrin-deficient mouse embryos at the stage of vessel remodeling are increased in diameter. This defect is accompanied by a failure of PC/pvSMCs, which normally express alpha4beta1 integrin, to spread uniformly along the vessels. We also find that fibronectin but not VCAM-1 is localized in the cranial vessels at this stage. Furthermore, cultured alpha4 integrin-null PC/pvSMCs plated on fibronectin display a delay in initiating migration, a reduction in migration speed, and a decrease in directional persistence in response to a polarized force of shear flow. These results suggest that specific motile activities of PC/pvSMCs regulated by mechanical signals imposed by the interstitial extracellular matrix may also be required in vivo for the distribution and function of the PC/pvSMCs during blood vessel development.     

Angiotensin II type 1 (AT1)-receptor blocker prevents impairment of endothelium-dependent cerebral vasodilation by acute cigarette smoking in rats

Our aim was to test for smoking-induced endothelial dysfunction in rat cerebral vessels, then to evaluate the effect of valsartan [angiotensin II type I (AT1)-receptor blocker] on that impairment. In pentobarbital-anesthetized, mechanically ventilated Sprague-Dawley rats, we used a cranial window preparation to measure changes in pial vessel diameters following topical applications of acetylcholine (Ach) (before and after smoking or intravenous nicotine infusion; n = 6 in each group), and adenosine (n = 6 for before and after smoking). Then, after intravenous valsartan pretreatment we reexamined the pial vasodilator response to topical Ach (before and after cigarette smoking). Under control conditions, cerebral arterioles were dilated by 6.9 +/- 4.2% and 13.6 +/- 4.8% by topical Ach (10(-6) M and 10(-5) M, respectively) and by 6.4 +/- 2.5% and 12.2 +/- 3.1% by topical adenosine (10(-5) M and 10(-4) M, respectively). One hour after a 1-min inhalation of mainstream smoke (1-mg nicotine cigarette), 10(-5) M Ach constricted cerebral arterioles (-4.4 +/- 4.1%), while 10(-4) M adenosine dilated them by 13.4 +/- 3.4%. One hour after a 1-min nicotine infusion (0.05 mg), 10(-5) M Ach dilated cerebral arterioles by 9.9 +/- 2.4%. Thus, vasodilator response to topical Ach was impaired after smoking, whereas that to adenosine was unaffected. However, the vasodilator response to Ach was unaffected by intravenous nicotine. Valsartan prevented smoking from impairing Ach-induced vasodilation. In conclusion, acute single-cigarette smoking causes a dysfunction of endothelium-dependent, but not endothelium-independent, vasodilation of rat cerebral vessels in vivo, and the effect was not mimicked by intravenous nicotine. AT1-receptor blockade prevented the above smoking-induced impairment of endothelium-dependent vasodilation.     

The relative importance of the deep and superficial vascular systems for delay of the transverse rectus abdominis musculocutaneous flap as demonstrated in a rat model

The use of some form of delay maneuver for "high-risk" patients before transfer of the superior pedicled lower transverse rectus abdominis musculocutaneous (TRAM) flap for breast reconstruction has augmented the rate of success in both the experimental and clinical arenas. A common method of vascular delay has been the bilateral division of both the superficial inferior epigastric and deep inferior epigastric vessels. Whether all of these must be divided to adequately effect the delay is unknown. For that matter, the relative importance of the superficial versus the deep vascular systems is unclear. To investigate this uncertainty, a delay was attempted in 61 Sprague-Dawley rats by division of either the superficial inferior epigastric or deep cranial epigastric vessels (the latter is the homologue to the human deep inferior epigastric) in unilateral or bilateral fashion. Division of the contralateral superficial inferior epigastric vessel resulted in significantly greater TRAM flap survival than either ipsilateral or bilateral superficial inferior epigastric vessel division (p = 0.0034 or p = 0.0093, respectively). Division of the ipsilateral or bilateral deep cranial epigastric vessel resulted in significantly greater flap survival than just contralateral deep cranial epigastric vessel division (p = 0.0034 or p = 0.006, respectively). No significant difference was observed between the group having contralateral superficial inferior epigastric or groups with ipsilateral deep cranial epigastric division, implying that either alone would be efficacious to achieve the desired delay effect. This would allow the other vascular system to be retained intact for later potential salvage maneuvers as needed.     

Dynamic viscous flow in distensible vessels of skeletal muscle microcirculation: application to pressure and flow transients

Blood flow in the microcirculation of the rat skeletal muscle during transient changes of arterial pressure is analyzed theoretically. Although flow in such small vessels is quasi-steady and has a very low Reynolds number, time-dependent nonuniform flows along the length of the blood vessels can be observed due to vessel distensibility. The governing equations for a single microvessel are derived using previously measured microvessel elasticity, and several solutions to different inflow and outflow pressures and flow conditions are investigated. The results indicate that when such distensible microvessels are subjected to a step increase of arterial pressure, the arterial flow shows a rapid overshoot followed by a progressive decay to steady-state. An arterial step flow induces a different response which takes the form of a monotonically increasing pressure. Pressure and flows are nonuniform along the vessel length during such transients. In-vitro whole organ pressure-flow data are presented in the dilated rat gracilis muscle which qualitatively agree with the theoretical predictions.     

Blood vascular system of the sea cucumber,Stichopus moebii

Stichopus moebii, a sea cucumber, has a closed circulatory system which is unique in its degree of development for the phylum Echinodermata. The gross anatomy, histology and fine structure of the system were studied. Blood vessels consist of a coelomic surface of ciliated epithelium, a layer of muscle and nerve cells, followed by connective tissue and luminal lining of endothelium. Basically the blood vascular system consists of two major vessels running parallel to the gut: the dorsal vessel pumps colorless blood via the vessels within the walls of the intestine into the ventral vessel. There are two specialized areas of the circulation: (1) At the upper small intestine 120 to 150 muscular single-chambered hearts pump blood from the dorsal vessel into a series of intestinal plates. (2) At the lower region of the small intestine the vasculature is associated with the left respiratory tree. Blood passing from the dorsal pulmonary vessel can take two routes to the gut, it either passes through myriads of minute respiratory shunt vessels entangled with the respiratory tree or it passes through a unique follicle network consisting of tiny channels periodically dilated into chambers filled with iron deposits, necrotic cells and developing coelomocytes.     

Long-Term Catheterization of the Intestinal Lymph Trunk and Collection of Lymph in Neonatal Pigs

Catheterization of the intestinal lymph trunk in neonatal pigs is a technique allowing for the long-term collection of large quantities of intestinal (central) efferent lymph. Importantly, the collection of central lymph from the intestine enables researchers to study both the mechanisms and lipid constitutes associated with lipid metabolism, intestinal inflammation and cancer metastasis, as well as cells involved in immune function and immunosurveillance. A ventral mid-line surgical approach permits excellent surgical exposure to the cranial abdomen and relatively easy access to the intestinal lymph trunk vessel that lies near the pancreas and the right ventral segment of the portal vein underneath the visceral aspect of the right liver lobe. The vessel is meticulously dissected and released from the surrounding fascia and then dilated with sutures allowing for insertion and subsequent securing of the catheter into the vessel. The catheter is exteriorized and approximately 1 L/24 hr of lymph is collected over a 7 day period. While this technique enables the collection of large quantities of central lymph over an extended period of time, the success depends on careful surgical dissection, tissue handling and close attention to proper surgical technique. This is particularly important with surgeries in young animals as the lymph vessels can easily tear, potentially leading to surgical and experimental failure. The video demonstrates an excellent surgical technique for the collection of intestinal lymph.     

The delay phenomenon: the story unfolds

Our previous studies have shown that when a flap is delayed, there is dilation of existing vessels within the flap not ingrowth of new vessels. The maximal anatomic effect on the arterial tree occurs at the level of the reduced-caliber "choke" anastomotic vessels that link adjacent vascular territories. To further investigate the sequence of anatomic changes that occurs during the delay phenomenon, a large series of 200 rabbits and 17 dogs underwent a flap delay procedure in either skin or muscle and the tissues were examined at postoperative periods between 1 hour and 1 year by using well-established fluorescein, angiographic, light microscopic, immunohistochemical, and electron microscopic techniques. These data in the rabbit skin consistently demonstrated an initial period of vasoconstriction that resolved within 3 hours postoperatively and was followed by an active and progressive dilation of choke vessels that was most dramatic between 48 and 72 hours. In vivo intravenous fluorescein dye testing revealed an interesting parallel in that there was a temporary barrier to the flow of fluorescein that occurred at the level of the choke vessels immediately after the flap was raised and that this temporary barrier-continued to impede the flow toward the flap tip in rabbits where flaps had been delayed for periods up to 72 hours. Thereafter, there was no obstruction to the flow of fluorescein along the flap. During this early delay period of 3 days, light microscopy revealed a decrease in vessel wall thickness associated with an increase in lumen diameter. Over the next 4 days, the luminal diameter continued to dilate to a lesser extent and the vessel wall thickened. Immunohistochemical analysis showed increased cell division, maximal between 24 and 72 hours, in all layers of the choke vessel wall. During this same postoperative interval, transmission electron microscopy revealed phenotypic changes in smooth muscle cells from contractile to synthetic cells. Hypertrophy of the smooth muscle cells was also observed. The vascular endothelium, which initially showed evidence of denudation, was restored to a healthy intact appearance within the first week after delay. When followed for longer periods, long-term studies of the delayed flap of up to 1 year demonstrated dramatically a permanent dilation of the choke vessel lumen and a thickening of the choke vessel wall. In canine studies, one rectus abdominis muscle was delayed by ligating the deep inferior epigastric artery. The time sequence of choke vessel dilation, studied by sequential angiograms in vivo, was comparable to that of the rabbit skin model. To ascertain the permanence and irreversibility of this dilation, the normal circulation of the delayed rectus abdominis muscle was restored by reanastomosing the deep inferior epigastric artery. Even after a recovery period of up to 3 months, the choke vessels remained dilated and tortuous instead of reverting to their original narrow diameters. From this work, it is suggested that the choke vessel dilation seen in the delay period is a permanent and irreversible event. It is an active process associated with both an increase (hyperplasia) and an enlargement (hypertrophy) of the cells in all layers of the choke artery wall and a resultant increase in caliber of these vessels. The time sequence for delay appears to be similar in different species and in different tissues, suggesting the possibility of a universal process for delay.     

Ccm3 functions in a manner distinct from Ccm1 and Ccm2 in a zebrafish model of CCM vascular disease

Cerebral cavernous malformations (CCMs) are vascular anomalies of the central nervous system that arise due to mutations in genes encoding three unrelated proteins: CCM1 (KRIT1); CCM2 (Malcavernin/OSM) and CCM3 (PDCD10). Both biochemical and mutant studies suggest that CCM1 and CCM2 act as part of a physical complex to regulate vascular morphogenesis and integrity. In contrast, mouse Ccm3 mutant and in vitro cell culture data suggests an independent role for Ccm3. In this study, we sought to use the zebrafish model system to examine for the first time the role of ccm3 in cranial vessel development. We report that inhibition of zebrafish ccm3a/b causes heart and circulation defects distinct from those seen in ccm1 (santa) and ccm2 (valentine) mutants, and leads to a striking dilation and mispatterning of cranial vessels reminiscent of the human disease pathology. ccm3, but not ccm2, defects can be rescued upon overexpression of stk25b, a GCKIII kinase previously shown to interact with CCM3. Morpholino knockdown of the GCKIII gene stk25b results in heart and vasculature defects similar to those seen in ccm3 morphants. Finally, additional loss of ccm3 in ccm2 mutants leads to a synergistic increase in cranial vessel dilation. These results support a model in which CCM3 plays a role distinct from CCM1/2 in CCM pathogenesis, and acts via GCKIII activity to regulate cranial vasculature integrity and development. CCM3/GCKIII activity provides a novel therapeutic target for CCMs, as well as for the modulation of vascular permeability.     

基质盐度对木榄叶柄导管分子形态特征的影响

对温室中培养在不同盐度下一年生木榄[Bruguiera gymnorrhiza(L.)Poil]植株上成熟叶的叶柄离析研究的结果表明：1）木榄叶柄导管分子以梯纹导管为主,其次为螺纹导管及它们之间的过渡类型;随着盐度的升高,螺纹导管及它们之间的过渡类型有增多的趋势;2）而叶柄长度,梯纹导管分子的直径、长度及两端梯状穿孔板的横隔条数都与盐度呈抛物线关系,而它们的最大值出现在20‰-30‰范围内;3）培养于盐度10‰的海水中的木榄叶柄中导管分子一端有出现两个朝向不同的梯状穿孔板现象;4）在低盐条件下,随着基质盐度的提高,导管分子的形态朝着有利于加快水分运输的方向发展,而在高盐环境下,导管分子的形态朝着增加水分运输的安全性方向发展。讨论了叶柄导管分子解剖学特征的适应意义。     

Smad7 Misexpression during Embryonic Angiogenesis Causes Vascular Dilation and Malformations Independently of Vascular Smooth Muscle Cell Function

Numerous in vitro and in vivo studies implicate transforming growth factor-beta (TGFbeta) superfamily signaling in vascular development and maintenance. Mice and humans with mutations in TGFbeta superfamily signaling pathway genes exhibit a range of vascular defects that include dilated, fragile and hemorrhagic vessels, defective angiogenic remodeling, severe vascular malformations including arterio-venous malformations, and disrupted vascular smooth muscle cell recruitment and maintenance. Despite a wealth of data, the functions of TGFbeta superfamily signals during angiogenesis are poorly defined, since early embryonic lethality and difficulty distinguishing between primary and secondary defects frequently confound phenotypic interpretation. To perturb TGFbeta superfamily signaling during angiogenesis, we have misexpressed Smad7, an intracellular antagonist of TGFbeta superfamily signaling, in the developing chick limb and head. We find that the great vessels are strikingly dilated and frequently develop intra and intervascular shunts. Neither noggin nor dominant negative BMP receptor misexpression causes similar vascular phenotypes. However, simultaneous misexpression of constitutively active BMP receptors with Smad7 suppresses the Smad7-induced phenotype, suggesting that a BMP-like intracellular pathway is the target of Smad7 action. Despite the gross morphological defects, further analyses find no evidence of hemorrhage and vessel structure is normal. Furthermore, enlarged vessels and vascular malformations form in either the presence or absence of vascular smooth muscle, and vascular smooth muscle cell recruitment is unperturbed. Our data define the TGFbeta superfamily pathway as an integral regulator of vessel caliber that is also essential for appropriate vessel connectivity. They demonstrate that dilation need not result in vessel rupture or hemorrhage, and dissociate vessel maintenance from the presence of a vascular smooth muscle cell coat. Furthermore they uncouple vascular smooth muscle cell recruitment and differentiation from TGFbeta superfamily signaling.     

Oxygen distribution in microcirculation after arginine vasopressin-induced arteriolar vasoconstriction

The microvascular distribution of oxygen was studied in the arterioles and venules of the awake hamster window chamber preparation to determine the contribution of vascular smooth muscle contraction to oxygen consumption of the microvascular wall during arginine vasopressin (AVP)-induced vasoconstriction. AVP was infused intravenously at the clinical dosage (0.0001 IU.kg(-1).min(-1)) and caused a significant arteriolar constriction, decreased microvascular flow and functional capillary density, and a substantial rise in arteriolar vessel wall transmural Po(2) difference. AVP caused tissue Po(2) to be significantly lowered from 25.4 +/- 7.4 to 7.2 +/- 5.8 mmHg; however, total oxygen extraction by the microcirculation increased by 25%. The increased extraction, lowered tissue Po(2), and increased wall oxygen concentration gradient are compatible with the hypothesis that vasoconstriction significantly increases vessel wall oxygen consumption, which in this model appears to constitute an important oxygen-consuming compartment. This conclusion was supported by the finding that the small percentage of the vessels that dilated in these experiments had a vessel wall oxygen gradient that was smaller than control and which was not determined by changes in tissue Po(2). These findings show that AVP administration, which reduces oxygen supply by vasoconstriction, may further impair tissue oxygenation by the additional oxygen consumption of the microcirculation.     

Smooth muscle-endothelial cell communication activates Reelin signaling and regulates lymphatic vessel formation

Active lymph transport relies on smooth muscle cell (SMC) contractions around collecting lymphatic vessels, yet regulation of lymphatic vessel wall assembly and lymphatic pumping are poorly understood. Here, we identify Reelin, an extracellular matrix glycoprotein previously implicated in central nervous system development, as an important regulator of lymphatic vascular development. Reelin-deficient mice showed abnormal collecting lymphatic vessels, characterized by a reduced number of SMCs, abnormal expression of lymphatic capillary marker lymphatic vessel endothelial hyaluronan receptor 1 (LYVE-1), and impaired function. Furthermore, we show that SMC recruitment to lymphatic vessels stimulated release and proteolytic processing of endothelium-derived Reelin. Lymphatic endothelial cells in turn responded to Reelin by up-regulating monocyte chemotactic protein 1 (MCP1) expression, which suggests an autocrine mechanism for Reelin-mediated control of endothelial factor expression upstream of SMC recruitment. These results uncover a mechanism by which Reelin signaling is activated by communication between the two cell types of the collecting lymphatic vessels--smooth muscle and endothelial cells--and highlight a hitherto unrecognized and important function for SMCs in lymphatic vessel morphogenesis and function.     

Spreds are essential for embryonic lymphangiogenesis by regulating vascular endothelial growth factor receptor 3 signaling

Spred/Sprouty family proteins negatively regulate growth factor-induced ERK activation. Although the individual physiological roles of Spred-1 and Spred-2 have been investigated using gene-disrupted mice, the overlapping functions of Spred-1 and Spred-2 have not been clarified. Here, we demonstrate that the deletion of both Spred-1 and Spred-2 resulted in embryonic lethality at embryonic days 12.5 to 15.5 with marked subcutaneous hemorrhage, edema, and dilated lymphatic vessels filled with erythrocytes. This phenotype resembled that of Syk^−/− and SLP-76^−/− mice with defects in the separation of lymphatic vessels from blood vessels. The number of LYVE-1-positive lymphatic vessels and lymphatic endothelial cells increased markedly in Spred-1/2-deficient embryos compared with WT embryos, while the number of blood vessels was not different. Ex vivo colony assay revealed that Spred-1/2 suppressed lymphatic endothelial cell proliferation and/or differentiation. In cultured cells, the overexpression of Spred-1 or Spred-2 strongly suppressed vascular endothelial growth factor-C (VEGF-C)/VEGF receptor (VEGFR)-3-mediated ERK activation, while Spred-1/2-deficient cells were extremely sensitive to VEGFR-3 signaling. These data suggest that Spreds play an important role in lymphatic vessel development by negatively regulating VEGF-C/VEGFR-3 signaling.     

Risk factors for fouling biomass: evidence from small vessels in Australia

Abstract

Invasive non-indigenous species (NIS) are a threat to marine biodiversity and marine reliant industries. Recreational vessels are recognised as an important vector of NIS translocation, particularly domestically. This paper reports on a novel application of multilevel modelling and multiple imputation in order to quantify the relationship between biofouling biomass (wet weight) and the vessel-level characteristics of recreational and fishing vessels. It was found that the number of days since the vessel was last cleaned strongly related to the biofouling biomass, yet differed dependent on vessel type. Similarly, the median number of trips undertaken was related to the biofouling biomass, and varied according to the type of antifouling paint (AF) used. No relationship was found between vessel size and biofouling biomass per sample unit. To reduce the spread of NIS, vessel owners should use an AF paint suitable to their vessel’s operational profile, and follow a maintenance schedule according to the paint manufacturer’s specifications.     

Application of Thinned-Skull Cranial Window to Mouse Cerebral Blood Flow Imaging Using Optical Microangiography

In vivo imaging of mouse brain vasculature typically requires applying skull window opening techniques: open-skull cranial window or thinned-skull cranial window. We report non-invasive 3D in vivo cerebral blood flow imaging of C57/BL mouse by the use of ultra-high sensitive optical microangiography (UHS-OMAG) and Doppler optical microangiography (DOMAG) techniques to evaluate two cranial window types based on their procedures and ability to visualize surface pial vessel dynamics. Application of the thinned-skull technique is found to be effective in achieving high quality images for pial vessels for short-term imaging, and has advantages over the open-skull technique in available imaging area, surgical efficiency, and cerebral environment preservation. In summary, thinned-skull cranial window serves as a promising tool in studying hemodynamics in pial microvasculature using OMAG or other OCT blood flow imaging modalities.     

Readdressing the issue of thermally significant blood vessels using a countercurrent vessel network

A physiologically realistic arterio-venous countercurrent vessel network model consisting of ten branching vessel generations, where the diameter of each generation of vessels is smaller than the previous ones, has been created and used to determine the thermal significance of different vessel generations by investigating their ability to exchange thermal energy with the tissue. The temperature distribution in the 3D network (8178 vessels; diameters from 10 to 1000 microm) is obtained by solving the conduction equation in the tissue and the convective energy equation with a specified Nusselt number in the vessels. The sensitivity of the exchange of energy between the vessels and the tissue to changes in the network parameters is studied for two cases; a high temperature thermal therapy case when tissue is heated by a uniformly distributed source term and the network cools the tissue, and a hypothermia related case, when tissue is cooled from the surface and the blood heats the tissue. Results show that first, the relative roles of vessels of different diameters are strongly determined by the inlet temperatures to those vessels (e.g., as affected by changing mass flow rates), and the surrounding tissue temperature, but not by their diameter. Second, changes in the following do not significantly affect the heat transfer rates between tissue and vessels; (a) the ratio of arterial to venous vessel diameter, (b) the diameter reduction coefficient (the ratio of diameters of successive vessel generations), and (c) the Nusselt number. Third, both arteries and veins play significant roles in the exchange of energy between tissue and vessels, with arteries playing a more significant role. These results suggest that the determination of which diameter vessels are thermally important should be performed on a case-by-case, problem dependent basis. And, that in the development of site-specific vessel network models, reasonable predictions of the relative roles of different vessel diameters can be obtained by using any physiologically realistic values of Nusselt number and the diameter reduction coefficient.     

Defective paracrine signalling by TGFbeta in yolk sac vasculature of endoglin mutant mice: a paradigm for hereditary haemorrhagic telangiectasia

Hereditary haemorrhagic telangiectasia (HHT) is an autosomal dominant disorder in humans that is characterised by multisystemic vascular dyplasia and recurrent haemorrhage. Germline mutations in one of two different genes, endoglin or ALK1 can cause HHT. Both are members of the transforming growth factor (TGF) beta receptor family of proteins, and are expressed primarily on the surface of endothelial cells (ECs). Mice that lack endoglin or activin receptor like kinase (ALK) 1 die at mid-gestation as a result of defects in the yolk sac vasculature. Here, we have analyzed TGFbeta signalling in yolk sacs from endoglin knockout mice and from mice with endothelial-specific deletion of the TGFbeta type II receptor (TbetaRII) or ALK5. We show that TGFbeta/ALK5 signalling from endothelial cells to adjacent mesothelial cells is defective in these mice, as evidenced by reduced phosphorylation of Smad2. This results in the failure of vascular smooth muscle cells to differentiate and associate with endothelial cells so that blood vessels remain fragile and become dilated. Phosphorylation of Smad2 and differentiation of smooth muscle can be rescued by culture of the yolk sac with exogenous TGFbeta1. Our data show that disruption of TGFbeta signalling in vascular endothelial cells results in reduced availability of TGFbeta1 protein to promote recruitment and differentiation of smooth muscle cells, and provide a possible explanation for weak vessel walls associated with HHT.     

Recalcitrant vulnerability curves: methods of analysis and the concept of fibre bridges for enhanced cavitation resistance

Vulnerability curves (VCs) generally can be fitted to the Weibull equation; however, a growing number of VCs appear to be recalcitrant, that is, deviate from a Weibull but seem to fit dual Weibull curves. We hypothesize that dual Weibull curves in Hippophae rhamnoides L. are due to different vessel diameter classes, inter‐vessel hydraulic connections or vessels versus fibre tracheids. We used dye staining techniques, hydraulic measurements and quantitative anatomy measurements to test these hypotheses. The fibres contribute 1.3% of the total stem conductivity, which eliminates the hypothesis that fibre tracheids account for the second Weibull curve. Nevertheless, the staining pattern of vessels and fibre tracheids suggested that fibres might function as a hydraulic bridge between adjacent vessels. We also argue that fibre bridges are safer than vessel‐to‐vessel pits and put forward the concept as a new paradigm. Hence, we tentatively propose that the first Weibull curve may be accounted by vessels connected to each other directly by pit fields, while the second Weibull curve is associated with vessels that are connected almost exclusively by fibre bridges. Further research is needed to test the concept of fibre bridge safety in species that have recalcitrant or normal Weibull curves.     

基质盐度对木榄叶柄导管分子形态特征的影响

对温室中培养在不同盐度下一年生木榄[Bruginera gyninorrhiza(L.)Poil]植株上成熟叶的叶柄离析研究的结果表明:1)木榄叶柄导管分子以梯纹导管为主,其次为螺纹导管及它们之间的过渡类型;随着盐度的升高,螺纹导管及它们之间的过渡类型有增多的趋势;2)而叶柄长度,梯纹导管分子的直径、长度及两端梯状穿孔板的横隔条数都与盐度呈抛物线关系,而它们的最大位出现在20‰-30‰,范围内;3)培养于盐度10‰的海水中的木榄叶柄中导管分子一端有出现两个朝向不同的梯状穿孔板现象;4)在低盐条件下,随着基质盐度的提高,导管分子的形态朝着有利于加快水分运输的方向发展,而在高盐环境下,导管分子的形态朝着增加水分运输的安全性方向发展。讨论了叶柄导管分子解剖学特征的适应意义。     

Exogenous Auxin and N-1 -Naphthylphthalamic Acid Effects on Populus deltoides Xylogenesis

A method was developed for evaluating the empirical alterationof xylem vessel differentiation in the central leaf trace ofPopulus deltoides, a species that exhibits helical phyllotaxis.Effects of experimental treatments for a period of six plastochronswere evaluated by vessel parameter ratios = 2.P_T/ (P_T+1 + P_T–1),where P was either vessel number or mean transverse vessel areameasured at mid-intern ode at Leaf Plastochron Indices of T– 1, T, and T + 1. Excising leaf laminae reduced vesselnumber and mean vessel area in the associated central leaf traceby 50% and 70%, respectively, compared to unexcised laminaecontrols. Replacing excised laminae with a concentration seriesof exogenous indoleacetic acid (IAA) resulted in a 5% increaseper log mol m^–3 of IAA in the number of vessels differentiatingin the associated central leaf traces compared to excised controls.Mean vessel areas within these leaf traces were 50% of thoseof intact leaf traces. No significant effects of different concentrationsof exogenously applied IAA on mean vessel area could be demonstrated.A lanolin paste ring of N-1 -naphthylphthalamic acid (NPA),an auxin transport inhibitor, around the petioles of intactleaves reduced the number of differentiating vessels by 7% andmean vessel area by 29% per log mol m^–3 of NPA comparedto central leaf traces of leaves ringed with plain lanolin paste.The results suggest that NPA treatments may be used to distinguishexperimentally, at least in part, the cell division from thecell enlargement phases of primary xylogenesis within centralleaf traces of P. deltoides stems. Key words: Auxin transport, Vessel area, Vessel number