© 1995 American Heart Association, Inc.
Articles |
Expression of ICAM-1 and VCAM-1 and Monocyte Adherence in Arteries Exposed to Altered Shear Stress
From The Max Bell Research Centre, The Toronto Hospital Research Institute, Banting and Best Diabetes Centre and Centre for Cardiovascular Research, Department of Pathology, University of Toronto, Ontario, Canada (P.L.W., A.I.G., B.L.L.), and the Vascular Research Division, Department of Pathology, Brigham and Women's Hospital and Harvard Medical School, Boston, Mass (M.I.C.).
Correspondence to B. Lowell Langille, PhD, The Toronto Hospital Research Institute, The Max Bell Research Centre, 200 Elizabeth St, Toronto, ON M5G 2C4, Canada.
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Abstract Local shear stresses generated by blood flow exert direct mechanical effects on adhesion of circulating leukocytes to vascular endothelium, but their effects on expression of endothelial-leukocyte adhesion molecules have not been determined. Shear stress in rabbit carotid arteries was increased by 170% or decreased by 73% in 5 days by surgical manipulations. En face immunofluorescence staining with the monoclonal antibody Rb1/9 revealed that vascular cell adhesion molecule–1 (VCAM-1) expression was greatly increased under low shear stress, but the distribution of staining was patchy. Thus, 71.4±7.8% of fields were VCAM-1 positive versus 2.4±0.47% of fields in control arteries. Frequently, large regions showed consistent but heterogeneous staining. Occasionally, small islands of cells were labeled intensely. Monocytes, detected by use of the monocyte-specific antibody HAM 56, adhered to endothelium under low shear stress; 64.5±8.2% of the monocytes colocalized with detectable VCAM-1, although many (83.2±2.8%) VCAM-1–positive regions were devoid of monocytes. VCAM-1 expression also increased significantly but to a lesser extent when shear stress was approximately doubled. Thus, 8.7±1.5% of fields were VCAM-1 positive under high shear versus 2.5±0.87% under normal shear stress. No monocytes were detected at high shear stress. At normal shear stresses, intercellular adhesion molecule–1 (ICAM-1), detected by use of the monoclonal antibody Rb2/3, was extensively distributed; thus, 53.5±5.5% of fields contained ICAM-1–positive cells. The junctional regions of the cells were heavily stained. Experimental increases in shear stress significantly upregulated ICAM-1 expression (88.3±2.0% of fields were ICAM-1 positive; P<.05). Staining was again concentrated in the cell junctional regions. Reduced shear stress suppressed ICAM-1 expression (16.6±10.3% of fields were positive), and ICAM-1 was more commonly, but not exclusively, distributed diffusely. Junctional ICAM-1 may participate in endothelial cell-cell adhesion; alternatively, a pool of ICAM-1 concentrated between cell junctions may be inaccessible to circulating leukocytes until endothelial cell activation presents the molecule to the vessel lumen.
Key Words: adhesion • ELAM • atherosclerosis
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Introduction |
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Cell adhesion molecules are critical regulators of direct cell-cell interactions. Embryonic morphogenesis,1 2 wound healing,3 and inflammatory responses4 are directed by temporal and spatial regulation of expression of these molecules. Cell adhesion molecules also influence many disease processes, including atherogenesis5 and tumor metastasis.6 7
Many of the functions mediated by cell adhesion molecules involve slow and orderly reorganization of cell-cell adhesion as one or both of the adherent cells migrate through an environment they create and control.1 8 However, very different dynamics characterize adhesion of circulating leukocytes to vascular endothelium and their subsequent emigration to the extravascular space. In this case, adhesion and related events occur rapidly, and they do so in a mechanical microenvironment that is not conducive to cell-cell adhesion. Continuous blood flow limits the residence time of leukocytes in the vicinity of adhesion sites, and the shear forces associated with blood flow can mechanically disrupt adhesion processes.9 10 11 Consequently, an organized cascade of three separate events mediated by three types of adhesion molecules has evolved. These include loose adhesion that results in leukocytes rolling along the endothelial surface, tight adherence of leukocytes that immobilizes the cells, and transmigration of leukocytes across the endothelium. Loose adhesion is mediated by selectins and their interactions with cell surface carbohydrates.12 The slow rolling associated with loose adherence permits tight endothelium-leukocyte adhesion through binding of other adhesion molecules to their leukocyte counterreceptors. Most notably, vascular cell adhesion molecule–1 (VCAM-1) binds to very late activation antigen–4, intercellular adhesion molecule–1 (ICAM-1) binds lymphocyte function-associated antigen–1, and E-selectin binds cell surface carbohydrates.13 14 Finally, recent evidence indicates that platelet–endothelial cell adhesion molecule–1, an endothelial cell junctional protein, is required for transmigration of leukocytes across the endothelium.15
We developed methods to alter shear stress in vivo in straight, unbranched portions of rabbit carotid arteries so that shear fluctuations and other flow complexities were avoided.16 17 18 Surprisingly, low shear stress alone was an adequate stimulus to induce monocyte adhesion and emigration.18 It is possible that monocyte emigration was due entirely to reduced physical disruption of adhesion by mechanical forces acting on the adhering cells. Alternatively, shear stress may influence expression of adhesion molecules by endothelial cells. In this regard, there is much evidence that shear stress affects many endothelial cell functions19 20 ; furthermore, sites of monocyte traffic in experimental atherosclerosis in rabbits exhibit expression of VCAM-1, an endothelial adhesion molecule that binds monocytes.5 21 In this study we examined the effects of both increased and decreased shear stress on the expression of two important adhesion molecules, VCAM-1 and ICAM-1. We report that expression of both molecules is sensitive to shear stress, although in different ways. Low shear stress upregulates VCAM-1 and downregulates ICAM-1, whereas both molecules are upregulated when shear stress is elevated. These findings have important implications for atherogenesis, which involves monocyte emigration at sites of unusual shear stress, and for other conditions that elicit leukocyte emigration. Leukocytes emigrate at different sites in the vascular tree where different shear stresses prevail5 11 22 23 ; furthermore, the conditions that elicit emigration, eg, inflammation, often alter local blood flow. Shear-dependent modulation of adhesion molecule expression may greatly influence the emigration process.
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Methods |
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Experimental Alteration of Shear Stress
Full surgical anesthesia of adult male New Zealand White rabbits weighing 2.5 to 3.5 kg was induced with intramuscular injection of 0.25 mL of xylazine (20 mg/mL) and 2.25 mL of ketamine (100 mg/mL) and maintained with continuous infusion of the 1:9 (vol/vol) xylazine-ketamine mixture (0.153 mL/min). A cervical incision along the ventral midline was made caudal to the thyroid cartilage, then the left common carotid artery was exposed and ligated just rostral to the origin of the thyroid branch with 2.0 silk. The incision was closed in layers, and the animal was allowed to recover. One milliliter of Penlong XL (150 000 U of benzathine penicillin G and 150 000 U of procaine penicillin) was given by intramuscular injection on the day of surgery. Animals were maintained for 5 days on a diet of standard lab chow. Sham-operated control surgeries were performed in which suture was passed around the carotid but not ligated. Previously, we showed that this surgical procedure results in a 170% increase (from 11.3±1.6 dynes/cm2 to 30.5±4.6 dynes/cm2) in shear stress in the experimental right common carotid artery and a 73% reduction (from 12.1±1.6 dynes/cm2 to 3.26±0.58 dynes/cm2) in shear stress in the experimental left common carotid artery after 5 days, compared with sham-operated animals.18 Volume flow rates were positive throughout the cardiac cycle under all flow conditions, with diastolic flows ranging from approximately 20% to 50% of peak flow.
Tissue Preparation for Fluorescence Microscopy
Heparin (1 mL, 1000 U) was infused through an ear catheter 5
days after ligation of the left common carotid artery. One minute later
the rabbits were killed by infusing into the same ear vein catheter 1.0
mL of euthanasia solution, 200 mg/mL
N-[2-m-methophenyl-2-ethylbutl-(1)]-2
hydroxybutyramide, 50 mg/mL 4,40' methylene bis
(cyclohexyltrimethylammonium iodide), and 5 mg/mL tetracaine
hydrochloride (T-61, Hoechst Canada, Inc). After a rapid thoracotomy,
the descending thoracic aorta was retrogradely cannulated, and 60 mL of
phosphate-buffered saline (PBS) was flushed through the aorta and the
carotid arteries. A cannula connected to a manometer was inserted into
the left subclavian artery. The carotid arteries were fixed by
perfusion through the aortic cannula of 3% paraformaldehyde in 0.1
mol/L phosphate buffer and 0.1 mmol/L CaCl2 (pH 7.4), then
they were washed with PBS (pH 7.4) for 15 minutes. Perfusion pressures
were maintained at 100 mm Hg for fixation and washing. The carotid
arteries were excised, cut into four sections, and opened ventrally.
These sections were pinned onto sheets of dental wax, with the
endothelial surface facing up.
Immunostaining for VCAM-1
The carotid artery samples from five experimental animals and
five controls were stained en face with 100 µL of Rb1/9, a mouse
monoclonal IgG antibody against VCAM-1,5 at 1:10 dilution
for 1 hour. After four 5-minute washes with PBS, the sections were
stained for 30 minutes with 100 µL of fluorescein isothiocyanate
(FITC)–conjugated donkey anti-mouse IgG, diluted 1:20 (Jackson
Immunoresearch Labs). After four more 5-minute washes with PBS, the
samples were mounted en face on glass slides under glass coverslips,
using 1:9 glycerol in PBS. Controls for nonspecific staining were
stained only with the secondary antibody. Sham-operated animals were
subjected to the same immunostaining protocol. In some samples from
both groups, propidium iodide (Calbiochem; 10 mg/mL in 1:100 dilutions)
was used to stain endothelial cell nuclei. Propidium iodide binds to
both RNA and DNA, and therefore tissues were incubated with 100 µg/mL
RNAse (Qiagen Inc) at 37°C for 30 minutes before staining. These
tissue sections were examined with a laser confocal microscope (BioRad
MRC 600) with a krypton/argon laser.
For double labeling, carotid arteries of another group of four experimental rabbits were prepared for confocal microscopy as described above. After three 5-minute washes with PBS, they were incubated for 1 hour with Rb1/9 (IgG) in 1:10 dilutions and HAM 56 (IgM), a monoclonal antibody against monocytes and macrophages, in 1:20 dilutions (Enzo Diagnostics).24 After three more 5-minute washes with PBS, these specimens were stained with FITC-conjugated anti-IgG in 1:20 dilutions and Texas Red–conjugated anti-IgM in 1:40 dilutions (Jackson Immunoresearch Labs) for 30 minutes. Controls for nonspecific staining were stained only with the secondary antibodies. The tissue was mounted on glass slides under glass coverslips with glycerol in PBS (1:9), with the lumen side facing up. These specimens also were examined with the laser confocal microscope.
Immunostaining for ICAM-1
Five experimental rabbits and five sham-operated controls were
subjected to the same experimental protocol as for VCAM-1 except that
the tissue was stained with Rb2/3, a mouse monoclonal IgG antibody
against ICAM-1, in 1:10 dilutions.5
Analysis of VCAM-1 and ICAM-1 Staining
Staining was assessed by confocal microscopy at predefined
points on a grid defined by means of the micrometer drives on the
microscope stage. More than 400 fields for each artery were observed
under x60 magnification for VCAM-1 or ICAM-1 staining. Well-defined,
brightly stained endothelial cells were counted as positively stained
cells. A field was considered positive when at least one cell exhibited
staining. The number of positive cells per field also was recorded.
Subsequently, fields with positive VCAM-1 staining were grouped
according to whether 1, 2 to 5, or 6 or more cells were positive for
VCAM-1. For ICAM-1, positive fields were grouped according to whether
fields with 1, 2 to 5, 6 to 10, or more than 10 cells were positive.
Fields in which all cells were positive also were recorded.
Statistical analysis was based on unpaired t tests between sham-operated and experimental animals. Differences were considered significant at P<.05, with n=5 rabbits per group for all comparisons.
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Results |
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VCAM-1 Staining
VCAM-1 staining in both left and right common carotid arteries of sham-operated animals was very modest. Rare fields were VCAM-1 positive, and most of these fields contained only one or a few positive cells (Fig 1A
). Staining of these
cells was diffuse. No staining was observed when the secondary antibody
alone was used.
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Endothelium exhibited much greater VCAM-1 staining 5 days after
reducing shear stress, with three distinct patterns observed. Most
frequently, fields contained many VCAM-1–positive cells that exhibited
variable staining, with intervening endothelial cells showing no
staining (Fig 1B
). Less frequently, islands of endothelial cells showed
uniformly intense staining (Fig 1C). Rarely, isolated endothelial cells
exhibited positive staining that was similar to that of positive cells
in control vessels. In general, VCAM-1 staining was distributed
diffusely, with concentration at cell junctions in some (Fig 1B) but
not all (Fig 1D) cells.
Morphometry confirmed that low shear stress caused upregulation of
VCAM-1 expression. Far more fields were positive (71.4±7.8% of
fields) compared with sham-operated controls (2.4±0.47% of fields)
(Fig 2), and the number of stained cells per field
increased (Fig 3A). Under control conditions, most
positive fields contained only one positive cell, a very low percentage
contained 2 to 5 positive cells, and no fields contained more than 5
positive cells. In contrast, most fields contained more than 6 positive
cells when shear stress was low.
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When the shear stress was increased by 170%, single cells or groups of
2 to 5 cells showed VCAM-1 staining (Fig 1E). The diffuse cellular
distribution of VCAM-1 was similar to that found with low shear stress.
Morphometry (Fig 2) showed a significant increase in number of fields
positive for VCAM-1 (8.7±1.5% of fields) compared with sham-operated
controls (2.5±0.87% of fields), but the upregulation was much less
than that observed with low shear stress. No fields contained 6 or more
VCAM-1–positive cells (Fig 3B).
In sham-operated controls, most positive fields contained one
positively stained endothelial cell (Fig 3B). High shear stress caused
a significant increase in the fields with 1 positive cell compared with
sham-operated controls, but there was no significant change in the
number of fields with 2 to 5 positively stained endothelial cells.
VCAM-1 Expression and Monocyte Adhesion
Double staining with HAM-56 and Rb1/9 in arteries with low shear
stress demonstrated that 64.5±8.2% of adherent monocytes were
colocalized with VCAM-1 (Fig 1F); however, 83.2±2.8% of fields
positively stained with VCAM-1 did not have adherent monocytes.
ICAM-1 Staining
Both the left and the right common carotid arteries of
sham-operated animals showed positive ICAM-1 staining (Fig 4A) in approximately half the fields observed (Fig 5). ICAM-1 staining was confined mainly to the periphery
of the endothelial cells, indicating a junctional distribution. All
cells were stained in only 2.8±1.8% of fields. There were no
monocytes adhering to endothelium in these vessels.
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Low shear stress caused a reduction and change in distribution in
ICAM-1 expression compared with sham-operated controls. Single cells or
groups of cells stained positively for ICAM-1, and staining of these
cells was diffuse in most fields (Fig 4B), with only rare fields
showing the junctional staining seen in sham-operated animals. Reduced
staining resulted in a statistically significant change in the total
number of fields that exhibited positive labeling with low shear stress
(Fig 5). Monocytes stained with HAM 56 colocalized with positive ICAM-1
staining in some areas.
In contrast to low shear stress, there was extensive ICAM-1 staining in
arteries with high shear stress compared with sham-operated controls
(Fig 4C). The staining was confined mainly to the vicinity of cell
junctions (Fig 4C). Almost all fields were ICAM-1 positive (88.3±2.0%
of fields), a significant increase compared with sham-operated controls
(53.5±5.5% of fields) (Fig 5). The number of fields in which all
cells stained for VCAM-1 rose dramatically from 2.82±1.79% to
32.5±4.8% of fields. Occasionally, single cells or groups of 2 to 5
cells showed diffuse, stippled staining among the cells showing
junctional pattern of staining. There were no monocytes adhering to the
endothelium in these vessels.
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Discussion |
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These experiments indicate that local shear stress regulates expression of at least two critical adhesion molecules, VCAM-1 and ICAM-1; thus, shear stress may modulate leukocyte-endothelial cell adhesion by inducing active changes in cell surface properties as well as by imposing physical forces on the adhesion process. Furthermore, the regulation was molecule-specific rather than stereotypic: low shear stress upregulated VCAM-1 expression but downregulated ICAM-1 expression. Both molecules were upregulated when shear stress was elevated. Upregulation of VCAM-1 and ICAM-1 with increased shear stress did not induce leukocyte adherence. The increases in expression were perhaps inadequate to bind leukocytes in the presence of increased mechanical forces that may disrupt adhesion.10 11 25 Responses to shear stress in combination with endothelial activation, eg, by cytokines, may ensure a response that is adequate to recruit leukocytes despite an unfavorable mechanical environment.
We have no data on the mechanisms by which shear stress regulates VCAM-1 and ICAM-1. It may be a direct cellular response to signaling through shear transduction pathways that regulate many endothelial cell functions20 26 27 28 29 30 31 ; however, these pathways are only now being characterized. Activation of the inositol pathway32 33 appears to mediate at least one important endothelial response to shear stress, cell shape change and orientation,33 and cytosolic calcium is elevated by shear stress,34 35 36 37 probably, at least in part, as a result of an associated diacylglycerol release. An alternative pathway involves cyclic GMP elevation that is secondary to shear-induced nitric oxide release.38 The events downstream of early signal transduction that might affect adhesion molecule expression are not known; however, the promoter region of the ICAM-1 gene apparently contains the shear stress–responsive element that is responsible for shear regulation of the B chain of platelet-derived growth factor.30 This element may control shear dependence of ICAM-1 expression as well. The VCAM-1 promoter does not contain this responsive element,30 and therefore other regulatory mechanisms must control its expression.
Alternatively, shear stress may modulate VCAM-1 and/or ICAM-1 expression indirectly through autocrine or paracrine pathways. For example, endothelin release by endothelium is shear sensitive,39 40 41 and endothelin can alter ICAM-1, VCAM-1, and E-selectin expression in endothelium.42 Finally, chronic shear alterations cause structural remodeling of arteries, and VCAM-1 regulation may be secondary to early events in the remodeling process. This possibility is less likely since we observed significant responses to increased shear stress after 5 days, whereas remodeling at high shear stress is initiated after a period of weeks.43
We observed intense staining for VCAM-1 next to sites that were negative for VCAM-1. Both isolated cells and islands of cells that stained positively were surrounded by unstained cells. These observations indicate that endothelium does not respond uniformly to shear stress, since significant local variations in shear stress in the straight, unbranched carotid arteries are improbable. Possibly, each island of positive cells represents a clone of a common parent cell that was predisposed to respond to shear stress. Alternatively, isolated VCAM-1–positive cells may attract monocytes that then release cytokines such as interleukin-1 to induce VCAM-1 expression in neighboring cells. Finally, we previously reported deletion of endothelial cells in the rabbit carotid artery carrying reduced flow.18 Thus, focal endothelial cell death could cause the release of cytokines, such as interleukin-1 and/or tumor necrosis factor, which may induce local VCAM-1 production. Even among VCAM-1–positive cells, we observed marked heterogeneity of VCAM-1 expression. Either all positive endothelial cells do not produce VCAM-1 to the same extent or VCAM-1 expression is transient, so that different cells are at different stages of expression at the time of fixation.
The massive upregulation of VCAM-1 by low shear stress was particularly important because it coincided with adhesion of monocytes, a colocalization that also occurs in experimental atherogenesis.5 21 If that colocalization reflects binding of monocytes by VCAM-1, these results provide in vivo evidence for a mechanism linking low shear stress to a critical early event in atherogenesis. Approximately one third of adherent monocytes were attached to cells that did not exhibit VCAM-1 staining. Other mediators may be responsible for adherence of these monocytes; alternatively, VCAM-1 may be expressed at levels below that detected with the antibody. However, a role for additional mediators may be indicated by our observation that many sites that stained quite intensely for VCAM-1 were devoid of monocytes. Previous studies have indicated additive or synergistic interactions of adhesion molecules during leukocyte emigration,44 and it may be that coexpression of these molecules promotes binding of monocytes when shear stress is reduced.
It was noteworthy that the 170% increase in shear stress also upregulated VCAM-1, albeit to a lesser degree than did low shear stress. Monocytes did not adhere, possibly because of relatively low expression and a hemodynamic environment unfavorable to adhesion.9 10 11 Many sites in large arteries are exposed to higher shear stresses than we induced,45 46 47 and further increases in VCAM-1 may elicit adhesion. This concept is important because experimental atherosclerosis in some species occurs in high-shear regions.48 Ultimately, both extremes of shear stress may be atherogenic. In some species, eg, rabbits, a balance of atherogenic factors including shear stress may favor disease formation in high-shear regions, whereas a different balance predisposes low (or fluctuating) shear sites to disease in other species.
There was substantial expression of ICAM-1 at normal shear stress. Further upregulation of ICAM-1 by increased shear stress, without detectable leukocyte adhesion, was surprising. It is possible that expression of other regulators is an absolute requirement for leukocyte adhesion in these vessels. However, there are other possibilities. ICAM-1 staining was concentrated around endothelial cell junctions, which are complex, interdigitating structures. ICAM-1 may be localized to the intercellular junctional regions, where it is inaccessible to circulating leukocytes, in preference to the luminal surface of the cells. Junctional ICAM-1 may participate in endothelial cell–endothelial cell adhesion; thus, upregulation with increased shear stress may be an adaptation to increased mechanical loads that pose a threat to endothelial integrity. In this case, increased cell-cell adhesion would accompany the enhanced cell-substrate adhesion afforded by stress fiber formation and altered substrate adhesion complexes.26 49 It is important to note, however, that counterreceptors for ICAM-1 have not been identified on endothelium, and therefore their role in endothelial cell-cell interactions is unknown.
It is also possible that ICAM-1 is sequestered in a junctional pool inaccessible to circulating leukocytes so that it can be delivered to the luminal surface rapidly to bind leukocytes when the cell is appropriately activated. Recently, Sugama and coworkers50 provided evidence for such a pool when they noted that thrombin-induced increases in luminal ICAM-1 occurred even after protein synthesis was blocked. Shear-induced increases in this junctional pool of ICAM-1 may ensure that enough ICAM-1 is available for rapid mobilization to bind leukocytes even when the shear forces that impede adhesion are high.
We considered the impact of our results on atherogenesis because this is the most important disease affecting large arteries of the type examined in our study. However, many other pathological processes, including inflammatory responses, immune responses, and tumor cell metastases, probably are influenced by shear-dependent modulation of adhesion molecules. These influences will depend strongly on the site of leukocyte emigration since shear stresses vary greatly throughout the vascular system. Thus, shear stresses are higher in smaller arteries and arterioles than in large arteries, they fluctuate greatly with passage of individual cells in capillaries, and they are lower in venules, a common site of leukocyte emigration.51 Furthermore, the vasomotion and edema that accompany many pathological states will alter local blood flows and shear stresses to further modulate the expression of endothelial-leukocyte adhesion molecules, and local cytokines and other factors will undoubtedly modulate the effects of shear stress. Finally, the endothelium itself exhibits much regional heterogeneity, and therefore endothelial cells at different sites may respond differently to shear stress.52 Consequently, much work is needed to elucidate the impact of local flow conditions on leukocyte participation in disease.
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Acknowledgments |
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This study was supported by grant-in-aid No. MA10029 from the Medical Research Council of Canada. Support to Dr Cybulsky was received from NIH grant No. HL45563. Dr Langille is a Career Investigator of the Heart and Stroke Foundation of Ontario, and Dr Walpola is a Trainee of the Heart and Stroke Foundation of Canada.
Received March 2, 1994; accepted July 9, 1994.
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J. L. Unthank, S. W. Fath, H. M. Burkhart, S. C. Miller, and M. C. Dalsing Wall Remodeling During Luminal Expansion of Mesenteric Arterial Collaterals in the Rat Circ. Res., November 1, 1996; 79(5): 1015 - 1023. [Abstract] [Full Text]
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J. Lambert, M. Aarsen, A. J.M. Donker, and C. D.A. Stehouwer Endothelium-Dependent and -Independent Vasodilation of Large Arteries in Normoalbuminuric Insulin-Dependent Diabetes Mellitus Arterioscler Thromb Vasc Biol, May 1, 1996; 16(5): 705 - 711. [Abstract] [Full Text]
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C. Wunder, R. W Brock, S. D McCarter, A. Bihari, K. Harris, O. Eichelbronner, and R. F Potter Inhibition of haem oxygenase activity increases leukocyte accumulation in the liver following limb ischaemia-reperfusion in mice J. Physiol., May 1, 2002; 540(3): 1013 - 1021. [Abstract] [Full Text] [PDF]
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