Evaluation of the role of intercellular adhesion molecule 1 in a rodent model of chronic venous hypertension

Tara L. Hahn, Robert Whitfield, James Salter, D. Neil Granger, Joseph L. Unthank, Stephen G. Lalka

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Abstract

Purpose. To evaluate the role of intercellular adhesion molecule 1 (ICAM-1) in cutaneous leukocyte trapping in venous disease, we used our rodent model of venous hypertension (VH). Materials and methods. VH was created in adult rats by ligation of the inferior vena cava, bilateral common iliac veins, and bilateral common femoral veins. In the Phase I experimental (exptl) group, anti-ICAM-1 monoclonal antibody (1A29) was given intravenously prior to venous ligations. Acute venous pressures were measured in the exptl and control (ctrl) (ligation only) groups. Bilateral forelimb and hindlimb skin specimens were harvested for myeloperoxidase (MPO) assay. In Phase II, VH was created in a chronic group; in a sham-operated group, ties were placed around the same vessels without ligations. Two weeks later, venous pressures were measured and radiolabeled (125I and 131I) monoclonal antibody (mAb) to ICAM-1 was injected and allowed to circulate for 5 min before the level of radiolabeled antibody within forelimb and hindlimb specimens was measured. Results. In the acute study with 1A29, hindlimb pressures were significantly elevated in both the ctrl (n = 4) and exptl (n = 4) hindlimbs (15.4 ± 0.239 and 13.8 ± 1.89 mm Hg, respectively) compared with ctrl and exptl forelimbs (1.38 ± 0.554 and 1.50 ± 0.612 mm Hg, respectively). However, MPO activity was significantly elevated in the hindlimbs of the ctrl group compared with the hindlimbs of the exptl animals (19.8 ± 1.54 U vs 6.71 ± 2.46 U). In the chronic VH rats (n = 5) given radiolabeled anti-ICAM- 1 mAb, the hindlimb pressures (10.1 ± 4.52 mm Hg) were significantly elevated (P < 0.05) compared with forelimb pressures (1 ± 0.447 mm Hg) and compared with the forelimb and hindlimb pressures in the sham-operated animals (n = 4) (1.63 ± 0.813 and 4.25 ± 2.13 mm Hg, respectively). However, there was not a significant difference in the quantity of ICAM-1 - hindlimb versus forelimb or chronic VH versus sham. Conclusions. Anti-ICAM-1 mAb decreased MPO activity in hypertensive hindlimb skin, supporting the instrumental role of ICAM-1 in cutaneous leukocyte trapping. However, the constituent endothelial ICAM-1 is not elevated by VH. (C) 2000 Academic Press.

Original languageEnglish
Pages (from-to)150-154
Number of pages5
JournalJournal of Surgical Research
Volume88
Issue number2
DOIs
StatePublished - Feb 2000

Fingerprint

Intercellular Adhesion Molecule-1
Hindlimb
Rodentia
Forelimb
Hypertension
Ligation
Monoclonal Antibodies
Peroxidase
Pressure
Skin
Venous Pressure
Leukocytes
Iliac Vein
Femoral Vein
Inferior Vena Cava
Control Groups
Antibodies

Keywords

  • Cellular adhesion molecules
  • Leukocytes
  • Venous hypertension

ASJC Scopus subject areas

  • Surgery

Cite this

Evaluation of the role of intercellular adhesion molecule 1 in a rodent model of chronic venous hypertension. / Hahn, Tara L.; Whitfield, Robert; Salter, James; Granger, D. Neil; Unthank, Joseph L.; Lalka, Stephen G.

In: Journal of Surgical Research, Vol. 88, No. 2, 02.2000, p. 150-154.

Research output: Contribution to journalArticle

Hahn, Tara L. ; Whitfield, Robert ; Salter, James ; Granger, D. Neil ; Unthank, Joseph L. ; Lalka, Stephen G. / Evaluation of the role of intercellular adhesion molecule 1 in a rodent model of chronic venous hypertension. In: Journal of Surgical Research. 2000 ; Vol. 88, No. 2. pp. 150-154.
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abstract = "Purpose. To evaluate the role of intercellular adhesion molecule 1 (ICAM-1) in cutaneous leukocyte trapping in venous disease, we used our rodent model of venous hypertension (VH). Materials and methods. VH was created in adult rats by ligation of the inferior vena cava, bilateral common iliac veins, and bilateral common femoral veins. In the Phase I experimental (exptl) group, anti-ICAM-1 monoclonal antibody (1A29) was given intravenously prior to venous ligations. Acute venous pressures were measured in the exptl and control (ctrl) (ligation only) groups. Bilateral forelimb and hindlimb skin specimens were harvested for myeloperoxidase (MPO) assay. In Phase II, VH was created in a chronic group; in a sham-operated group, ties were placed around the same vessels without ligations. Two weeks later, venous pressures were measured and radiolabeled (125I and 131I) monoclonal antibody (mAb) to ICAM-1 was injected and allowed to circulate for 5 min before the level of radiolabeled antibody within forelimb and hindlimb specimens was measured. Results. In the acute study with 1A29, hindlimb pressures were significantly elevated in both the ctrl (n = 4) and exptl (n = 4) hindlimbs (15.4 ± 0.239 and 13.8 ± 1.89 mm Hg, respectively) compared with ctrl and exptl forelimbs (1.38 ± 0.554 and 1.50 ± 0.612 mm Hg, respectively). However, MPO activity was significantly elevated in the hindlimbs of the ctrl group compared with the hindlimbs of the exptl animals (19.8 ± 1.54 U vs 6.71 ± 2.46 U). In the chronic VH rats (n = 5) given radiolabeled anti-ICAM- 1 mAb, the hindlimb pressures (10.1 ± 4.52 mm Hg) were significantly elevated (P < 0.05) compared with forelimb pressures (1 ± 0.447 mm Hg) and compared with the forelimb and hindlimb pressures in the sham-operated animals (n = 4) (1.63 ± 0.813 and 4.25 ± 2.13 mm Hg, respectively). However, there was not a significant difference in the quantity of ICAM-1 - hindlimb versus forelimb or chronic VH versus sham. Conclusions. Anti-ICAM-1 mAb decreased MPO activity in hypertensive hindlimb skin, supporting the instrumental role of ICAM-1 in cutaneous leukocyte trapping. However, the constituent endothelial ICAM-1 is not elevated by VH. (C) 2000 Academic Press.",
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AU - Unthank, Joseph L.

AU - Lalka, Stephen G.

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N2 - Purpose. To evaluate the role of intercellular adhesion molecule 1 (ICAM-1) in cutaneous leukocyte trapping in venous disease, we used our rodent model of venous hypertension (VH). Materials and methods. VH was created in adult rats by ligation of the inferior vena cava, bilateral common iliac veins, and bilateral common femoral veins. In the Phase I experimental (exptl) group, anti-ICAM-1 monoclonal antibody (1A29) was given intravenously prior to venous ligations. Acute venous pressures were measured in the exptl and control (ctrl) (ligation only) groups. Bilateral forelimb and hindlimb skin specimens were harvested for myeloperoxidase (MPO) assay. In Phase II, VH was created in a chronic group; in a sham-operated group, ties were placed around the same vessels without ligations. Two weeks later, venous pressures were measured and radiolabeled (125I and 131I) monoclonal antibody (mAb) to ICAM-1 was injected and allowed to circulate for 5 min before the level of radiolabeled antibody within forelimb and hindlimb specimens was measured. Results. In the acute study with 1A29, hindlimb pressures were significantly elevated in both the ctrl (n = 4) and exptl (n = 4) hindlimbs (15.4 ± 0.239 and 13.8 ± 1.89 mm Hg, respectively) compared with ctrl and exptl forelimbs (1.38 ± 0.554 and 1.50 ± 0.612 mm Hg, respectively). However, MPO activity was significantly elevated in the hindlimbs of the ctrl group compared with the hindlimbs of the exptl animals (19.8 ± 1.54 U vs 6.71 ± 2.46 U). In the chronic VH rats (n = 5) given radiolabeled anti-ICAM- 1 mAb, the hindlimb pressures (10.1 ± 4.52 mm Hg) were significantly elevated (P < 0.05) compared with forelimb pressures (1 ± 0.447 mm Hg) and compared with the forelimb and hindlimb pressures in the sham-operated animals (n = 4) (1.63 ± 0.813 and 4.25 ± 2.13 mm Hg, respectively). However, there was not a significant difference in the quantity of ICAM-1 - hindlimb versus forelimb or chronic VH versus sham. Conclusions. Anti-ICAM-1 mAb decreased MPO activity in hypertensive hindlimb skin, supporting the instrumental role of ICAM-1 in cutaneous leukocyte trapping. However, the constituent endothelial ICAM-1 is not elevated by VH. (C) 2000 Academic Press.

AB - Purpose. To evaluate the role of intercellular adhesion molecule 1 (ICAM-1) in cutaneous leukocyte trapping in venous disease, we used our rodent model of venous hypertension (VH). Materials and methods. VH was created in adult rats by ligation of the inferior vena cava, bilateral common iliac veins, and bilateral common femoral veins. In the Phase I experimental (exptl) group, anti-ICAM-1 monoclonal antibody (1A29) was given intravenously prior to venous ligations. Acute venous pressures were measured in the exptl and control (ctrl) (ligation only) groups. Bilateral forelimb and hindlimb skin specimens were harvested for myeloperoxidase (MPO) assay. In Phase II, VH was created in a chronic group; in a sham-operated group, ties were placed around the same vessels without ligations. Two weeks later, venous pressures were measured and radiolabeled (125I and 131I) monoclonal antibody (mAb) to ICAM-1 was injected and allowed to circulate for 5 min before the level of radiolabeled antibody within forelimb and hindlimb specimens was measured. Results. In the acute study with 1A29, hindlimb pressures were significantly elevated in both the ctrl (n = 4) and exptl (n = 4) hindlimbs (15.4 ± 0.239 and 13.8 ± 1.89 mm Hg, respectively) compared with ctrl and exptl forelimbs (1.38 ± 0.554 and 1.50 ± 0.612 mm Hg, respectively). However, MPO activity was significantly elevated in the hindlimbs of the ctrl group compared with the hindlimbs of the exptl animals (19.8 ± 1.54 U vs 6.71 ± 2.46 U). In the chronic VH rats (n = 5) given radiolabeled anti-ICAM- 1 mAb, the hindlimb pressures (10.1 ± 4.52 mm Hg) were significantly elevated (P < 0.05) compared with forelimb pressures (1 ± 0.447 mm Hg) and compared with the forelimb and hindlimb pressures in the sham-operated animals (n = 4) (1.63 ± 0.813 and 4.25 ± 2.13 mm Hg, respectively). However, there was not a significant difference in the quantity of ICAM-1 - hindlimb versus forelimb or chronic VH versus sham. Conclusions. Anti-ICAM-1 mAb decreased MPO activity in hypertensive hindlimb skin, supporting the instrumental role of ICAM-1 in cutaneous leukocyte trapping. However, the constituent endothelial ICAM-1 is not elevated by VH. (C) 2000 Academic Press.

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KW - Leukocytes

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