Venular Constriction of Submucosal Arterioles Induced by Dextran Sodium Sulfate

Harris, Norman R.; Whatley, Joseph R.; Carter, Patsy R.; Specian, Robert D.

doi:10.1097/01.mib.0000178262.95980.65

Cited by 19 publications

(27 citation statements)

References 28 publications

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“…In spontaneously hypertensive rats, treatment with cyclooxygenase inhibition or thromboxane receptor antagonists abolished the constriction observed in arterial rings [1]. Additionally, intestinal inflammation induced by dextran sodium sulfate (a model of colitis) was found to induce thromboxane-dependent arteriolar constriction, but only in arterioles closely paired with venules having adherent leukocytes and platelets [12].…”

Section: Discussionmentioning

confidence: 99%

“…The antagonist partially reduced the vasoconstriction, suggesting that one or more other constricting mediators could be involved in their model of ischemia-reperfusion [22]. Thromboxane also appears to play a role in the venule-dependent arteriolar constriction observed in a model of intestinal inflammation induced by dextran sodium sulfate [14].…”

Section: Introductionmentioning

confidence: 99%

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Mediators of CD18/P-selectin-dependent constriction of venule-paired arterioles in hypercholesterolemia

Kim

Granger

2007

Microvascular Research

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This study addresses the role of venule-derived mediators in the arteriolar constriction that accompanies hypercholesterolemia. Constriction was assessed by measuring the tone of small arterioles closely paired with venules in the mesentery of normal cholesterol rats (NC), high cholesterol rats (HC), HC rats injected with antibodies against CD18 and P-selectin (HC/mAbs), HC rats treated with the thromboxane synthase inhibitor, ozagrel (HC/ozagrel), and HC rats pretreated with anti-platelet serum (HC/APS). Venule-paired arterioles in the untreated HC group demonstrated enhanced tone compared with arterioles in the NC group, while no difference was found between unpaired arterioles of the two groups. Perivascular nitric oxide (NO) concentrations were found to be significantly decreased in venule-paired arterioles of HC rats (238±14 nM) compared with those of NC rats (426±42 nM). The injection of anti-adhesion antibodies successfully attenuated the enhanced arteriolar tone and venular leukocyte adherence in the HC group, and tended to increase levels of NO in venule-paired arterioles by 33% (to 326±19 nM; still lower than that of the NC group). Ozagrel and platelet depletion attenuated the enhanced arteriolar tone by 53% and 33%, respectively, without affecting NO concentrations. These findings indicate that the mechanism of blood celldependent arteriolar constriction during hypercholesterolemia may be dependent on thromboxane, a decrease in NO, and the proximity of the arterioles to postcapillary venules.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Mediators of CD18/P-selectin-dependent constriction of venule-paired arterioles in hypercholesterolemia

Kim

Granger

2007

Microvascular Research

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“…We and others (16,20,40) have earlier observed that the degree of inflammation in DSS-induced colitis tends to be greater in the distal than in the proximal colon. This is confirmed here in the histological sections as well as in the P-selectin expression, which was three times higher in the distal compared with the proximal and transverse colon.…”

Section: Discussionmentioning

confidence: 99%

Lactobacillus reuteriprevents colitis by reducing P-selectin-associated leukocyte- and platelet-endothelial cell interactions

Schreiber¹,

Petersson²,

Phillipson³

et al. 2009

American Journal of Physiology-Gastrointestinal and Liver Physi

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Schreiber O, Petersson J, Phillipson M, Perry M, Roos S, Holm L. Lactobacillus reuteri prevents colitis by reducing P-selectin-associated leukocyte-and platelet-endothelial cell interactions. Am J Physiol Gastrointest Liver Physiol 296: G534 -G542, 2009. First published January 15, 2009 doi:10.1152/ajpgi.90470.2008.-Recent findings indicate that dextran sodium sulfate (DSS)-induced colitis is associated with a prothrombogenic phenotype, with P-selectin playing a major role in platelet recruitment. It has been suggested that probiotics may ameliorate colonic inflammation. We therefore investigated how treatment with Lactobacillus reuteri influenced P-selectin expression, leukocyte and platelet endothelial cell interactions, and colitis severity in DSS-treated rats. Rats were divided into the following four groups: nontreated, DSS treated (5% in drinking water for 9 days), L. reuteri, and L. reuteri and DSS treated. The rats were anesthetized with Inactin (120 mg/kg ip), and the dual radiolabeled monoclonal antibody technique was used to quantify P-selectin expression. Leukocyte-endothelial and platelet-endothelial cell interactions were studied in colonic venules with intravital microscopy. Colitis severity was assessed using a disease activity index. Disease activity index increased, as did the expression of P-selectin in the entire colon after DSS treatment, but both were reduced to control levels with L. reuteri pretreatment. The increased platelet-and leukocyte-endothelial cell interactions after DSS treatment were abolished by pretreatment with L. reuteri. L. reuteri protects against DSS-induced colitis in rats. The protection is associated with reduced P-selectin expression and a decrease in leukocyte-and plateletendothelial cell interactions.

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“…A recent study revealed that platelet adhesion within postcapillary venules was highly dependent on leukocyte adhesion, with ϳ45% of adherent leukocytes binding platelets in a model of ischemia-reperfusion (4). Activated platelets can release the potent vasoconstrictor thromboxane, which has been implicated in a recent study (8) in which platelet adherence in venules was associated with constriction of closely paired arterioles in a model of dextran sodium sulfate-induced inflammation. Figure 8 shows the mechanism that has been proposed to explain the role of venular adenosine and adherent leukocytes in regulation of the resting diameter of closely paired arterioles.…”

Section: Discussionmentioning

confidence: 99%

“…In contrast to normal physiological conditions, the presence of inflammatory cells in venules may have a major influence on arteriolar constriction (8,33). Zamboni et al (33) found that arterioles in reperfused (previously ischemic) skeletal muscle, but only arterioles near inflamed venules (as assessed by the presence of adherent leukocytes), were constricted.…”

mentioning

confidence: 99%

Leukocyte adherence inhibits adenosine-dependent venular control of arteriolar diameter and nitric oxide

Kim

2006

American Journal of Physiology-Heart and Circulatory Physiology

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Kim, Min-ho, and Norman R. Harris. Leukocyte adherence inhibits adenosine-dependent venular control of arteriolar diameter and nitric oxide. Am J Physiol Heart Circ Physiol 291: H724 -H731, 2006. First published March 31, 2006 doi:10.1152/ajpheart.01215.2005.-Venular control of arteriolar perfusion has been the focus of several investigations in recent years. This study investigated 1) whether endogenous adenosine helps control venule-dependent arteriolar dilation and 2) whether venular leukocyte adherence limits this response via an oxidant-dependent mechanism in which nitric oxide (NO) levels are decreased. Intravital microscopy was used to assess changes in arteriolar diameters and NO levels in rat mesentery. The average resting diameter of arterioles (27.5 Ϯ 1.0 m) paired with venules with minimal leukocyte adherence (2.1 Ϯ 0.3 per 100-m length) was significantly larger than that of unpaired arterioles (24.5 Ϯ 0.8 m) and arterioles (23.3 Ϯ 1.3 m) paired with venules with higher leukocyte adherence (9.0 Ϯ 0.5 per 100-m length). Local superfusion of adenosine deaminase (ADA) induced significant decreases in diameter and perivascular NO concentration in arterioles closely paired to venules with minimal leukocyte adherence. However, ADA had little effect on arterioles closely paired to venules with high leukocyte adherence or on unpaired arterioles. To determine whether the attenuated response to ADA for the high-adherence group was oxidant dependent, the responses were also observed in arterioles treated with 10 Ϫ4 M Tempol. In the high-adherence group, Tempol fully restored NO levels to those of the low-adherence group; however, the ADA-induced constriction remained attenuated, suggesting a possible role for an oxidant-independent vasoconstrictor released from the inflamed venules. These findings suggest that adenosine-and venule-dependent dilation of paired arterioles may be mediated, in part, by NO and inhibited by venular leukocyte adherence. leukocyte adhesion; Tempol RESTING ARTERIOLAR TONE can be determined by various endogenous vasoactive substances, the release of which depends on the metabolic state of the tissue, as well as on hemodynamic factors such as shear stress and pressure. In addition, when an arteriole is closely paired with a venule, vasoactive substances released from the venule also play an important role in regulating arteriolar diameter, depending on various stimulated conditions such as an increase in venular shear rate (26), an increase in muscle stimulation (16), and an exogenous venular infusion of vasoactive substances (5, 11). Nitric oxide (NO), prostaglandins, and adenosine have been implicated as mediators of venule-induced arteriolar dilation. Anatomically, various sizes of arterioles from large to small are paired with venules within a short diffusion distance in most tissues, and this close arrangement enables venular-arteriolar diffusion of vasoactive substances.In this study, we hypothesized that endogenous adenosine induces venule-dependent dilation of closely paired arte...

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Venular Constriction of Submucosal Arterioles Induced by Dextran Sodium Sulfate

Abstract: The results are consistent with a proposed mechanism in which thromboxane constricts submucosal arterioles when the arterioles are closely paired with platelet-bearing venules in DSS-induced inflammation.

Cited by 19 publications

References 28 publications

Mediators of CD18/P-selectin-dependent constriction of venule-paired arterioles in hypercholesterolemia

Mediators of CD18/P-selectin-dependent constriction of venule-paired arterioles in hypercholesterolemia

Lactobacillus reuteriprevents colitis by reducing P-selectin-associated leukocyte- and platelet-endothelial cell interactions

Leukocyte adherence inhibits adenosine-dependent venular control of arteriolar diameter and nitric oxide

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