Early collateral and microvascular adaptations to intestinal artery occlusion in rat

Unthank, Joseph L.; Nixon, J. C.; Burkhart, Harold M.; Fath, Steven W.; Dalsing, Michael C.

doi:10.1152/ajpheart.1996.271.3.h914

Cited by 49 publications

(94 citation statements)

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“…For example, regression of medial thickness may result from the reduction in the levels of angiotensin II or the decrease in wall stress, whereas the widening of the lumen may have resulted from the increase in blood flow associated with the increase in arterial pressure following cessation of therapy. [37][38][39] An additional objective was to determine whether the depressor response or the removal of a trophic factor was the critical component in producing persistent changes in MAP and vascular structure. Two groups of SHR received the same degree of ACE inhibition and therefore a similar reduction in the trophic factor angiotensin II, with one group receiving a diet that was low in sodium.…”

Section: Discussionmentioning

confidence: 99%

Time Course of Vascular Structural Changes During and After Short-Term Antihypertensive Treatment

et al. 2003

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Abstract-The present study characterized the persistent changes (ie, off-treatment) resulting from short-term antihypertensive treatments on mean arterial pressure (MAP) and structurally based vascular resistance. Rats were treated for 14 days with enalapril (30 mg · kg Ϫ1 · d Ϫ1 ) with regular (ENAL, 0.4%) or low salt (ELS, 0.04%) diets, or a triple therapy (Triple: hydralazine 45 mg · kg Ϫ1 · d Ϫ1

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Section: Discussionmentioning

confidence: 99%

Time Course of Vascular Structural Changes During and After Short-Term Antihypertensive Treatment

et al. 2003

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“…After experimentation, animals were euthanized with an overdose of anesthetic and aortic transection. A collateral artery model (41) was created within young and mature male Wistar rats (Harlan; Indianapolis, IN) weighing ϳ200 g (ϳ2 mo old) and ϳ600 g (Ͼ8 mo old), respectively. Acute animal studies were completed with both groups for determination of blood flow and shear rate.…”

Section: Methodsmentioning

confidence: 99%

“…After laparotomy, the ileal portion of the bowel and the cecum were gently placed into a support chamber attached to the rat's abdomen and bathed in 37°C PBS. A collateral-dependent region of the bowel containing 45-55 first-order arterioles was created by the sequential ligation of 3-4 ileal arteries located near the cecum (41). This selectively increases flow in the ileal arteries immediately adjacent to the collateral-dependent region.…”

Section: Methodsmentioning

confidence: 99%

Impaired collateral development in mature rats

Tuttle¹,

Hahn²,

Sanders³

et al. 2002

American Journal of Physiology-Heart and Circulatory Physiology

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The effect of maturation on collateral development of resistance arteries was investigated. Three to four sequential mesenteric arteries were ligated to create collateral pathways in anesthetized young (ϳ200 g) and mature (ϳ600 g) rats. Blood flow was similarly elevated in collaterals of young and mature animals. In vivo inner arterial diameter was increased only within young collaterals (33 Ϯ 7%, P Ͻ 0.001). Increases in number of intimal nuclei (57 Ϯ 10% vs. 52 Ϯ 14%) and cross-sectional medial area (33 Ϯ 13% vs. 38 Ϯ 5%) were similar between young and mature collaterals. Relative to the same animal controls, collateral endothelial nitric oxide synthase mRNA was increased as much in mature as in young rats. Proteomic analysis revealed significant differences in protein expression with maturation between control arteries as well as flow-loaded collateral vessels. The results indicate that, whereas intimal and medial remodeling events were similar in collaterals of young and mature rats, luminal expansion occurred only in young rats. Alteration in arterial protein expression with maturation and altered responses to stimuli for collateral development may contribute to this impairment. luminal expansion; resistance artery; proteomic analysis; eNOS; arterial remodeling DURING THE MATURATION OF PHYSIOLOGICAL SYSTEMS, many of the mechanisms governing various functional outcomes are altered. With increasing age, these alterations may in turn lead to functional impairments and exacerbate disease. The vascular system has been shown to follow this path with regard to a variety of functions, including blood vessel reactivity (20, 35) and vascular growth and remodeling (3,24,27). Studies from our laboratory have focused on understanding processes involved in collateral artery remodeling after chronic elevation of blood flow. Currently, little is known about how maturation and aging affect the capacity for collateral development. The clinical observation/experience is that collateral growth (32) and flow-induced luminal enlargement of arteries (8) occur in adult humans. However, flow-mediated remodeling in large conduit arteries, which has many mechanistic similarities to collateral/resistance artery remodeling, has been observed to be impaired with maturation (3, 24).Arterial remodeling occurs after chronic elevation of blood flow and is a complex process involving flow/ shear stimulus transduction and endothelial activation (5, 26). After transduction and activation, remodeling of the entire arterial wall is accomplished through changes in protein expression/activity and cell growth. Luminal dimensions are altered to normalize wall shear stress (3,24,40,46). Age-dependent alterations in any of the mechanisms involved in flow-induced arterial remodeling could influence the capacity for luminal adjustment in response to altered shear. The primary purpose of the current study was to determine whether flow-induced expansion of resistance arteries forming collateral pathways is impaired with maturation and to provide insight r...

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“…Recently, similar outward remodeling has been observed in vivo (11). Increased wall shear stress, known to cause acute vasodilatation in many vascular beds (27,28), was shown by Pistea et al (36) to prevent inward remodeling in pressurized vessels in vitro and has been shown in a number of studies to cause outward remodeling in vivo (45,46). Finally, in human essential hypertension, there are indications that pharmacological normalization of the structural hypertensive changes in microvessels depend on vasodilatation (32).…”

Section: Critique Of the Modelmentioning

confidence: 70%

A mechanism for arteriolar remodeling based on maintenance of smooth muscle cell activation

Jacobsen¹,

Mulvany²,

Holstein‐Rathlou³

2008

American Journal of Physiology-Regulatory, Integrative and Comp

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Jacobsen JC, Mulvany MJ, Holstein-Rathlou N-H. A mechanism for arteriolar remodeling based on maintenance of smooth muscle cell activation. Am J Physiol Regul Integr Comp Physiol 294: R1379-R1389, 2008. First published January 9, 2008 doi:10.1152/ajpregu.00407.2007.-Structural adaptation in arterioles is part of normal vascular physiology but is also seen in disease states such as hypertension. Smooth muscle cell (SMC) activation has been shown to be central to microvascular remodeling. We hypothesize that, in a remodeling process driven by SMC activation, stress sensitivity of the vascular wall is a key element in the process of achieving a stable vascular structure. We address whether the adaptive changes in arterioles under different conditions can arise through a common mechanism: remodeling in a stress-sensitive wall driven by a shift in SMC activation. We present a simple dynamic model and show that structural remodeling of the vessel radius by rearrangement of the wall material around a lumen of a different diameter and driven by differences in SMC activation can lead to vascular structures similar to those observed experimentally under various conditions. The change in structure simultaneously leads to uniform levels of circumferential wall stress and wall strain, despite differences in transmural pressure. A simulated vasoconstriction caused by increased SMC activation leads to inward remodeling, whereas outward remodeling follows relaxation of the vascular wall. The results are independent of the specific myogenic properties of the vessel. The simulated results are robust in the face of parameter changes and, hence, may be generalized to vessels from different vascular beds. essential hypertension; microcirculation; eutrophic remodeling VESSELS OF THE MICROCIRCULATION must continuously meet the changing demands of the tissues. On short time scales, vascular diameter and, hence, tissue perfusion are regulated by variation in smooth muscle cell (SMC) activation. On longer time scales, resistance vessels adapt structurally to maintain dimensions optimal for acute flow regulation. In microvascular networks in vivo, such adaptation depends on a complex interplay between various stimuli, including pressure, shear stress, and metabolic status of the tissue (38).As noted six decades ago by Folkow and co-workers (15), in human essential hypertension, resistance vessels develop a reduced lumen size and an increased wall thickness. These changes are apparently caused by redistribution of the wall material around a smaller lumen, i.e., inward eutrophic remodeling (33), and allow the vessel to operate at normal or near-normal levels of activation, despite increased pressure (14).Another example of structural adaptation is the surprising observation by Bakker et al. (7) that, in unbranched segments of first-order rat cremaster arterioles, structural diameter does, in fact, increase distally along the vessel. This increase in diameter is not associated with an increase in wall transsectional area. Rather, analogous ...

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Early collateral and microvascular adaptations to intestinal artery occlusion in rat

Cited by 49 publications

References 0 publications

Time Course of Vascular Structural Changes During and After Short-Term Antihypertensive Treatment

Time Course of Vascular Structural Changes During and After Short-Term Antihypertensive Treatment

Impaired collateral development in mature rats

A mechanism for arteriolar remodeling based on maintenance of smooth muscle cell activation

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