Comparison of microvascular pressures in normal and spontaneously hypertensive rats

Bohlen, H. G.; Gore, Robert W.; Hutchins, Phillip M.

doi:10.1016/0026-2862(77)90121-2

Cited by 131 publications

(76 citation statements)

References 5 publications

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“…Zweifach et al (51) showed that, in the rat spinotrapezius, ϳ60% of the pressure drop occurs before the transverse arterioles (diameter 8-30 m). Similar results have been observed in other tissues (7,35,48), although the distribution of resistances in larger, conscious animals has not been determined.…”

Section: Anatomical Evidence For Venular-arteriolar Communicationsupporting

confidence: 78%

Venular-arteriolar communication in the regulation of blood flow

Hester

Hammer

2002

American Journal of Physiology-Regulatory, Integrative and Comp

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Hester, Robert L., and Leah W. Hammer. Venular-arteriolar communication in the regulation of blood flow. Am J Physiol Regulatory Integrative Comp Physiol 282: R1280-R1285, 2002; 10.1152/ajpregu. 00744.2001.-Muscle blood flow is regulated to meet the metabolic needs of the tissue. With the vasculature arranged as a successive branching of arterioles and the larger, Ͼ50 m, arterioles providing the major site of resistance, an increasing metabolic demand requires the vasodilation of the small arterioles first then the vasodilation of the more proximal, larger arterioles. The mechanism(s) for the coordination of this ascending vasodilation are not clear and may involve a conducted vasodilation and/or a flow-dependent response. The close arteriolar-venular pairing provides an additional mechanism by which the arteriolar diameter can be increased due to the diffusion of vasoactive substances from the venous blood. Evidence is presented that the venular endothelium releases a relaxing factor, a metabolite of arachidonic acid, that will vasodilate the adjacent arteriole. The stimulus for this release is not known, but it is hypothesized that hypoxia-induced ATP release from red blood cells may be responsible for the stimulation of arachidonic release from the venular endothelial cells. Thus the venous circulation is in an optimal position to monitor the overall metabolic state of the tissue and thus provide a feedback regulation of arteriolar diameter. vasodilation; venular endothelium; relaxing factor TISSUE BLOOD FLOW is regulated to meet the metabolic needs of each tissue and can change quite dramatically. Increases in tissue metabolism cause increases in blood flow (functional hyperemia), whereas excess oxygen delivery causes a decrease in blood flow. Blood flow to skeletal or cardiac muscle increases proportionally with increases in metabolic rate to ensure adequate delivery of nutrients and removal of waste products. Although the precise mechanisms governing this close relationship between metabolic state of the tissue and blood flow remain to be elucidated, the anatomical arrangement of arteries and veins may provide a unique mechanism allowing the exchange of information or "cross-talk" between the pre-and postcapillary vessels.The vasculature is arranged as a series of blood vessels ranging in size from several millimeters to several micrometers, with the largest contribution of total resistance to blood flow coming from the large "feed" arterioles. Thus, to achieve optimal increases in blood flow during periods of increased muscle metabolism, large decreases in resistance of these arterioles must occur. As these upstream or feed vessels are not necessarily in contact with the metabolically active tissue, mechanisms other than or in addition to direct stimulation by tissue metabolites must be important in functional hyperemia. Mechanisms that have been proposed to regulate the diameter of upstream vessels include 1) conducted vasodilation (14), 2) flow-dependent vasodilation (29), and 3) myogenic vasodilation ...

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Section: Anatomical Evidence For Venular-arteriolar Communicationsupporting

confidence: 78%

Venular-arteriolar communication in the regulation of blood flow

Hester

Hammer

2002

American Journal of Physiology-Regulatory, Integrative and Comp

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“…While it is possible that there could be a difference in the number of enlarging collaterals, the similar enlargement of the major collaterals suggests that the mechanisms responsible for collateral growth are not impaired. Previous studies in the Nox2 Ϫ/Ϫ mouse have shown clear impairment of angiogenesis, but capillaries comprise such a small component of skeletal muscle microvascular resistance (3,27) that is is not clear that the difference in perfusion between hindlimbs of BL6 and Rac2 Ϫ/Ϫ and Nox2 Ϫ/Ϫ mice after femoral excision can be attributed to differences in capillarity. Other studies (34,56) have shown that perfusion subsequent to femoral artery occlusion is not correlated with capillarity.…”

Section: Discussionmentioning

confidence: 98%

Suppressed hindlimb perfusion in Rac2^−/− and Nox2^−/− mice does not result from impaired collateral growth

Distasi

Case

Ziegler

et al. 2009

American Journal of Physiology-Heart and Circulatory Physiology

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arteriogenesis; hindlimb ischemia; necrosis; regeneration; NADPH oxidase 2 IN THE PERIPHERAL CIRCULATION, the dilation and enlargement of preexisting vessels that form collateral pathways subsequent to arterial occlusion are the primary vascular compensations that preserve tissue viability and maintain function. These vessels dilate within seconds (25,39,45,70) and undergo expansion for weeks (20,25,45,69). In various species, the preexisting vessels are the size of the smallest arteries, and they enlarge ϳ100% (14,20,35,45,56). Available clinical studies have indicated that subsequent to arterial occlusion in the peripheral circulation, the primary vessels that enlarge as collaterals are preexisting arteries (4,29,57). The largest of the preexisting vessels are typically those that become the dominant collaterals (35,45,51). Combined anatomic and modeling studies have predicted that hindlimb flow subsequent to femoral artery occlusion is primarily determined by these collaterals (22,56). This is consistent with studies of segmental resistances that demonstrated that compensation in the collateral vessels is of significantly greater hemodynamic importance than adaptations in the distal microvasculature (43,71,75). Nevertheless, few studies investigating the mechanisms of vascular compensation subsequent to arterial occlusion in mice have specifically identified and studied these preexisting vessels that form the primary collateral pathways. Such investigations are needed because angiogenesis and collateral growth are initiated by different stimuli, and differences exist in the molecules and mechanisms that mediate these important processes (7, 11).Leukocytes, especially lymphocytes (63, 74) and macrophages (2,33,37), have been shown to have an important role in vascular compensation to hindlimb ischemia. Recent studies by Tojo et al. (66) and Urao et al. (72) have established that NADPH oxidase 2 (Nox2)-derived ROS from bone marrowderived cells (BMDCs) have an important role in neovascularization in the ischemic mouse hindlimb. The initial report (66) concluded from microsphere data that collateral growth was impaired, but did not specifically identify collateral bypass vessels or measure their diameters.To investigate the hypothesis that Nox2-derived NAD(P)H oxidase mediates primary collateral growth subsequent to arterial occlusion, the present study used Rac2-null (Rac2 Ϫ/Ϫ ) and Nox2-null (Nox2 Ϫ/Ϫ ) mice and a novel method of identifying primary hindlimb collaterals. Rac2 is expressed primarily, if not exclusively, in hematopoietic cells (38, 52) and binds to and activates Nox2-containing NAD(P)H oxidase (24,40). In addition, leukocytes from Rac2 Ϫ/Ϫ and Nox2 Ϫ/Ϫ mice have impaired function related to reduced ROS production (47,66,72). We present a method to identify the dominant or primary collateral that should be the major collateral supplying flow to

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“…The major breakthrough entailed opening the muscle, detaching it from the testicle and spreading it radially as a flat sheet for transillumination under a compound microscope 4 . While shown to be a valuable preparation to study the physiology of the microcirculation in rats 5 and hamsters 6 , the cremaster muscle in mice 7 has proven particularly useful in dissecting cellular pathways involved in regulating microvascular function [8][9][10][11] and real-time imaging of intercellular signaling 12 .…”

Section: Introductionmentioning

confidence: 99%

The Mouse Cremaster Muscle Preparation for Intravital Imaging of the Microcirculation

Bagher

Segal

2011

JoVE

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Throughout the body, the maintenance of homeostasis requires the constant supply of oxygen and nutrients concomitant with removal of metabolic by-products. This balance is achieved by the movement of blood through the microcirculation, which encompasses the smallest branches of the vascular supply throughout all tissues and organs. Arterioles branch from arteries to form networks that control the distribution and magnitude of oxygenated blood flowing into the multitude of capillaries intimately associated with parenchymal cells. Capillaries provide a large surface area for diffusional exchange between tissue cells and the blood supply. Venules collect capillary effluent and converge as they return deoxygenated blood towards the heart. To observe these processes in real time requires an experimental approach for visualizing and manipulating the living microcirculation.The cremaster muscle of rats was first used as a model for studying inflammation using histology and electron microscopy post mortem 1,2 . The first in vivo report of the exposed intact rat cremaster muscle investigated microvascular responses to vasoactive drugs using reflected light 3 . However curvature of the muscle and lack of focused illumination limited the usefulness of this preparation. The major breakthrough entailed opening the muscle, detaching it from the testicle and spreading it radially as a flat sheet for transillumination under a compound microscope 4 . While shown to be a valuable preparation to study the physiology of the microcirculation in rats 5 and hamsters 6 , the cremaster muscle in mice 7 has proven particularly useful in dissecting cellular pathways involved in regulating microvascular function [8][9][10][11] and real-time imaging of intercellular signaling 12 .The cremaster muscle is derived from the internal oblique and transverse abdominus muscles as the testes descend through the inguinal canal 13. It serves to support (Greek: cremaster = suspender) and maintain temperature of the testes. As described here, the cremaster muscle is prepared as a thin flat sheet for outstanding optical resolution. With the mouse maintained at a stable body temperature and plane of anesthesia, surgical preparation involves freeing the muscle from surrounding tissue and the testes, spreading it onto transparent pedestal of silastic rubber and securing the edges with insect pins while irrigating it continuously with physiological salt solution. The present protocol utilizes transgenic mice expressing GCaMP2 in arteriolar endothelial cells. GCaMP2 is a genetically encoded fluorescent calcium indicator molecule 12 . Widefield imaging and an intensified charge-coupled device camera enable in vivo study of calcium signaling in the arteriolar endothelium. Video LinkThe video component of this article can be found at https://www.jove.com/video/2874/ Protocol 1. Mouse board, muscle pedestal, body wedge and superfusion solution 1. Mouse board: A transparent rectangular Plexiglas board (6" wide X 8" long X 3/16" thick) is made to fit on the...

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Comparison of microvascular pressures in normal and spontaneously hypertensive rats

Cited by 131 publications

References 5 publications

Venular-arteriolar communication in the regulation of blood flow

Venular-arteriolar communication in the regulation of blood flow

Suppressed hindlimb perfusion in Rac2^−/− and Nox2^−/− mice does not result from impaired collateral growth

The Mouse Cremaster Muscle Preparation for Intravital Imaging of the Microcirculation

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Comparison of microvascular pressures in normal and spontaneously hypertensive rats

Cited by 131 publications

References 5 publications

Venular-arteriolar communication in the regulation of blood flow

Venular-arteriolar communication in the regulation of blood flow

Suppressed hindlimb perfusion in Rac2−/− and Nox2−/− mice does not result from impaired collateral growth

The Mouse Cremaster Muscle Preparation for Intravital Imaging of the Microcirculation

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Product

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Suppressed hindlimb perfusion in Rac2^−/− and Nox2^−/− mice does not result from impaired collateral growth