Microvascular pressure distribution in skeletal muscle and the effect of vasodilation

Fronek, K.; Zweifach, BW

doi:10.1152/ajplegacy.1975.228.3.791

Cited by 196 publications

(114 citation statements)

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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: 99%

“…Studies have shown that chronic reductions in flow and pressure can result in enhanced constriction and inward remodeling characterized by wall thinning (1,6,8,17,19,41,49,50,64,67), characteristics that occur in human critical limb ischemia (17)(18)(19). Thus, the profound decrease in distal microvascular flow and pressure could result in similar decompensatory events in the precapillary arterioles and small arteries that control the majority of microvascular resistance (3,27,42,77). Such a decompensatory response could be exaggerated in Rac2 Ϫ/Ϫ and Nox2 Ϫ/Ϫ mice.…”

Section: Discussionmentioning

confidence: 99%

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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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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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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“…Some initial reports suggested that NO was more important than EDHF in producing endothelium-dependent relaxation (15,16). These experiments were performed in the isolated ring specimens and in arteries of bigger size than those controlling peripheral resistance in skeletal muscle (20). On the other hand, using hind limb perfusion models, it was shown that the endotheliumdependent relaxation in response to acetylcholine was completely resistant to the inhibition of NOS or cyclooxygenase (21 -23).…”

Section: Discussionmentioning

confidence: 99%

Mediators Involved in Decreasing Peripheral Vascular Resistance With Carbachol in the Rat Hind Limb Perfusion Model

et al. 2005

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Abstract. We examined the involvement of nitric oxide (NO) and / or endothelium-derived hyperpolarizing factor (EDHF) in decreasing peripheral vascular resistance in the rat hind limb perfusion model and analyzed the identity of EDHF in this model. The potency of carbachol (CCh) to produce relaxation was quantitatively similar to sodium nitroprusside (SNP). CChinduced relaxation was abolished after endothelial denudation, but resistant to nitroarginine and indomethacin. The relaxation was inhibited by tetraethylammonium, ouabain, charybdotoxin plus apamin, and under depolarization. SNP-induced relaxation was accompanied by increased cGMP production, which was inhibited by ODQ (1H-[1,2,4]oxadiazolo[4,3-a]quinoxaline-l-one). Although CCh produced a similar extent of relaxation to SNP, the cGMP level was 24 times lower than that with SNP. Low KCl produced a definite relaxation, which was inhibited by ouabain, but independent of NO, prostacyclin, and endothelium. 1-EBIO (1-ethyl-2-benzimidazolinone) as an activator of IK Ca channel also produced a concentration-dependent relaxation, which was inhibited by charybdotoxin, ouabain, and depolarization, but independent of NO and prostacyclin. Clotrimazole and 17-octadecynoic acid as inhibitors of P 450 monooxygenase inhibited the CCh-induced relaxation. Meanwhile, catalase at a concentration sufficient to inhibit H 2 O 2 -induced relaxation did not exert definite inhibition of the CCh-induced relaxation. These results suggest that CCh produces an endothelium-dependent, EDHF-dependent, and NO-cGMPindependent relaxation and that K + and metabolite(s) of P 450 monooxygenase possibly play an important role for this relaxation.

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“…Arterioles can be considered to be vessels smaller than ~100µm [8] and are important in regulating the pressure in the capillaries by modulating their diameter and 50-60% of the pressure drop in the vasculature occurs in the arterioles. [21] Arterioles sequentially bifurcate and eventually feed into capillaries. Capillary diameters are generally similar to or less than the major diameter of the RBCs, i.e.…”

Section: The Vascular System and Retinal Microvasculaturementioning

confidence: 99%

“…Approximately 15% of the total vascular pressure drop occurs in the capillary bed. [21] Retinal capillaries essentially consist of an endothelial monolayer covering the basal lamina, allowing diffusion of water, small solutes and lipid soluble materials in physiological states. However, the diffusion of RBCs and plasma proteins is inhibited.…”

Section: The Vascular System and Retinal Microvasculaturementioning

confidence: 99%

Red blood cells in retinal vascular disorders

Agrawal

Sherwood

Chhablani

et al. 2016

Blood Cells, Molecules, and Diseases

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Microvascular circulation plays a vital role in regulating physiological functions, such as vascular resistance, and maintaining organ health. Pathologies such as hypertension, diabetes, or hematologic diseases affect the microcirculation posing a significant risk to human health. The retinal vasculature provides a unique window for non-invasive visualisation of the human circulation in vivo and retinal vascular image analysis has been established to predict the development of both clinical and subclinical cardiovascular, metabolic, renal and retinal disease in epidemiologic studies. Blood viscosity which was otherwise thought to play a negligible role in determining blood flow based on Poiseuille's law up to the 1970s has now been shown to play an equally if not a more important role in controlling microcirculation and quantifying blood flow. Understanding the hemodynamics/rheology of the microcirculation and its changes in diseased states remains a challenging task; this is due to the particulate nature of blood, the mechanical properties of the cells (such as deformability and aggregability) and the complex architecture of the microvasculature. In our review, we have tried to postulate a possible role of red blood cell (RBC) biomechanical properties and laid down future framework for research related to hemorrheological aspects of blood in patients with retinal vascular disorders

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Microvascular pressure distribution in skeletal muscle and the effect of vasodilation

Cited by 196 publications

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

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

Mediators Involved in Decreasing Peripheral Vascular Resistance With Carbachol in the Rat Hind Limb Perfusion Model

Red blood cells in retinal vascular disorders

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Microvascular pressure distribution in skeletal muscle and the effect of vasodilation

Cited by 196 publications

References 0 publications

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

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

Mediators Involved in Decreasing Peripheral Vascular Resistance With Carbachol in the Rat Hind Limb Perfusion Model

Red blood cells in retinal vascular disorders

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

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