In vivo measurement of structural changes in the microcirculation of the skeletal muscle under long term blood flow loading

Previous studies from this laboratory suggest that during juvenile growth, structural changes in the arteriolar network are accompanied by changes in some of the mechanisms responsible for regulation of tissue blood flow. To test the hypothesis that arteriolar myogenic behavior is altered with growth, we studied gracilis muscle arterioles isolated from Sprague-Dawley rats at two ages: 21–28 and 42–49 days. When studied at their respective in vivo pressures, the myogenic index (instantaneous slope of the active pressure-diameter curve) of arterioles from 42–49-day-old rats was more negative than that of arterioles from 21–28-day-old rats, indicating greater myogenic responsiveness. Endothelial denudation, or prostaglandin H2 (PGH2)/thromboxane A2 (TxA2) receptor antagonism without denudation, significantly reduced the myogenic responsiveness of arterioles from the older rats over a wide range of pressures but had no consistent effects on the myogenic responsiveness of arterioles from the younger rats. The heme oxygenase inhibitor chromium (III) mesoporphyrin IX chloride had no effect on the myogenic activity of arterioles from either age group. These findings indicate that microvascular growth in young animals is accompanied by an increase in the myogenic behavior of arterioles, possibly because PGH2 or TxA2 assumes a role in reinforcing myogenic activity over this period. As a result, the relative contribution of myogenic activity to blood flow regulation in skeletal muscle may increase during rapid juvenile growth.

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Effects of aging and exercise training on spinotrapezius muscle microvascular Po2 dynamics and vasomotor control

Journal of Applied Physiology ◽

10.1152/japplphysiol.01084.2010 ◽

2011 ◽

Vol 110 (3) ◽

pp. 695-704 ◽

Cited By ~ 19

Author(s):

Danielle J. McCullough ◽

Robert T. Davis ◽

James M. Dominguez ◽

John N. Stabley ◽

Christian S. Bruells ◽

...

Keyword(s):

Skeletal Muscle ◽

Blood Flow ◽

Exercise Training ◽

Sodium Nitroprusside ◽

Vascular Function ◽

Treadmill Running ◽

Aged Rats ◽

Phosphorescence Quenching

With advancing age, there is a reduction in exercise tolerance, resulting, in part, from a perturbed ability to match O2 delivery to uptake within skeletal muscle. In the spinotrapezius muscle (which is not recruited during incline treadmill running) of aged rats, we tested the hypotheses that exercise training will 1) improve the matching of O2 delivery to O2 uptake, evidenced through improved microvascular Po2 (PmO2), at rest and throughout the contractions transient; and 2) enhance endothelium-dependent vasodilation in first-order arterioles. Young (Y, ∼6 mo) and aged (O, >24 mo) Fischer 344 rats were assigned to control sedentary (YSED; n = 16, and OSED; n = 15) or exercise-trained (YET; n = 14, and OET; n = 13) groups. Spinotrapezius blood flow (via radiolabeled microspheres) was measured at rest and during exercise. Phosphorescence quenching was used to quantify PmO2 in vivo at rest and across the rest-to-twitch contraction (1 Hz, 5 min) transition in the spinotrapezius muscle. In a follow-up study, vasomotor responses to endothelium-dependent (acetylcholine) and -independent (sodium nitroprusside) stimuli were investigated in vitro. Blood flow to the spinotrapezius did not increase above resting values during exercise in either young or aged groups. Exercise training increased the precontraction baseline PmO2 (OET 37.5 ± 3.9 vs. OSED 24.7 ± 3.6 Torr, P < 0.05); the end-contracting PmO2 and the time-delay before PmO2 fell in the aged group but did not affect these values in the young. Exercise training improved maximal vasodilation in aged rats to acetylcholine (OET 62 ± 16 vs. OSED 27 ± 16%) and to sodium nitroprusside in both young and aged rats. Endurance training of aged rats enhances the PmO2 in a nonrecruited skeletal muscle and is associated with improved vascular smooth muscle function. These data support the notion that improvements in vascular function with exercise training are not isolated to the recruited muscle.

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Long-Term Progestin-Only Contraceptives Result in Reduced Endometrial Blood Flow and Oxidative Stress

The Journal of Clinical Endocrinology & Metabolism ◽

10.1210/jc.2006-0724 ◽

2006 ◽

Vol 91 (9) ◽

pp. 3633-3638 ◽

Cited By ~ 22

Author(s):

M. Hickey ◽

G. Krikun ◽

P. Kodaman ◽

Frederick Schatz ◽

C. Carati ◽

...

Keyword(s):

Blood Flow ◽

Western Australia ◽

Access To Health Care ◽

Abnormal Uterine Bleeding ◽

Yale University ◽

Discontinue Therapy ◽

Endometrial Blood Flow

Abstract Context: Because of their safety and efficacy, long-term progestin-only contraceptives (LTPOCs) are well-suited for women with restricted access to health care. However, abnormal uterine bleeding (AUB) causes half of all users to discontinue therapy within 12 months. Endometria of LTPOC-treated patients display aberrant angiogenesis with abnormally enlarged, thin-walled, fragile blood vessels, inflammation, and focal hemorrhage. In this study, similar effects were observed with a new third-generation implantable LTPOC. Objective: We hypothesized that LTPOC reduces uterine and endometrial blood flow, leading to hypoxia/reperfusion, which triggers the generation of reactive oxygen species. The latter induce aberrant angiogenesis, causing AUB. Design: Endometrial perfusion was measured by laser-Doppler fluxmetry in women requesting LTPOCs. Endometrial biopsies were obtained for in vivo and in vitro experiments. Setting: The study was conducted in the Yale University School of Medicine and Family-Planning Center in Western Australia. Patients: Seven women 18 yr or older requesting implantable LTPOCs were recruited in Western Australia. Intervention: Women received etonorgestrel implants. Main Outcome: LTPOC treatment resulted in reduced endometrial perfusion and increased endometrial oxidative damage. Conclusions: We propose that LTPOCs result in hypoxia reperfusion, which leads to aberrant angiogenesis resulting in AUB.

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Microdialysis of skeletal muscle at rest

Proceedings of The Nutrition Society ◽

10.1017/s0029665199001226 ◽

1999 ◽

Vol 58 (4) ◽

pp. 919-923 ◽

Cited By ~ 28

Author(s):

Jan Henriksson

Keyword(s):

Skeletal Muscle ◽

Blood Flow ◽

Human Skeletal Muscle ◽

Human Metabolism ◽

High Expectations ◽

Perfusate Flow ◽

Muscle Research ◽

Interstitial Glucose

Techniques in human skeletal muscle research are by necessity predominantly 'descriptive'.Microdialysis has raised high expectations that it could meet the demand for a method that allows 'mechanistic' investigations to be performed in human skeletal muscle. In the present review, some views are given on how well the initial expectations on the use of the microdialysis technique in skeletal muscle have been fulfilled, and the areas in which additional work is needed in order to validate microdialysis as an important metabolic technique in this tissue. The microdialysis catheter has been equated to an artificial blood vessel, which is introduced into the tissue. By means of this 'vessel' the concentrations of compounds in the interstitial space can be monitored. The concentration of substances in the collected samples is dependent on the rate of perfusate flow. When perfusate flow is slow enough to allow complete equilibration between interstitial and perfusate fluids, the concentration in the perfusate is maximal and identical to the interstitial concentration. Microdialysis data may be influenced by changes in blood flow, especially in instances where the tissue diffusivity limits the recovery in vivo, i.e. when recovery in vitro is 100 %, whereas the recovery in vivo is less than 100 %. Microdialysis data indicate that a significant arterial-interstitial glucose concentration gradient exists in skeletal muscle but not in adipose tissue at rest. While the concentrations of glucose and lactate in the dialysate from skeletal muscle are close to the expected values, the glycerol values obtained for muscle are still puzzling. Ethanol added to the perfusate will be cleared by the tissue at a rate that is determined by the nutritive blood flow (the microdialysis ethanol technique). It is concluded that microdialysis of skeletal muscle has become an important technique for mechanistic studies in human metabolism and nutrition.

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Skeletal muscle contractions uncoupled from gravitational loading directly increase cortical bone blood flow rates in vivo

Journal of Orthopaedic Research® ◽

10.1002/jor.20780 ◽

2008 ◽

Vol 27 (5) ◽

pp. 651-656 ◽

Cited By ~ 8

Author(s):

Carrie Caulkins ◽

Edward Ebramzadeh ◽

Howard Winet

Keyword(s):

Skeletal Muscle ◽

Blood Flow ◽

Cortical Bone ◽

Muscle Contractions ◽

Bone Blood Flow ◽

Flow Rates ◽

Gravitational Loading

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In Vivo Study of the Long Term Structural Changes Induced by Macular Argon Laser

Current Eye Research ◽

10.1080/02713683.2017.1419572 ◽

2017 ◽

Vol 43 (4) ◽

pp. 511-516

Author(s):

Joel Hanhart ◽

Yishay Weill ◽

Yaakov Rozenman

Keyword(s):

Structural Changes ◽

Argon Laser ◽

In Vivo Study

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Endothelium regulates skeletal muscle microcirculation by a blood flow velocity-sensing mechanism

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1990.258.3.h916 ◽

1990 ◽

Vol 258 (3) ◽

pp. H916-H920 ◽

Cited By ~ 32

Author(s):

A. Koller ◽

G. Kaley

Keyword(s):

Skeletal Muscle ◽

Endothelial Cells ◽

Blood Flow ◽

Flow Velocity ◽

Cremaster Muscle ◽

Positive Linear Correlation ◽

Skeletal Muscle Microcirculation ◽

Per Se ◽

Dependent Flow

In rat cremaster muscle, utilizing parallel arteriolar occlusion, we found that an increase in red blood cell (RBC) velocity (3.5-26.5 mm/s) per se induced an increase in diameter (1.5-9.4 microns) of arterioles (mean control diam 21.5 +/- 0.6 microns; n = 25). The dilation of arterioles appeared only when RBC velocity increased and started always with a delay (mean 8.4 +/- 0.5 s) after the increase in flow velocity. A positive linear correlation was found between peak changes in RBC velocity and diameter (r = 0.87, P less than 0.05). The velocity sensor as well as the mechanism(s) that mediates this response is likely to be located in endothelial cells, because the dilation to increased RBC velocity was completely eliminated after impairment of arteriolar endothelium with light-dye (L-D) treatment. The in vivo demonstration of this phenomenon in arterioles suggests the existence of a new endothelium-dependent, flow velocity-sensitive mechanism for the regulation of blood flow in the microcirculation.

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