Reactive hyperemia in individual capillaries of skeletal muscle

Burton, KS; Pc, Johnson

doi:10.1152/ajplegacy.1972.223.3.517

Cited by 104 publications

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“…Using a frequency modulated monitoring system that has sufficient fidelity to assess changes in ST segment height, evidence for ischemia can be obtained during ambulatory dual lead monitoring. 26,27 The advantages of this system include little need for patient skill or participation, the ability to record events over a longer period of time, and ability to monitor for ischemia during routine daily activities. Disadvantages include the large variability in numbers of ischemic episodes from day to day, the non-specificity of ST changes on the ECG, and the need for more extensive recording time, with sensitivity of the test being maximal after 72 h of monitoring.…”

Section: Diagnosis Of Silent Ischemiamentioning

confidence: 99%

Silent Myocardial Ischemia

Gutterman

2009

Circ J

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Although much progress has been made in reducing mortality from ischemic cardiovascular disease, this condition remains the leading cause of death throughout the world. This might in part be due to the fact that over half of patients have a catastrophic event (heart attack or sudden death) as their initial manifestation of coronary disease. Contributing to this statistic is the observation that the majority of myocardial ischemic episodes are silent, indicating an inability or failure to sense ischemic damage or stress on the heart. This review examines the clinical characteristics of silent myocardial ischemia, and explores mechanisms involved in the generation of angina pectoris. Possible mechanisms for the more common manifestation of injurious reductions in coronary flow; namely, silent ischemia, are also explored. A new theory for the mechanism of silent ischemia is proposed. Finally, the prognostic importance of silent ischemia and potential future directions for research are discussed. (Circ J 2009; 73: 785 -797)

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Section: Diagnosis Of Silent Ischemiamentioning

confidence: 99%

Silent Myocardial Ischemia

Gutterman

2009

Circ J

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“…Propagating the ROI through the 120-image data set resulted in a plot of mean signal intensity (SI), averaged over the ROI, as a function of time. The mean SI at each time-point was then normalized to the mean signal intensity of the first 20 baseline images: SI normalized ϭ SI i /mean SI [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20] (SI i ϭ mean SI, averaged over the ROI, at a given time-point; mean SI 1-20 ϭ mean signal intensity of the first 20 images). Peak height (PH) and time to peak (TTP) of the hyperemic curve were quantified using MATLAB (The Mathworks, Natick, MA, USA).…”

Section: Bold Mrimentioning

confidence: 99%

Reactive hyperemia and BOLD MRI demonstrate that VEGF inhibition, age, and atherosclerosis adversely affect functional recovery in a murine model of peripheral artery disease

Greve

Williams

Bernstein³

et al. 2008

Magnetic Resonance Imaging

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Purpose: To develop magnetic resonace imaging (MRI) methods for functional assessment of arteriogenesis in a murine model of peripheral artery disease to quantify the influences of vascular endothelial growth factor (VEGF), age, and atherosclerosis. Materials and Methods:Reactive hyperemia (RH), which was induced using a device designed for remote and transient occlusion of the aorta and vena cava, was measured by blood-oxygen-level-dependent MRI. Twenty-eight days after femoral artery ligation, peak height (PH) and time to peak (TTP) of the RH response was compared with shamoperated animals in 10-week-old C57Bl6, 9-month-old C57Bl6, and 9-month-old Ldlr Ϫ/Ϫ Apobec Ϫ/Ϫ mice. The contribution of VEGF to functional recovery was assessed in young mice. Angiogenesis was quantified using an anti-PECAM1 radioimmunoassay. Results:In young animals, angiogenesis was maximal 7 days after ligation, whereas functional recovery took 28 days. Inhibition of VEGF eliminated the angiogenesis seen at 7 days and reduced RH (PH, P Ͻ 0.05). At day 28, RH was altered in old (TTP, P Ͻ 0.05) and atherosclerotic (PH, P Ͻ 0.05; TTP, P Ͻ 0.05) animals. RH was different in young, old, and atherosclerotic sham animals. Old and atherosclerotic mice showed reduced angiogenesis. Conclusion:The method presented herein can provide a sensitive assay for the functional assessment of arteriogenesis and highlights the contribution of VEGF, age, and atherosclerosis to this process.

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“…Reactive hyperemia in this muscle following occlusions of Ͻ45 s is not related to a shift to anaerobic metabolism in tissue regions adjacent to the capillary network, where PO 2 levels are lowest (45). The myogenic response has long been considered an important factor in reactive hyperemia, particularly after short occlusions (3,6,25). In vivo and in vitro studies have shown that the steadystate diameter of arterioles is inversely related to intravascular pressure (19,26).…”

Section: Mechanisms Of Reactive Hyperemiamentioning

confidence: 92%

Contribution of anaerobic metabolism to reactive hyperemia in skeletal muscle

Tóth

Pál

Intaglietta

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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Tó th A, Pal M, Intaglietta M, Johnson PC. Contribution of anaerobic metabolism to reactive hyperemia in skeletal muscle. Am J Physiol Heart Circ Physiol 292: H2643-H2653, 2007. First published February 16, 2007 doi:10.1152/ajpheart.00207.2006.-Elevated blood flow (reactive hyperemia) is seen in many organs after a period of blood flow stoppage. This hyperemia is often considered to be due in part to a shift to anaerobic metabolism during tissue hypoxia. The aim of our study was to test this hypothesis in skeletal muscle. For this purpose we measured NADH fluorescence at localized tissue areas in cat sartorius muscle during and after arterial occlusions of 5-300 s. In parallel studies, red blood cell (RBC) velocity was measured in venules. Tissue NADH fluorescence rose significantly with occlusions of 45 s or greater, reaching a maximum of 44% above control at 180 s. Peak RBC velocity rose to four times control as occlusion duration was increased from 5 to 45 s, but hyperemia duration was stable at ϳ70 s. With occlusions of 45-240 s, hyperemia duration increased progressively to 210 s while peak flow was unchanged. However, after 300-s occlusions, peak flow rose to six times above control and hyperemia duration fell to 140 s. With occlusions of 45-300 s the time integral both of increased NADH fluorescence and of reduced fluorescence following occlusion release showed a high degree of correlation with the additional hyperemia. We conclude that in this muscle anaerobic vasodilator metabolites are responsible for the increase in reactive hyperemia with arterial occlusions longer than 45 s. Since the durations of reactive hyperemia and reduced fluorescence are substantially different, vasodilator metabolite removal may be due to washout by the bloodstream rather than metabolic uptake. anoxia; vasodilator metabolites; metabolic feedback; NADH fluorescence; red blood cell velocity; microcirculation; blood flow regulation REACTIVE HYPEREMIA is the increase in blood flow above resting levels that occurs after a period of blood flow stoppage, usually induced by arterial occlusion. This phenomenon has been demonstrated in a wide variety of vascular beds including skeletal muscle (4), myocardium (9), liver (14), kidney (16), intestine (36), and skin (27). The hyperemia is often attributed to accumulation of vasodilator metabolites produced by anaerobic metabolism during tissue hypoxia (1,13,28,47). However, occlusions of a few seconds' duration also elicit a hyperemic response, although this is too brief to deplete oxygen stores as noted initially by Bayliss in 1902 (3). This finding suggests that other mechanisms such as the myogenic response may contribute, since a fall in intravascular pressure during arterial occlusion would lead to arteriolar relaxation and a subsequent hyperemia when the pressure is restored. Studies on skeletal muscle (21, 25) supported the suggestion that the response following short-term (5-30 s) occlusions in resting skeletal muscle is primarily myogenic. However, with reports of additional flo...

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Reactive hyperemia in individual capillaries of skeletal muscle

Cited by 104 publications

References 0 publications

Silent Myocardial Ischemia

Silent Myocardial Ischemia

Reactive hyperemia and BOLD MRI demonstrate that VEGF inhibition, age, and atherosclerosis adversely affect functional recovery in a murine model of peripheral artery disease

Contribution of anaerobic metabolism to reactive hyperemia in skeletal muscle

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