Effect of occlusion duration on reactive hyperemia in sartorius muscle capillaries

Pc, Johnson; Burton, KS; Henrich, H; Henrich, U

doi:10.1152/ajplegacy.1976.230.3.715

Cited by 72 publications

(41 citation statements)

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“…In regards to the post-occlusive reactive hyperemia after AO alone, an initial vasodilation following blood flow perfusion could be caused by a loss of myogenic tone (Bayliss, 1902), whereas accumulating vasodilator metabolites may be responsible for the increase in excess blood flow (Johnson et al, 1976). The present data is well supported by previous findings.…”

Section: Post-exercise Hyperemia Vs Post-occlusive Hyperemiasupporting

confidence: 90%

Post-exercise Hyperemia after Ischemic and Non-ischemic Isometric Handgrip Exercise

Osada

Katsumura

Murase

et al. 2003

J. Physiol. Anthropol.

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Post-exercise related time course of muscle oxygenation during recovery provides valuable information on peripheral vascular disease. The purpose of the present study was to examine post-exercise hyperemia (forearm blood flow; FBF, Doppler ultrasound) assessed by peak FBF, excess FBF and the time constant for FBF (FBF Tc ) following isometric handgrip exercise (IHE). Post-exercise hyperemia was assessed in an ischemic and non-ischemic state at different exercise intensities and durations. Peak FBF and excess FBF were defined as the maximum FBF during recovery, and the total amount of FBF volume, respectively. FBF Tc represents the time to reach approximately 37% of the change in FBF between peak FBF and resting FBF (delta peak FBF). Ten subjects performed IHE at "10% and 30% maximum voluntary contraction (MVC)" for 2 min with or without arterial occlusion (AO), followed by 2 min of AO alone (Study I). In Study II, six subjects performed 30%MVC-IHE with AO for "100%, 66%, 33% and 10% of the exhausted exercise duration" (time to exhaustion). In Study I, although peak FBF and excess FBF were significantly higher in ischemic than non-ischemic IHE for both 10% and 30%MVC (pϽ0.05), FBF Tc was similar in the ischemic and non-ischemic conditions. The peak FBF, excess FBF and FBF Tc were all significantly higher at 30% than at 10%MVC (pϽ0.05). In Study II, the peak FBF and excess FBF increased linearly compared to the absolute and relative exercise durations for ischemic IHE. FBF Tc increased exponentially when compared to the absolute and relative exercise durations. These data suggest the ischemic exercise has a larger hyperemic response compared to the non-ischemic exercise. In conclusion, the peak FBF, excess FBF and FBF Tc seen during post-exercise hyperemia are closely correlated with exercise intensity and duration, not only in non-ischemic, but also in the ischemic exercise. In combination with the ischemic exercise, these parameters could potentially prove to be valuable indicators of peripheral vascular disease.

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Section: Post-exercise Hyperemia Vs Post-occlusive Hyperemiasupporting

confidence: 90%

Post-exercise Hyperemia after Ischemic and Non-ischemic Isometric Handgrip Exercise

Osada

Katsumura

Murase

et al. 2003

J. Physiol. Anthropol.

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“…[21][22][23] An occlusion of 4 minutes, as applied in the present study, is thus expected to cause vasodilatation not only through the mechanism of myogenic vasodilatation but also through an additional metabolic vasodilatatory stimulus. 17,24 The role of the endothelium in modulating the myogenic response is controversial, 25 but in hypertension, arteriolar vasomotor responses to changes in intraluminal pressure are due to at least 2 mechanisms: one that is intrinsic to vascular smooth muscle (ie, myogenic) and a second that involves the endothelium. 26 Therefore, an increased sensitivity to vasoconstrictor stimuli 27 or a reduced endotheliumdependent vasodilatation 28 of small precapillary arterioles may be a mechanism explaining the impaired recruitment of capillaries in essential hypertension.…”

Section: Discussionmentioning

confidence: 99%

Impaired Skin Capillary Recruitment in Essential Hypertension Is Caused by Both Functional and Structural Capillary Rarefaction

et al. 2001

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Abstract-Capillary rarefaction occurs in many tissues in patients with essential hypertension and may contribute to an increased vascular resistance and impaired muscle metabolism. Rarefaction may be caused by a structural (anatomic) absence of capillaries, functional nonperfusion, or both. The aim of this study was to assess the extent of structural versus functional capillary rarefaction in the skin of subjects with essential hypertension. We examined skin capillary density with video microscopy before and during maximization of the number of perfused capillaries by venous congestion (structural capillary number) and before and during postocclusive reactive hyperemia (capillary recruitment, which may have a structural and/or functional basis). The study group was composed of 26 patients with never-treated essential hypertension and 26 normotensive control subjects. In both groups, intermittently perfused capillaries in the resting state were an important functional reserve for recruitment during postocclusive hyperemia. Recruitment of perfused capillaries during postocclusive reactive hyperemia was decreased in the hypertensive subjects compared with normotensive control subjects (47.9Ϯ6.8 versus 55.3Ϯ8.2 capillaries/mm 2 , respectively; PϽ0.01). During venous occlusion, maximal capillary density was significantly lower in the hypertensive subjects than in the control subjects (52.5Ϯ6.6 versus 57.2Ϯ8.6 capillaries/mm 2 , respectively; PϽ0.05), suggesting structural rarefaction. However, in the hypertensive subjects compared with the normotensive subjects, a smaller proportion of the maximal number of capillaries was perfused during postocclusive hyperemia (91.6Ϯ7.5% versus 97.2Ϯ2.7%, respectively; PϽ0.05), suggesting an additional functional impairment of capillary recruitment. If the difference in capillary numbers during venous congestion (Ϸ4.6 capillaries/mm 2 ) truly reflects the structural difference between the normotensive and hypertensive subjects, then, at most, 62% (4.6/7.4ϫ100%) of the difference in capillary numbers during postocclusive hyperemia (Ϸ7.4 capillaries/mm 2 ) can be explained by structural defects, and at least 38% can be explained by functional defects. In conclusion, in patients with essential hypertension, recruitment of perfused capillaries is impaired, which can be explained by both functional and structural rarefaction.

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“…Changes in the arterial vessel wall tone caused by vas cular occlusion are usually assumed to be accomplished by myogenic and metabolic mechanisms [17], Because of the slow cuff deflation, time-dependent changes in the arterial vessel wall tone due to myogenic mechanisms arc prevented [14], Changes in the arterial vessel wall tone by metabolic factors will mainly appear when vessels which are involved in metabolic exchange, i.e. the smallest ves sels, start to refill [ 18], Because the arterial blood volumes are derived from parameters estimated at cuff pressures above 10 mm Hg, with the contribution of the smallest vessels calculated using extrapolation to cuff pressures below 10 mm Hg [14], the estimated blood volumes will hardly be influenced by changes in arterial vessel wall tone caused by metabolic mechanisms.…”

Section: Discussionmentioning

confidence: 99%

Age-Related Differences in Elastic Properties of the Upper Arm Vascular Bed in Healthy Adults

Muntinga

Schut²,

Visser³

et al. 1997

J Vasc Res

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The significance of age-related changes in arterial stiffness has remained largely uncertain in healthy subjects. This appears to be partly due to difficulties in the interpretation of methods for measuring arterial stiffness in vivo. Therefore, a recently developed electrical bioimpedance method was used for studying elastic properties of a vascular bed as a function of age. In 66 healthy subjects, aged 22-82 years, we investigated the vascular bed of an upper arm segment. This vascular bed showed an age-related decrease in the venous blood volume (r = -0.31, p& < 0.01) and in the distensibility, the inverse of stiffness, of the larger arteries (r = -0.38, p& < 0.001). The distensibility of the arterial bed as a whole at normotensive blood pressure, however, appeared to increase with age (r = 0.32, p& < 0.005). The arterial and venous blood volumes, arterial compliance and extravascular fluid volume were significantly higher in the males than in the females. Practically all investigated vascular properties appeared to be related with height, body mass or body mass index. We concluded that comparative studies concerning vascular properties should preferably be performed in subjects matched as to age, gender, height and body mass. In healthy subjects the smaller arteries adjust to the age-related decrease in large artery distensibility by means of an age-related increase in distensibility. These age-related changes in arterial distensibility are caused by changes in the females, and seem to be associated with age-related changes in body mass index rather than with aging per se.

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Effect of occlusion duration on reactive hyperemia in sartorius muscle capillaries

Cited by 72 publications

References 0 publications

Post-exercise Hyperemia after Ischemic and Non-ischemic Isometric Handgrip Exercise

Post-exercise Hyperemia after Ischemic and Non-ischemic Isometric Handgrip Exercise

Impaired Skin Capillary Recruitment in Essential Hypertension Is Caused by Both Functional and Structural Capillary Rarefaction

Age-Related Differences in Elastic Properties of the Upper Arm Vascular Bed in Healthy Adults

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