Influence of arterial pressure on reactive hyperemia in skeletal muscle capillaries

1978 ◽  
Vol 234 (4) ◽  
pp. H352-H360
Author(s):  
H. Henrich ◽  
P. C. Johnson
1986 ◽  
Vol 250 (5) ◽  
pp. H838-H845 ◽  
Author(s):  
S. D. House ◽  
P. C. Johnson

It has been suggested from whole organ studies that the viscosity of blood in skeletal muscle venules varies inversely with flow over physiological flow ranges. If this is the case, the hydrostatic pressure gradient in venules should change less than flow as flow is altered. To test this hypothesis, pressure in venules of cat sartorius muscle was measured during stepwise arterial pressure reduction to 20 mmHg. Large vein pressure remained constant at about 5 mmHg. Average pressures in the large venules (40–185 microns) ranged from 13.6 to 10.0 mmHg. The difference between pressure in these venules and large vein pressure fell in proportion to the reduction in blood pressure and blood flow. Pressures in the smallest venules studied (25 microns) averaged 19.7 +/- 6.2 (SD) mmHg. The pressure difference between the smallest venules and the large vein fell less than the arteriovenous pressure difference or blood flow when arterial pressure was reduced. During reactive hyperemia the pressure gradient between the smallest venules and the large vein rose proportionately less than blood flow. The stability of pressure in the smallest venules is consistent with the hypothesis that blood viscosity varies inversely with flow rate.


1990 ◽  
Vol 112 (4) ◽  
pp. 437-443 ◽  
Author(s):  
Shou-Yan Lee ◽  
G. W. Schmid-Scho¨nbein

Although blood flow in the microcirculation of the rat skeletal muscle has negligible inertia forces with very low Reynolds number and Womersley parameter, time-dependent pressure and flow variations can be observed. Such phenomena include, for example, arterial flow overshoot following a step arterial pressure, a gradual arterial pressure reduction for a step flow, or hysteresis between pressure and flow when a pulsatile pressure is applied. Arterial and venous flows do not follow the same time course during such transients. A theoretical analysis is presented for these phenomena using a microvessel with distensible viscoelastic walls and purely viscous flow subject to time variant arterial pressures. The results indicate that the vessel distensibility plays an important role in such time-dependent microvascular flow and the effects are of central physiological importance during normal muscle perfusion. In-vivo whole organ pressure-flow data in the dilated rat gracilis muscle agree in the time course with the theoretical predictions. Hemodynamic impedances of the skeletal muscle microcirculation are investigated for small arterial and venous pressure amplitudes superimposed on an initial steady flow and pressure drop along the vessel.


2019 ◽  
Author(s):  
Ian M Williams ◽  
P Mason McClatchey ◽  
Deanna P Bracy ◽  
Jeffrey S Bonner ◽  
Francisco A Valenzuela ◽  
...  

ABSTRACTDelivery of insulin to the surface of myocytes is required for skeletal muscle (SkM) insulin action. Previous studies have shown that SkM insulin delivery is reduced in the setting of obesity and insulin resistance (IR). The key variables that control SkM insulin delivery are 1) microvascular perfusion and 2) the rate at which insulin moves across the continuous endothelium of SkM capillaries. Obesity and IR are associated with reduced insulin-stimulated SkM perfusion. Whether an impairment in trans-endothelial insulin transport (EIT) contributes to SkM IR, however, is unknown. We hypothesized that EIT would be delayed in a mouse model of diet-induced obesity (DIO) and IR. Using intravital insulin imaging, we found that DIO male mice have a ~15% reduction in EIT compared to their lean counterparts. This impairment in EIT is associated with a 45% reduction in the density of endothelial vesicles. Despite impaired EIT, hyperinsulinemia sustained delivery of insulin to the interstitial space in DIO male mice. Even with maintained interstitial insulin delivery DIO male mice still showed SkM IR, indicating severe myocyellular IR in this model. Interestingly, there was no difference in EIT, endothelial ultrastructure or SkM insulin sensitivity between lean and high fat diet-fed female mice. These results suggest that, in male mice, obesity results in damage to the capillary endothelium which limits the capacity for EIT.


1977 ◽  
Vol 150 (1) ◽  
pp. 213-218 ◽  
Author(s):  
Ralph V. McKinney ◽  
Baldev B. Singh ◽  
Phyllis D. Brewer

Author(s):  
Miles F. Bartlett ◽  
Scott M. Jordan ◽  
Dennis M. Hueber ◽  
Michael D. Nelson

Near-infrared diffuse correlation spectroscopy (DCS) is increasingly utilized to study relative changes in skeletal muscle blood flow. However, most diffuse correlation spectrometers assume that tissue optical properties- such as absorption (μa) and reduced scattering (μ's) coefficients- remain constant during physiological provocations, which is untrue for skeletal muscle. Here, we interrogate how changes in tissue μa and μ's affect DCS calculations of blood flow index (BFI). We recalculated BFI using raw autocorrelation curves and μa/μ's values recorded during a reactive hyperemia protocol in 16 healthy young individuals. First, we show that incorrectly assuming baseline μa and μ's substantially affects peak BFI and BFI slope when expressed in absolute terms (cm2/s, p<0.01) but these differences are abolished when expressed in relative terms (% baseline). Next, to evaluate the impact of physiologic changes in μa and μ's, we compared peak BFI and BFI slope when μa and μ's were held constant throughout the reactive hyperemia protocol versus integrated from a 3s-rolling average. Regardless of approach, group means for peak BFI and BFI slope did not differ. Group means for peak BFI and BFI slope were also similar following ad absurdum analyses, where we simulated supraphysiologic changes in μa/μ's. In both cases, however, we identified individual cases where peak BFI and BFI slope were indeed affected, with this result being driven by relative changes in μa over μ's. Overall, these results provide support for past reports in which μa/μ's were held constant but also advocate for real-time incorporation of μa and μ's moving forward.


1977 ◽  
Vol 232 (6) ◽  
pp. H571-H575 ◽  
Author(s):  
E. J. Messina ◽  
R. Weiner ◽  
G. Kaley

Several studies implicate endogenously synthesized prostaglandins in the mediation of reactive hyperemic responses in the coronary, renal, and skeletal muscle circulations. We sought additional evidence to involve locally released prostaglandins in the mediation of reactive hyperemia in skeletal muscle at the level of the microcirculation. The cremaster muscle of pentobarbital-anesthetized Wistar-strain rats was prepared for direct in vivo observation and measurement of postocclusive responses of single arterioles. Responses of individual arterioles were reproducible over a 3-h test period. The postocclusion increase in diameter and the duration of response were dependent upon the duration of the occlusion. Repetitive occlusions did not influence arteriolar responsiveness to vasoactive substances. Indomethacin and 5-8-11-14-eicosatetraynoic acid, inhibitors of prostaglandin synthesis, did not affect resting arteriolar diameters; however, both drugs decreased the maximum increase in diameter and duration of the vasodilator response following release of the arteriolar occlusion. These findings suggest that in this microcirculatory bed, prostaglandins contribute little to resting vascular tone; in contrast, temporary arteriolar occlusion elicits the local release of dilator prostaglandins which contribute to the reactive hyperemic response.


1962 ◽  
Vol 202 (6) ◽  
pp. 1055-1058 ◽  
Author(s):  
Lloyd R. Yonce

Circulatory reactivity to vascular occlusion for periods of 30, 60, and 120 sec was determined on eight isolated canine gracilis muscles under normothermic and hypothermic conditions (approx. 37.5 C, 25 C, 18 C, and 7 C). Control blood flow either increased or decreased when the temperature was lowered but was quite stable at each temperature step. The amount of reactive hyperemia always decreased with hypothermia and was statistically independent of effect from the control blood flow as the temperature was lowered. Recovery from reactive hyperemia required approximately the same time for the three periods of occlusion at each temperature step. The effect of hypothermia on control blood flow appears to determine the time required for recovery from reactive hyperemia.


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