Sympathetic a-adrenergic control of large-bore arterial vessels, arterioles and veins, and of capillary pressure and fluid exchange in whole-organ cat skeletal muscle

1990 ◽  
Vol 138 (4) ◽  
pp. 509-521 ◽  
Author(s):  
M. MASPERS ◽  
J. BJÖRNBERG ◽  
P.-O. GRÄNDE ◽  
S. MELLANDER
Keyword(s):  
Skeletal Muscle ◽  
Capillary Pressure ◽  
Fluid Exchange ◽  
Adrenergic Control

scholarly journals The Colloid Osmotic Pressure Across the Glycocalyx: Role of Interstitial Fluid Sub-Compartments in Trans-Vascular Fluid Exchange in Skeletal Muscle

2021 ◽  
Vol 9 ◽  
Author(s):  
Fitzroy E. Curry ◽  
C. Charles Michel
Keyword(s):  
Skeletal Muscle ◽  
Steady State ◽  
Osmotic Pressure ◽  
Capillary Pressure ◽  
Interstitial Fluid ◽  
Protein Composition ◽  
Colloid Osmotic Pressure ◽  
Endothelial Glycocalyx ◽  
Fluid Exchange ◽  
Small Pore

The primary purpose of these investigations is to integrate our growing knowledge about the endothelial glycocalyx as a permeability and osmotic barrier into models of trans-vascular fluid exchange in whole organs. We describe changes in the colloid osmotic pressure (COP) difference for plasma proteins across the glycocalyx after an increase or decrease in capillary pressure. The composition of the fluid under the glycocalyx changes in step with capillary pressure whereas the composition of the interstitial fluid takes many hours to adjust to a change in vascular pressure. We use models where the fluid under the glycocalyx mixes with sub-compartments of the interstitial fluid (ISF) whose volumes are defined from the ultrastructure of the inter-endothelial cleft and the histology of the tissue surrounding the capillaries. The initial protein composition in the sub-compartments is that during steady state filtration in the presence of a large pore pathway in parallel with the “small pore” glycocalyx pathway. Changes in the composition depend on the volume of the sub-compartment and the balance of convective and diffusive transport into and out of each sub-compartment. In skeletal muscle the simplest model assumes that the fluid under the glycocalyx mixes directly with a tissue sub-compartment with a volume less than 20% of the total skeletal muscle interstitial fluid volume. The model places limits on trans-vascular flows during transient filtration and reabsorption over periods of 30–60 min. The key assumption in this model is compromised when the resistance to diffusion between the base of the glycocalyx and the tissue sub-compartment accounts for more than 1% of the total resistance to diffusion across the endothelial barrier. It is well established that, in the steady state, there can be no reabsorption in tissue such as skeletal muscle. Our approach extends this idea to demonstrate that transient changes in vascular pressure favoring initial reabsorption from the interstitial fluid of skeletal muscle result in much less fluid exchange than is commonly assumed. Our approach should enable critical evaluations of the empirical models of trans-vascular fluid exchange being used in the clinic that do not account for the hydrostatic and COPs across the glycocalyx.

Microvascular pressure, surface area, and permeability in isolated hindquarters of SHR

1985 ◽  
Vol 249 (3) ◽  
pp. H498-H504
Author(s):  
R. J. Korthuis ◽  
C. R. Kerr ◽  
M. I. Townsley ◽  
A. E. Taylor
Keyword(s):  
Skeletal Muscle ◽  
Capillary Pressure ◽  
Surface Area ◽  
Convective Transport ◽  
Microvascular Permeability ◽  
Spontaneously Hypertensive ◽  
Pressure Surface ◽  
Total Plasma Protein ◽  
Wistar Kyoto ◽  
Osmotic Reflection Coefficient

The transvascular escape rate (TER) of labeled albumin is reported to increase in essential hypertension. However, the mechanism for this augmented rate of protein efflux is uncertain and may be related to increased microvascular permeability, surface area, and/or pressure. To determine the possible contributions of these mechanisms to increased TER of protein, the osmotic reflection coefficient for total plasma protein, capillary filtration coefficient, and effective capillary pressure were estimated in isolated hindquarters of age-matched (12-13 wk) spontaneously hypertensive (SHR), Wistar-Kyoto (WKY), and Wistar (WR) rats. Estimates of the reflection and filtration coefficients were not significantly different in SHR, WKY, and WR. However, capillary pressure was significantly greater in SHR than in normotensive controls. These results indicate that 1) skeletal muscle microvascular permeability and surface area are similar in SHR, WKY, and WR; 2) effective capillary pressure is greater in SHR than WKY or WR; and 3) if TER for protein is elevated in hypertensive skeletal muscle, the primary mechanism for this process may be increased convective transport of protein secondary to elevated microvascular hydrostatic pressure.

Fluid exchange in skeletal muscle with viscoelastic blood vessels

1987 ◽  
Vol 253 (6) ◽  
pp. H1548-H1556
Author(s):  
J. Lee ◽  
E. P. Salathe ◽  
G. W. Schmid-Schonbein
Keyword(s):  
Experimental Data ◽  
Mathematical Model ◽  
Skeletal Muscle ◽  
Blood Cells ◽  
Constant Pressure ◽  
Tissue Fluid ◽  
Flow State ◽  
Governing Equations ◽  
Fluid Exchange ◽  
Better Than

A mathematical model of capillary-tissue fluid exchange in a viscoelastic blood vessel is presented, and the Landis occlusion experiment is simulated. The model assumes that the fluid exchange is governed by Starling's law and that the protein and red blood cells are conserved in the capillary. Before occlusion, in the steady flow state, the pressure in the capillary decreases from the arterial to venous end due to viscous dissipation. After occlusion a constant pressure is established along the capillary. We assume the capillary to be distensible with viscoelastic wall properties. Immediately following occlusion an instantaneous distension of the capillary occurs. The vessel continues to expand viscoelastically while fluid is filtered for a period of several minutes, until it reaches an equilibrium state. A full numerical solution of the governing equations has been obtained. We use this model to compute the distance variation between two labeled erythrocytes as obtained in the Landis occlusion experiment and compare the results with experimental data obtained recently for the spinotrapezius muscle in our laboratory. The new model can fit the experimental data better than previous models that neglect the distensibility of the capillaries.

Autoregulation of capillary pressure and filtration rate in isolated rat hindquarters

1985 ◽  
Vol 248 (6) ◽  
pp. H835-H842 ◽  
Author(s):  
R. J. Korthuis ◽  
D. N. Granger ◽  
M. I. Townsley ◽  
A. E. Taylor
Keyword(s):  
Skeletal Muscle ◽  
Arterial Pressure ◽  
Capillary Pressure ◽  
Filtration Rate ◽  
Venous Occlusion ◽  
Aortic Pressure ◽  
Capillary Filtration ◽  
Abdominal Aortic ◽  
Capillary Pressures ◽  
Isolated Rat

The hypothesis that skeletal muscle capillary pressure and/or capillary filtration rate are autoregulated was tested in 10 isolated rat hindquarters. Capillary pressure was directly assessed with the venous occlusion technique as abdominal aortic pressure was reduced in 25-mmHg decrements from 125 to 25 mmHg. Capillary pressure was not altered by reduction of arterial pressure from 125 to 100 mmHg, but it decreased progressively when arterial pressure was reduced from 100 to 25 mmHg. As perfusion pressure was reduced, capillary filtration rate decreased progressively, while the capillary filtration coefficient increased. The progressive decrease in capillary pressures was less than that predicted for a totally passive system, implying that capillary pressure was autoregulated to some degree. However, analysis of pre- to postcapillary resistance ratios suggested that the degree of capillary pressure autoregulation was minimal when perfusion pressures varied over a range of 100–25 mmHg. Capillary filtration rate was maintained better than would be predicted from the measured fall in capillary pressure by readjustments of interstitial Starling forces. These results indicate that capillary pressure is poorly autoregulated in rat skeletal muscle but that compensatory readjustments in interstitial Starling forces help maintain fluid balance and prevent excess dehydration of the interstitium of skeletal muscle as arterial pressure is reduced.

Mathematical analysis of transport and exchange in skeletal muscle

1988 ◽  
Vol 234 (1276) ◽  
pp. 303-318 ◽  
Keyword(s):  
Skeletal Muscle ◽  
Oxygen Transport ◽  
Mathematical Analysis ◽  
Large Scale ◽  
Specific Reference ◽  
Fluid Exchange ◽  
New Approach ◽  
Scale Interaction ◽  
Macromolecular Transport

A new approach to modelling microcirculatory transport and exchange is introduced and developed with specific reference to skeletal muscle. The objective is to describe the large-scale interaction of a great number of differently perfused capillary groups and to interpret phenomena observed in a whole organ in terms of processes occurring within individual capillaries. We consider fluid exchange and the associated macromolecular transport, the exchange of small metabolites carried in the plasma, and oxygen transport to tissue.

A new method for estimating skeletal muscle capillary pressure

1984 ◽  
Vol 246 (6) ◽  
pp. H880-H885
Author(s):  
R. J. Korthuis ◽  
D. N. Granger ◽  
A. E. Taylor
Keyword(s):  
Skeletal Muscle ◽  
Capillary Pressure ◽  
Venous Pressure ◽  
Arterial Occlusion ◽  
Venous Occlusion ◽  
Fluid Filtration ◽  
Arterial Inflow ◽  
Capillary Pressures ◽  
Highly Correlated ◽  
Artificial Plasma

Venous (Pc,vo) and arterial occlusion capillary pressures were simultaneously compared with isogravimetric capillary pressure (Pci) in isolated rat hindquarters and canine gracilis muscles perfused with blood or an artificial plasma. Arterial or venous pressure transients following rapid occlusion of arterial inflow or venous outflow, respectively, were analyzed for the inflection point between rapid and slow components. This transition point was assumed to represent the beginning of discharge of blood stored in (arterial occlusion) or the addition of blood to (venous occlusion) skeletal muscle microvessels and was defined as the effective capillary pressure. In all preparations, Pc,vo was identical to Pci. Arterial occlusion pressures were the same as Pci and Pc,vo in artificial plasma-perfused preparations but were significantly greater (P less than 0.01) than Pci and Pc,vo obtained in blood-perfused preparations. This inequality between arterial occlusion pressure and Pci may be related to a critical closure of small precapillary vessels or the non-Newtonian behavior of blood. In addition, venous occlusion pressures were highly correlated (r = 0.95, P less than 0.01) to calculated capillary pressures obtained following simultaneous equivalent elevations of arterial and venous pressure. These results indicate that the primary sites of vascular compliance and fluid filtration reside at or very near one another in the skeletal muscle microcirculation and that the more easily determined venous occlusion capillary pressure is an adequate measure of the effective capillary pressure in skeletal muscle.

Sympathetic stimulation and intestinal capillary fluid exchange

1984 ◽  
Vol 247 (3) ◽  
pp. G279-G283 ◽  
Author(s):  
D. N. Granger ◽  
J. A. Barrowman ◽  
S. L. Harper ◽  
P. R. Kvietys ◽  
R. J. Korthuis
Keyword(s):  
Capillary Pressure ◽  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Filtration Rate ◽  
Lymph Flow ◽  
Filtration Coefficient ◽  
Fluid Exchange ◽  
Sympathetic Nerve Stimulation ◽  
Capillary Filtration ◽  
Capillary Filtration Coefficient

Sympathetic nerve stimulation is generally considered not to alter intestinal capillary pressure or filtration rate because of appropriate adjustments in the pre-to-postcapillary resistance ratio. To directly assess this possibility, we measured lymph flow, capillary pressure, capillary filtration coefficient, and the transcapillary oncotic pressure gradient in the cat small intestine. Measurements were taken under control conditions and during the steady-state phase of periarterial nerve stimulation, i.e., following completion of the escape phase. Venous outflow pressure was held constant (0 mmHg) during the entire experiment. Nerve stimulation resulted in a significant reduction of lymph flow (by 65%), capillary filtration coefficient (by 75%), and capillary pressure (by 15%). Interstitial fluid pressure, calculated from the measured parameters in the Starling equation, was also reduced (from -0.74 to -2.53 mmHg) by nerve stimulation. The results of this study indicate that intestinal capillary pressure and capillary filtration rate are not "autoregulated" during sympathetic nerve stimulation. Capillary derecruitment appears to be largely responsible for the dramatic reduction in filtration rate associated with adrenergic stimulation.

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