Simultaneous Measurement of Interstitial Fluid Pressure and Load in Rat Skin After Strain Application In Vitro

The administration of insulin is recommended to patients with severe sepsis and hyperglycemia. Previously, we demonstrated that insulin may have direct anti-inflammatory properties and counteracted fluid losses from the circulation by normalizing the interstitial fluid pressure (PIF). PIF is one of the Starling forces determining fluid flux over the capillary wall, and a lowered PIF is one of the driving forces in early edema formation in inflammatory reactions. Here we demonstrate that insulin restores a lipopolysaccharide (LPS)-lowered PIF via a mechanism involving integrin αvβ3. In C57 black mice ( n = 6), LPS lowered PIF from −0.2 ± 0.2 to −1.6 ± 0.3 ( P < 0.05) and after insulin averaged −0.8 ± 0.2 mmHg ( P = 0.098 compared with after LPS). Corresponding values in wild-type BALB/c mice ( n = 5) were −0.8 ± 0.1, −2.1 ± 0.3 ( P < 0.05), and −0.8 ± 0.3 mmHg ( P < 0.05 compared with LPS) after insulin administration. In BALB/c integrin β3-deficient (β3−/−) mice ( n = 6), LPS lowered PIF from −0.1 ± 0.2 to −1.5 ± 0.3 mmHg ( P < 0.05). Insulin did not, however, restore PIF in these mice (averaged −1.7 ± 0.3 mmHg after insulin administration). Cell-mediated collagen gel contraction can serve as an in vitro model for in vivo measurements of PIF. Insulin induced αvβ3-integrin-dependent collagen gel contraction mediated by C2C12 cells. Our findings suggest a beneficiary effect of insulin for patients with sepsis with regard to the fluid balance, and this effect may in part be due to a normalization of PIF by a mechanism involving the integrin αvβ3.

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Increased negativity of interstitial fluid pressure contributes to development of oedema in rat skin following application of xylene

Acta Physiologica Scandinavica ◽

10.1111/j.1748-1716.1990.tb09036.x ◽

1990 ◽

Vol 140 (4) ◽

pp. 581-586 ◽

Cited By ~ 13

Author(s):

S. Å. RODT ◽

H. WIIG ◽

R. K. REED

Keyword(s):

Interstitial Fluid ◽

Fluid Pressure ◽

Interstitial Fluid Pressure ◽

Rat Skin

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Measurement of renal interstitial fluid pressure with polyethylene matrix capsules

Journal of Applied Physiology ◽

10.1152/jappl.1975.38.5.937 ◽

1975 ◽

Vol 38 (5) ◽

pp. 937-941 ◽

Cited By ~ 20

Author(s):

C. E. Ott ◽

J. L. Cuche ◽

F. G. Knox

Keyword(s):

Hydrostatic Pressure ◽

Interstitial Fluid ◽

Matrix Material ◽

Fluid Pressure ◽

Interstitial Fluid Pressure ◽

Oncotic Pressure ◽

Polyethylene Matrix ◽

Measuring Device ◽

Polyethylene Capsule

The renal interstitial fluid pressure was measured in dogs from small chronically implanted solid capsules made of porous polyethylene matrix material (pore size approximately 60 mum). Tissue does not grow into the polyethylene and the matrix creates a permanent fluid-filled space in communication with the interstitium. The fluid pressure in the capsule matrix was measured from a tube leading from the capsule with an active servo-null pressure-measuring device. Renal interstitial fluid pressure measured from 28 hydropenic dogs averaged 6.1 plus or minus 0.51 mmHg (SE). Increasing oncotic pressure inside the capsule to 90 mmHg resulted in a small but significant increase in hydrostatic pressure inside the capsule of 3.3 plus or minus 0.46 mmHg. However, the hydrostatic pressure returned to control levels within 30 min. In vitro studies indicated that the pressure measured from the capsule was highly sensitive to change in surrounding hydrostatic pressure, but insensitive to change in surrounding oncotic pressure. Histological studies showed a small layer of connective tissue surrounding the capsule less than 100 mum thick in many areas. There was no evidence of inflammation or tissue rejection. It is concluded that the small chronically implanted polyethylene capsule is a reliable method for the measurement of renal interstitial fluid pressure.

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Increased negativity of interstitial fluid pressure during the onset stage of inflammatory edema in rat skin

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1991.260.6.h1985 ◽

1991 ◽

Vol 260 (6) ◽

pp. H1985-H1991 ◽

Cited By ~ 11

Author(s):

R. K. Reed ◽

S. A. Rodt

Keyword(s):

Interstitial Fluid ◽

Circulatory Arrest ◽

Fluid Pressure ◽

Interstitial Fluid Pressure ◽

System Control ◽

Rat Skin ◽

Glass Capillaries ◽

Inflammatory Edema ◽

Rat Paw ◽

Observation Period

Interstitial fluid pressure (Pif) was measured in skin of pentobarbital-anesthetized rats during anaphylaxis toward dextran and after subdermal injection of histamine by using sharpened glass capillaries (tip diam 5–7 microns) connected to a servo-controlled counterpressure system. Control Pif averaged -1.5 mmHg (SD = 1.0). After intravenous dextran Pif in the rat paw fell transiently to -3 mmHg up to 20 min and thereafter increased to +1-2 mmHg when edema had developed. To study the full magnitude of the increased negativity of Pif, circulatory arrest was induced 1 min after dextran injection. This procedure prevents accumulation of edema that will cause underestimation of Pif. In this group Pif fell to about -10 mmHg in 20 min and remained at this level throughout the observation period of 90 min. Subdermal injection of 1–10 micrograms histamine in 10 microliters saline reduced Pif to about -6 mmHg within 5 min after injection. Injection of 10 microliters saline increased Pif by +2 mmHg. Indomethacin or cyproheptadine did not alter the response in the above situations. The increased negativity in Pif of about 6–8 mmHg will add directly to normal transcapillary net filtration pressure of 0.5 mmHg and increase the latter pressure 10–20 times.

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The Mechanical Microenvironment in Breast Cancer

Cancers ◽

10.3390/cancers12061452 ◽

2020 ◽

Vol 12 (6) ◽

pp. 1452

Author(s):

Stephen J.P. Pratt ◽

Rachel M. Lee ◽

Stuart S. Martin

Keyword(s):

Breast Cancer ◽

Interstitial Fluid ◽

Fluid Pressure ◽

Normal Breast ◽

Interstitial Fluid Pressure ◽

Mechanical Stimuli ◽

Solid Stress ◽

Physical Cues

Mechanotransduction is the interpretation of physical cues by cells through mechanosensation mechanisms that elegantly translate mechanical stimuli into biochemical signaling pathways. While mechanical stress and their resulting cellular responses occur in normal physiologic contexts, there are a variety of cancer-associated physical cues present in the tumor microenvironment that are pathological in breast cancer. Mechanistic in vitro data and in vivo evidence currently support three mechanical stressors as mechanical modifiers in breast cancer that will be the focus of this review: stiffness, interstitial fluid pressure, and solid stress. Increases in stiffness, interstitial fluid pressure, and solid stress are thought to promote malignant phenotypes in normal breast epithelial cells, as well as exacerbate malignant phenotypes in breast cancer cells.

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