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R K Reed

Publications and source records attributed to R K Reed.

141 records · Page 8Linked to original sources

Interstitial fluid volume, colloid osmotic and hydrostatic pressures in rat skeletal muscle. Effect of venous stasis and muscle activity.

The effect of 24 h caval/iliac venous obstruction on interstitial fluid volume (IFV), hydrostatic (Pi) and colloid osmotic (COPi) pressure in hindlimb skeletal muscle was studied in three groups of rats: Group I (G I), Intact innervation, unrestricted motor activity. Group II (G II), Sympathectomized, unrestricted. Group III (G III), Motoric and sympathetic denervation + immobilization of the hindlimbs. Subcutaneous edema was present in all groups at femoral venous pressure (Pv) exceeding 13 mmHg. Skeletal muscle edema was seen in G III at Pv above 12 mmHg, in two rats in G II at Pv of 18 and 23 mmHg, but in no rats in GI. Without venous obstruction, control COPi was 8-10 mmHg in all groups. With increasing Pv, COP fell moderately in G I and G II: delta COPi/delta Pv = 0.22. In G III, COPi fell from a control of 8.2 to 3.5 mmHg at a Pv of 12 mmHg (delta COPi/delta Pv = 0.52), but remained constant with further rise in Pv. Pi was about 0 mmHg in controls and 1-2 mmHg in rats with muscle edema. IFV rose by 6% per mmHg increase in Pv in G III, and 2% in G I and G II. This expansion of IFV may explain about 70% of the fall in COPi, the remaining being due to lymphatic washout of interstitial proteins. It is concluded that normal muscle activity together with dilution and washout of interstitial proteins constitute the main edema preventing mechanisms in skeletal muscle.

Albumins↗

Interstitial fluid volume, colloid osmotic and hydrostatic pressures in rat skeletal muscle. Effect of hypoproteinemia.

Colloid osmotic pressures in plasma (COPp) and interstitial fluid (COPi), interstitial fluid pressure (Pi) as well as interstitial fluid volume (IFV) was measured in rat skeletal muscle during development of hypoproteinemia. The hypoproteinemia was induced with intraperitoneal injections of aminonucleoside puromucin causing a renal lesion similar to that in human nephrotic syndrome with renal loss of plasma protein and subsequent fall in COPp. When COPp fell from control values (about 20 mmHg) to about 10 mmHg, the fall was accompanied by an identical fall in COPi (in mmHg) while Pi did not change. Provided the pre- to postcapillary resistance ratio was unchanged, the pressure imbalance in the Starling forces (net filtration pressure) was similar to the control situation at this stage of the hypoproteinemia. With further fall in COPi, the absolute fall in COPi was less, - leading to increased net filtration pressure, and finally edema appeared. In presence of edema, Pi rose from average control values of -0.20 mmHg to an average of +1.5 mmHg. Interstitial fluid volume in hypoproteinemic rats without edema was similar to that of controls (about 0.30 ml/g dry tissue), and increases to 3 to 4 times this value in the presence of edema. Comparing the fall in COPi to IFV in the nephrotic rats without edema show that the fall in COPi must have been brought about by a lymphatic washout of interstitial proteins since IFV was similar to the controls when COPi had fallen to 1/3 that of control.

Animals↗

Compliance of the interstitial space in rats. I. Studies on hindlimb skeletal muscle.

Interstitial compliance, defined as the ratio between changes in interstitial fluid volume (delta IFV) and interstitial fluid pressure (delta IFP), was determined for rat skeletal muscle. IFV was measured as the extravascular distribution space for 51Cr-EDTA, while sharpened micropipettes connected to a servo-controlled counterpressure system were used to measure IFP. The experimental protocol was designed to bring about acute (2-4 h) and chronic (24-28h) tissue over- and dehydration. During dehydration, the average compliance was 0.056 ml/g dry weight . mmHg, corresponding to 1.40 ml/100 g wet tissue . mmHg, and was not significantly different in acute and chronic experiments. In hydration (acute and chronic), compliance increased several-fold when IFV increased. Even at greatly increased IFV, IFP did not rise more than 1 to 1.5 mmHg above control level. Since control IFV amounts to 10 ml/100 g wet tissue, IFV will decrease by 14% when IFP falls by 1 mmHg from this control level. Provided unchanged interstitial protein mass the dehydration will cause interstitial fluid colloid osmotic pressure to increase by somewhat more than 1 mmHg--from a control level of 9 mmHg. Furthermore, since IFP was not increased by more than 1 to 1.5 mmHg during hydration, an increase in IFP plays a minor role in edema-prevention compared to dilution and/or washout of interstitial proteins.

Animals↗

Compliance of the interstitial space in rats. II. Studies on skin.

Interstitial compliance, defined as the ratio between changes in interstitial fluid volume (delta IFV) and interstitial fluid pressure (delta IFP), has been measured for rat skin. IFP has been measured with sharpened glass capillaries connected to a servocontrolled counterpressure system, while IFV has been determined as the extravascular distribution space for 51Cr-EDTA. The measurements were performed at hydration and dehydration of various duration. Compliance was 0.162 ml/g dry tissue per mmHg in dehydration, corresponding to 5.4 ml/100 g wet tissue per mmHg. The volume-pressure curve was similar at 2-4 and 24-28h of dehydration. Up to 20% increase in IFV compliance was similar to that in dehydration, but thereafter increased severalfold upon further increase in IFV. Even at sixfold increase in IFV, IFP did not rise by more than 1 to 2 mmHg. Control IFV in skin amounts to 40 ml/100 g wet tissue and IFV will therefore change by 14% when IFP changes by 1 mmHg from the control level. This change in IFV will cause interstitial fluid colloid osmotic pressure to increase or decrease by somewhat more than 1 mmHg in dehydration or hydration respectively from a normal control level of about 9 mmHg. With further increase in IFV secondary to increased capillary filtration, the interstitial edmaprevention will depend on washout and/or dilution of interstitial proteins since IFP did not increase by more than 1 to 2 mmHg.

Animals↗

Pathogenesis of edema formation in burn injuries.

One of the obvious acute features of cutaneous thermal injury is the swelling of the involved tissue. This swelling is caused by a fluid shift from circulating plasma. Along with the evolution of intravenous fluid therapy in trauma and surgery, the implementation of such therapy to burn victims has improved survival. Edema generation aggravated by fluid therapy may, however, represent a source of increased morbidity. This paper presents a review of the literature on postburn edema generation, focusing mainly on fluid physiology. It is well documented that fluid is lost from the circulation into burned tissue because of a moderate increase in capillary permeability to fluid and macromolecules and a modest increase in hydrostatic pressure inside the perfusing microvessels. Recently it was discovered that a very negative interstitial pressure develops in thermally injured skin. This pressure constitutes a strong "suction" adding markedly to the edema generating effect of increased capillary permeability and pressure.

Animals↗

Hyaluronan, hydration and flow conductivity of rat dermis.

We have measured the flow conductivity, kappa/eta, of discs of rat dermis with and without digestion with hyaluronidase. We found no significant difference between the flow conductivity of hyaluronan digested (kappa/eta = 5.56 +/- 2.74 cm4/dyne.s (n = 13)) and untreated tissue (kappa/eta = 6.03 +/- 3.15 cm4/dyne.s (n = 13)). For the first time in such experiments the overall tissue hyaluronan content as well as the difference in concentration of this material across tissues subjected to conditions of flow was measured. Similarly, the overall hydration and the difference in fluid content across the tissue is also reported. We have demonstrated that approximately 99% of the tissue hyaluronan was digested as a result of activity of the enzyme. No difference in hyaluronan across the tissue was found in the flow experiments (i.e., with or without digestion). We found significant change in the overall tissue hydration for controls and for either of the two types of flow experiments performed. Likewise, we found significant hydration differences across the tissues under both types of flow conditions. A trend in decreasing hydration associated with digestion of hyaluronan in the flow experiments was found.

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Preliminary model of fluid and solute distribution and transport during hemorrhage.

The distribution and transport of fluid, ions, and other solutes (plasma proteins and glucose) are described in a mathematical model of unresuscitated hemorrhage. The model is based on balances of each material in both the circulation and its red blood cells, as well as in a whole-body tissue compartment along with its cells. Exchange between these four compartments occurs by a number of different mechanisms. The hemorrhage model has as its basis a validated model, due to Gyenge et al., of fluid and solute exchange in the whole body of a standard human. Hypothetical but physiologically based features such as glucose and small ion releases along with cell membrane changes are incorporated into the hemorrhage model to describe the system behavior, particularly during larger hemorrhages. Moderate (10%-30% blood volume loss) and large (> 30% blood loss) hemorrhage dynamics are simulated and compared with available data. The model predictions compare well with the available information for both types of hemorrhages and provide a reasonable description of the progression of a large hemorrhage from the compensatory phase through vascular collapse.

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Lymphatic hyaluronan flux from skin increases during increased lymph flow induced by intravenous saline loading.

Hyaluronan is a structural component of the interstitial matrix in skin and is catabolized locally in skin as well as by lymphatic removal and subsequent degradation in lymph nodes and liver. The present experiments were designed to evaluate the role of interstitial fluid flux in turnover of hyaluronan in skin by measuring the maximal lymphatic flux of hyaluronan. Lymph flow, total protein concentration, hyaluronan concentration, and flux were measured every 15 min in prenodal lymph from the hind paw in 12 pentobarbital-anesthetized mongrel dogs at normal and increased interstitial fluid flux. An intravenous saline load (15% of body weight during the course of 30 min) was followed by a one-step increase in local venous pressure 30 min later (to a maximum of 50 mm Hg) and maintained at this level for the next 240 min. Lymph flow and hyaluronan concentration during the control period averaged 25.6 +/- (SD) 23.2 (range 4.7-61.9) microliters/min and 8.6 +/- 2.8 (range 2.0-11.6) micrograms/ml, respectively. The hyaluronan concentration fell by 30% during the experimental period, while the lymph flow increased up to ten times above control. Total tissue water increased from 1.73 +/- 0.11 ml/g dry weight during the control period to 1.91 +/- 0.12 ml/g dry weight at the end of the experiment (p < 0.01). The corresponding tissue contents of hyaluronan averaged 3.5 +/- 0.9 and 3.6 +/- 0.6 mg/g dry weight, respectively (p > 0.05). The average lymphatic hyaluronan flux was 8.4 +/- 5.4 micrograms/h during the control period, peaked at about 60 micrograms/h, and averaged 33.6 +/- 13.9 micrograms/h during the last hour of the experimental period.(ABSTRACT TRUNCATED AT 250 WORDS)

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Increased hyaluronan flux in canine paw lymph is induced by histamine and the histamine-releasing agent compound 48/80.

The present experiments investigated hyaluronan (HYA) flux from skin of pentobarbital anesthetized mongrel dogs when transcapillary fluid flux was increased by local intraarterial injection of histamine (50 micrograms) or Compound 48/80 (C48/80) (100 micrograms) inducing mast cell degranulation. A prenodal lymphatic draining the hindpaw was cannulated and the paw flexed passively at 50 times/min. Grand mean (n = 18) of control lymph flow and HYA concentration was 16 +/- (SD) 14 microliters/min and 8.8 +/- 2.3 micrograms/ml, respectively. Lymph flow increased 11- and 15-fold within 10 min after histamine and C48/80 injection, respectively, and returned to control values after 3 h for histamine while it did not return fully in the C48/80 group. HYA concentration decreased by 30 and 40% during the first hour after histamine and C48/80, respectively, while HYA flux increased 11-15 times control. Control experiments (saline vehicle) showed an unexpected and gradual increase in HYA concentration during the 8-hour experimental period, regardless of unchanged lymph flow. This increase became statistically significant at the end of the experimental period, suggesting either an increased synthesis or increased rate of release of bound HYA from the paw. The present data show that HYA is loosely bound and easily mobilized from the interstitial matrix and that histamine and C48/80 cause a release of bound HYA from the interstitium. An increase in HYA concentration towards the end of the 8-hour experimental period most likely represents an increased synthesis of HYA.

Animals↗

Flow conductivity of rat dermis is determined by hydration.

The flow rate of phosphate buffered saline through dermis was measured as a function of applied pressure. Hyaluronan and collagen, the two principal materials which confirm resistance to flow in dermis, were not lost from the tissue during the experiments which lasted up to two days. From Darcy's Law, the average flow conductivities were 2 to 6 x 10(-12) cm4/dyn x s and decreased with increasing applied pressure. We conclude that the tissue is compacted in proportion to the applied pressure during the flow experiments. The hydraulic flow conductivity is described mathematically as a function of compaction induced by the applied pressure.

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