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Biomedical subjects

R K Reed

Publications and source records attributed to R K Reed.

At least 55 records · Page 3Linked to original sources
PubMed1997

Pressure-volume relationship for rat dermis: compression studies.

The relationship between tissue hydrostatic pressure and fluid content is an important determinant of the response of the microvascular exchange system to perturbations. However, only a limited number of studies relating these parameters have been reported. To add to this body of information, fully swollen rat dermis in vitro was subjected to successive compressive loads in an apparatus in which tissue thickness changes were monitored. At steady-state the mechanical load on the tissue was balanced by the interstitial fluid pressure within the tissue while the fluid content of the tissue was determined from the unstressed tissue fluid content and changes in tissue thickness. The range of conditions investigated was from moderate overhydration through normal tissue fluid content to significant dehydration. From the relationship between interstitial fluid pressure and tissue fluid content (expressed as mass of fluid per mass of fat-free dry tissue) the tissue compliance was determined. Compliance, defined as the rate of change of the tissue fluid content with changes in interstitial pressure, increased with tissue hydration. The compliance determined using compressive loads and steady-state response of tissue thickness compares favourably with the limited amount of information available about this tissue property which is critical in the determination of tissue fluid balance. Compliance ranged over one order of magnitude for the conditions studied and at normal hydration, tissue fluid volume changed by about 6.6% per mmHg in tissue hydrostatic pressure.

Animals↗
PubMed1997

Alloxan diabetes abolishes the increased negativity of interstitial fluid pressure in rat trachea induced by vagal nerve stimulation.

Increased negativity of interstitial fluid pressure (Pif) occurs concomitantly with oedema formation in acute airway inflammation. This observation is principally important because the loose connective tissues become 'active' and provide the driving force for the rapid oedema formation via Pif. The present study reports Pif in acute airway inflammation in alloxan diabetic rats. The basis for the study was, firstly, that inflammation is important in the pathogenesis of asthma. Secondly, that clinically there is almost a mutual exclusion between diabetes and asthma and, lastly, that the inflammatory response is attenuated in alloxan diabetic rats. Pif was measured on the ventral side of the trachea with sharpened glass capillaries (3-6 microns) connected to a servocontrolled counterpressure system. Measurements and nerve stimulation were performed after circulatory arrest, since oedema formation associated with inflammation will increase Pif, causing an underestimation of a potentially increased negativity of Pif. Control or diabetic rats (alloxan 45 mg kg-1 i.v. 5 days earlier) received either the mast cell degranulating substance compound 48/80 (100 micrograms), dextran 70 (60 mg) i.v. or vagal nerve stimulation. After dextran, Pif was -4.7 +/- 0.9 (SD) mmHg (n = 6) and -1.3 +/- 0.3 mmHg (n = 6) (P < 0.01) in normal and diabetic rats, respectively. Corresponding values after vagal nerve stimulation were -5.3 +/- 1.8 mmHg (n = 5) and -0.7 +/- 0.2 mmHg (P < 0.01). Insulin treatment restored the Pif response to dextran and vagal stimulation. Pif after Compound 48/80 did not differ between control and diabetic rats. Interstitial volume, total tissue water and transcapillary albumin extravasation increased significantly in controls after vagal nerve stimulation, but was attenuated in diabetic rats.

Albumins↗
PubMed1997

CGRP, but not substance P, induces an increased negativity of the interstitial fluid pressure in rat trachea.

Neurogenic inflammation is mediated by neuropeptides released from sensory nerves following electrical stimulation of the vagal nerve or by capsaicin. The released neuropeptides are, among others, calcitonin gene-related peptide and substance P, which both induce vasodilation, while only substance P induces plasma extravasation. Electrical stimulation of the vagal nerve induces increased negativity of interstitial fluid pressure (Pif), which will contribute to enhance oedema formation. Pif was measured, on the abluminal side of the surgically exposed trachea, with sharpened glass capillaries (4-10 microns) connected to a servo-controlled counterpressure system. Measurements were performed after circulatory arrest, since the oedema formation associated with acute inflammation will increase Pif in a positive direction, which may potentially underestimate the increased negativity of Pif. Experiments were carried out in pentobarbital anaesthetized (50 mg kg-1) Wistar-Møller rats. Pif in control rats averaged -1.2 +/- 0.9 (SD) mmHg (n = 9). Intravenous injection of capsaicin (65.0 nmol) and calcitonin gene-related peptide (1.3 nmol) increased the negativity of Pif to -4.0 +/- 1.2 mmHg (n = 8) (P < 0.01) and -4.7 +/- 2.0 mmHg (n = 9) (P < 0.01), respectively. Intravenous injection of substance P (7.4 nmol, n = 9; and 37.0 nmol, n = 8) did not affect Pif compared to control (P > 0.05). Similarly, potentiation of the available substance P with thiorphan or captopril did not increase the negative Pif, nor did injection of stable substance P analogues. Thus, the present study seems to support the theory that, in rat trachea, the increased negativity of Pif after intravenous injection of capsaicin and after vagal stimulation is caused by calcitonin gene-related peptide.

Animals↗
PubMed1996

A novel physiological function for platelet-derived growth factor-BB in rat dermis.

1. The present experiments describe a role for platelet-derived growth factor-BB and cellular adhesion receptors towards extracellular matrix molecules (beta 1-integrins) in control of interstitial fluid pressure (Pif). 2. Pif was measured in rat skin with sharpened glass capillaries (3-7 microns) connected to a servocontrolled counter-pressure system. 3. The collagen and laminin-binding alpha 2 beta 1-integrin is involved in the control of Pif since subdermal injection (5 microliters) of monoclonal hamster anti-rat alpha 2 beta 1-integrin IgG (anti-alpha 2 beta 1) resulted in increased negativity of Pif. Control Pif averaged -0.88 +/- 0.23 mmHg (+/- S.D.) and decreased to -2.50 +/- 0.35 mmHg (P < 0.05) and -3.88 +/- 1.45 mmHg (P < 0.05) at anti-alpha 2 beta 1 concentrations of 0.56 and 1.12 mg ml-1, respectively. 4. The effect of anti-alpha 2 beta 1 was abolished when platelet-derived growth factor-BB (PDGF-BB) (200 ng ml-1) was injected together with anti-alpha 2 beta 1. 5. The time- and dose-responses of PDGF-BB to counteract increased negativity of Pif were studied further using dextran anaphylaxis as an experimental model inducing increased negativity of Pif in skin. Control Pif averaged -0.33 +/- 0.43 mmHg and fell to -4.10 +/- 1.47 mmHg within 10 min after dextran (P < 0.01). Subsequent subdermal injection of PDGF-BB at 200 ng ml-1 normalized Pif in 10-20 min which became -1.37 +/- 1.23 mmHg (P < 0.01 versus dextran, P > 0.05 versus control). PDGF-BB had little or no effect at 50 ng ml-1. PDGF-AA and basic fibroblast growth factor had no effect on Pif. 6. The in vivo function reported for PDGF-BB has not been described previously and provides further evidence for active participation of connective tissue cells in control of Pif by altering tension on extracellular matrix structures.

Animals↗
PubMed1996

The relationship between interstitial fluid pressure and volume in rat trachea.

A change of interstitial fluid volume (IFV) will normally change the interstitial fluid pressure (Pif) so as to counteract further fluid movement across the capillaries and changes in IFV. Contrary to this, several acute inflammatory reactions in the trachea are associated with increased negativity of Pif, which will 'actively' generate oedema. To outline further the role of Pif in interstitial fluid balance in the trachea, interstitial compliance (delta IFV/delta Pif) was measured in pentobarbital anaesthetized rats. IFV was measured as the plasma equivalent extravascular distribution space of [51Cr]EDTA. Pif was measured in the same animal with sharpened glass pipettes (diameter 3-6 microns) connected to a servocontrolled counterpressure system. In dehydration (30 mL saline i.v., n = 10) interstitial compliance was 0.083 mL g dry wt-1 mmHg-1. Since control IFV was 1.046 mL g dry wt-1 (n = 10) the interstitial compliance is 8% of IFV per mmHg. In overhydration (30 mL NaCl, n = 10) and dextran anaphylaxis (1 mL dextran 70, n = 10) compliance remained the same for the first 15% increase in IFV and then increased several-fold since Pif did not increase more than 2 mmHg above control level. The increased negativity of Pif by -10 mmHg associated with acute inflammation will require a reduction of IFV by 80% when interstitial compliance is 8% per mmHg. A more likely explanation is therefore that structural rearrangements are responsible for the events leading to increased negativity of Pif in acute inflammation.

Animals↗
PubMed1996

Effect of increased interstitial fluid flux on fractional catabolic rate of high molecular weight [3H]hyaluronan injected in rabbit skin.

The removal rate of high molecular weight (M(r) 3 x 10(6) [3H]hyaluronan has been measured in rabbit paw skin in control and during increased local venous pressure induced by ligation of the femoral vein. The increased venous pressure resulted in a 20% increase of interstitial volume at 4 h after ligation, a value which relates to at least a doubling of lymph flow, i.e. also to doubling of fluid flux through the tissues. The fractional catabolic rate of hyaluronan was 0.0918 +/- 0.0170 h-1 (n = 10) and 0.0775 +/- 0.0206 h-1 (n = 11) in control and following increased venous pressure respectively (P > 0.05). Since the fractional catabolic rate of hyaluronan is not affected by increased venous pressure, the removal of hyaluronan via lymphatic drainage in rabbit paw skin must be small compared to the local turnover of the polysaccharide.

Animals↗
PubMed1996

Enterostatin efflux in cat intestinal lymph: relation to lymph flow, hyaluronan, and fat absorption.

The question addressed in this study was whether enterostatin, the pancreatic procolipase activation peptide, modulates intestinal hyaluronan turnover via lymph. In anesthetized cats, segments of ileum were surgically isolated from the proximal and distal gut, the draining lymphatic was cannulated, and the segment was autoperfused in situ. In several groups, concentrations of immunoreactive enterostatin in lymph were compared with that in plasma at baseline and elevated lymph flow and in the absence and presence of fat absorption. The baseline ratio of lymph enterostatin to that in plasma (L/P) in the absence of fat absorption was 1.44 +/- 0.29 compared with 4.93 +/- 0.42 after cream feeding (P < 0.05). In a separate group, when the intestinal lumen was perfused for 2 h with a mixture of oleic acid and taurocholate, enterostatin L/P doubled compared with baseline. At high lymph flows, enterostatin concentrations fell in all groups, resulting in an L/P of 0.47 +/- 0.09 (P < 0.05) in the absence of fat absorption, 0.77 +/- 0.35 after oleic acid, and 1.26 +/- 0.13 in the cream-fed group. These changes correlate with the pattern of hyaluronan efflux from the ileum into lymph after fat absorption [R.K. Reed, M.I Townsley, V.H. Pitts, T.C. Laurent, and A.E. Taylor. Am. J. Physiol, 263 (Gastrointest. Liver Physiol. 26): G6-G11, 1992] However, in separate groups when enterostatin was introduced into ileum, either as a close intra-arterial bolus or via the intestinal lumen, there were no resultant changes in efflux of hyaluronan from the intestine into lymph. In conclusion, despite the fact that delivery of pancreatic exocrine secretions to the ileal lumen was blocked in this model, enterostatin concentration in lymph increased after fat absorption. Nonetheless, it seems clear that enterostatin does not modify intestinal hyaluronan turnover.

Animals↗
PubMed1996

Lowering of interstitial fluid pressure will enhance edema in trachea of albumin-sensitized rats.

Interstitial fluid pressure (Pif) has recently been found to play an important role in edema formation in acute airway inflammation. Because airway inflammation is important in the pathogenesis of asthma, Pif was measured in rat trachea after albumin challenge to rats previously sensitized to chicken egg albumin. In pentobarbital anesthesia (50 mg/kg intraperitoneally) sensitized rats received an intravenous infusion of either saline or albumin, which circulated for 4 min. Circulatory arrest was then induced with saturated KCl intravenously to prevent further edema formation, which will increase Pif and thereby possibly cause an underestimation of an increased negativity of Pif. Pif was measured with sharpened glass capillaries (diameter 3-6 micrometer) connected to a servo-controlled counter pressure system. Pif was -1.3 +/- 0.4 mm Hg in controls and -5.8 +/- 0.5 mm Hg in sensitized rats (p < 0.01) after allergen challenge. Airway resistance was measured to verify the occurrence of airway narrowing and increased significantly in sensitized rats after allergen challenge but did not change in controls. The experimental anti-inflammatory drug, alpha-trinositol (D-myo-inositol-1,2,6-trisphosphate, 10 mg), given before or after allergen challenge abolished the increased negativity of Pif (p < 0.05), while hydrocortisone (6.25 mg) had no effect. Thus, allergen challenge is associated with a lowering of Pif, which was abolished by alpha-trinositol.

Airway Resistance↗
PubMed1995

A model of human microvascular exchange.

A compartmental model consisting of the circulation, a general interstitium, and the lymphatics, is formulated to describe the transport and distribution of fluid and plasma proteins (albumin) in the human microvascular exchange system. Transcapillary mass exchange is assumed to occur via a coupled Starling mechanism. Unknown or poorly quantified model parameters are estimated by statistical fitting of simulation predictions to five different sets of experimental data. The data consist of steady-state and transient plasma and interstitial volumes and colloid osmotic pressures measured under laboratory or clinical conditions for normal humans and for patients with nephrotic syndrome or mild heart disease. In all cases, it is assumed that the system response to perturbations imposed either artificially or through illness is due to changes in the Starling driving forces. The three best-fit parameters were found to be normal capillary hydrostatic pressure, Pc,o = 11.0 mm Hg; albumin reflection coefficient, sigma = 0.99; and lymph flow sensitivity, LS = 43.1 ml/mm Hg.hr. Three other parameters, which were unknown but related to the estimated parameters through steady-state mass balance equations, were determined to be fluid filtration coefficient, KF = 121.1 ml/mm Hg.hr; albumin permeability-surface area product, PS = 73.0 ml/hr; and normal lymph flow, JL,o = 75.7 ml/hr. The fully described model was validated by comparisons between (1) simulation predictions and data used in parameter estimation, (2) estimated transport parameters and available literature values, and (3) model predictions and an additional set of experimental data.

Cardiac Output, Low↗
PubMed1995

A model of fluid resuscitation following burn injury: formulation and parameter estimation.

A dynamic compartmental model is developed to describe the redistribution of fluid and albumin between the circulation and the intact and injured interstitia following burn injury in humans. Transcapillary fluid and albumin exchange is described by a coupled Starling mechanism, while the effect of the burn is represented by time-dependent perturbations to all three compartments. The unknown model parameters are determined for two groups of patients, having less than and greater than 25% total body surface area burns, by statistical fitting of model predictions to patient data from two sources. The parameters include the perturbations to the fluid filtration coefficients in uninjured and injured tissue, GkF,Tl and GkF,BT, respectively, the relaxation coefficient, r, which describes the exponential decay of the perturbations, and the exudation factor, EXFAC, which relates the protein concentration in the exudate to that in the injured tissue. Perturbations to other parameters, including the membrane permeability-surface area product and the albumin reflection coefficient in the injured and uninjured tissues, are determined based on interrelationships with GkF,Tl and GkF,BT. The values of GkF,BT, when corrected for tissue destruction and decreased post-injury perfusion, are in reasonable agreement with the limited experimental data available from the literature. The model and its parameters are further validated by comparing the simulated patient responses to the clinical data used in the parameter estimation as well as to data available from two additional sources.

Body Fluid Compartments↗
PubMed1995

Interstitial fluid accumulation does not influence oxygen uptake in the rabbit small intestine.

Crystalloid resuscitation increases interstitial fluid volume. Intestinal ischemia and impaired barrier function may contribute to the precipitation of multiple organ failure. Accordingly, the intestine was chosen as target organ to test whether interstitial oedema impairs oxygen extraction by the tissue. The portal vein in anaesthetized rabbits was partially obstructed for 30 min along with an intravenous infusion of 0.9% saline 60-90 ml kg-1 (oedema group, n = 7). Total water content of the small intestine increased from 3.4 ml g-1 dry weight in control (n = 8) to 3.9 ml g-1 in the oedema group (P = 0.049). Small intestinal O2 uptake was calculated from the arteriovenous O2 content and electromagnetic flow measurements in the superior mesenteric artery. Mesenteric flow was reduced stepwise by a snare occluder around the artery. Intestinal oxygenation was monitored indirectly as well, by means of mesenteric venous lactate, arterial base excess and by mucosal pH (pHi) assessed tonometrically. The oxygen extraction ratios were similar in the oedema and control group at similar oxygen supplies. After a 45 min flow reduction to 15% of baseline mesenteric venous lactate and pHi did not differ between the groups. pHi averaged 7.31 and fell to 6.74. Below an intestinal O2 uptake of 2.5 ml min-1, pHi correlated somewhat better with O2 uptake (r = 0.66) than did arterial base excess (r = 0.50). The results indicate that acute elevation of extracellular volume to the extent in the present study, does not impede oxygen uptake in the gut.

Acid-Base Imbalance↗
PubMed1995

Lymphatic transport and organ uptake of gelatin and hyaluronan injected into the rat mesentery.

The metabolic pathways of denatured collagen (gelatin) and hyaluronan were studied by injecting labelled macromolecules into the mesentery of rats. The label, [125]tyramine-cellobiose is trapped intracellularly after endocytosis, allowing localization of the site of uptake. Mesenteric and thoracic lymph was sampled for 6 h in anaesthetized rats. Separate rats were investigated after an awake period of 6 or 24 h. About 30% of the gelatin remained at the site of injection and of the remaining activity 1.7% was recovered in lymph, 11% in the liver and 15% in the kidneys, whereas 3 h after an intravenous injection of gelatin > 70% was recovered in the liver. The change in preferable site of uptake from the liver to the kidney was attributed to local degradation in the mesentery as confirmed by chromatography of tissue extracts and lymph. Following hyaluronan injection and 6 h lymph sampling approximately 30% was left at the site of injection and of the remaining activity 5.7% was recovered in lymph. After an awake period of 6 or 24 h, 30% was regained in the liver. The recoveries in other organs were negligible and mesenteric lymph nodes seem quantitatively unimportant in the uptake of hyaluronan or gelatin from lymph or blood. The liver has a central role in intestinal hyaluronan metabolism, while denatured collagen is more prone to local degradation with remote uptake shared between the liver and the kidney.

Animals↗
PubMed1994

Alpha-Trinositol inhibits edema generation and albumin extravasation in thermally injured skin.

Pharmacologic attempts to reduce edema generation and albumin extravasation into thermally injured skin have until recently been disappointing unless the drugs (usually antiphlogistic or anti-inflammatory drugs) were given before injury. We have studied the effect of alpha-trinositol (PP56, i.e., 1D-myo-inositol-1,2,6-trisphosphate) given after the injury in an experimental full-thickness 10% TBSA scald burn in anesthetized rats. Total tissue water content (TTW) and albumin extravasation (Ealb) were determined in injured and noninjured skin (series I, n = 12). Interstitial fluid hydrostatic pressure (Pif) was measured in injured skin (series II, n = 14). alpha-Trinositol was administered (alpha-trinositol groups) as an i.v. bolus (40 mg/kg) at 5 minutes after injury followed by an i.v. infusion (1.3 mg/kg/min). In both series a placebo group received burn injury and normal saline in equal volumes instead of alpha-trinositol. Compared with placebo, alpha-trinositol reduced TTW and Ealb as well as the increased negatively of Pif in injured tissue significantly. The effect on Ealb was most prominent, with a reduction from 153.9 +/- 35.6 (SEM) microL/g in the NaCl group to 23.1 +/- 6.3 after alpha-trinositol (p < 0.005). Total tissue water was reduced from 2.51 +/- 0.13 to 2.17 +/- 0.06 mL/g (p < 0.05) and Pif (measured between 21 and 40 minutes postinjury) from -24.7 +/- 4.1 to -3.2 +/- 1.1 mm Hg (p < 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)

Albumins↗
PubMed1994

Increased lymphatic hyaluronan output and preserved hyaluronan content of the rat small intestine in prolonged hypoproteinaemia.

Nephrotic syndrome was induced in seven rats by daily aminonucleoside injections. Experiments were performed in anaesthesia 6 or 7 d later when protein loss in urine had reduced serum colloid osmotic pressure (COP) to 8.2 +/- 0.9 (SD) mmHg compared with 20.2 +/- 2.2 mmHg in controls (P < 0.01). Due to the decreased COP in the nephrotic rats, lymph flow in the main mesenteric lymphatic was 29.5 +/- 11.5 microliters min-1 compared with 4.2 +/- 2.2 microliters min-1 in the control rats (P < 0.01). The corresponding hyaluronan concentrations were 3.4 +/- 0.9 micrograms ml-1 and 12.0 +/- 3.5 micrograms ml-1, respectively (P < 0.01). Nevertheless lymphatic hyaluronan output was doubled in the nephrotic rats, but this did not affect the hyaluronan content of the small intestine of 192 +/- 58 micrograms g-1 dry wt compared with 215 +/- 69 micrograms g-1 in controls (P > 0.05). During a 20 min intravenous 0.9% saline infusion of 4 ml 100 g-1 rat, the hyaluronan concentration increased to 18.3 (6.0) micrograms ml-1 in mesenteric lymph in controls, whereas the concentration in lymph from the nephrotic rats remained unchanged. Lymphatic output increased, however, in this group as well due to the elevated flow. The amount of hyaluronan cleared daily by the main mesenteric lymphatic in awake rats corresponds to about half the tissue hyaluronan content in the drained area (østgaard & Reed 1993 b).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Permeability of parietal pleura to liquid and proteins.

The permselectivity of the parietal pleura was determined in spontaneously breathing anesthetized rabbits and dogs. In rabbits, we injected intrapleurally 5 ml of 1-g/dl albumin solution containing 100 microCi of 131I-labeled albumin plus 100 microCi of either lactate dehydrogenase (LDH) or alpha 2-125I-macroglobulin. Dogs received 100 ml of 1-g/dl albumin solution containing 100 microCi of 131I-albumin plus 100 microCi of alpha 2-125I-macroglobulin. A transpleural pressure gradient was set, lowering the intracapsular pressure to -30 cmH2O. The solvent drag reflection coefficients (sigma f) were calculated as the ratio between tracer concentrations in capsular and pleural liquid collected at 60-180 min. In rabbits sigma f was 0.44 +/- 0.2 (SD) for albumin, 0.84 +/- 0.1 for LDH, and 0.93 +/- 0.05 for alpha 2-macroglobulin. In dogs sigma f was 0.30 +/- 0.19 for albumin and 0.53 +/- 0.15 for alpha 2-macroglobulin. The hydraulic conductivity of the parietal pleura was 2.18 +/- 1.54 microliters.h-1.cmH2O-1.cm-2 in rabbits and 1.22 +/- 1.13 microliters.h-1.cmH2O-1.cm-2 in dogs. The parietal pleura could be modeled by two pore populations with radii of 83-89 and 156-222 A. The permeability coefficient averaged 0.08-0.21 x 10(-6) cm/s for albumin, 0.06-0.09 x 10(-6) cm/s for LDH, and 0.01-0.03 x 10(-6) cm/s for alpha 2-macroglobulin.

Animals↗
PubMed1994

The anti-inflammatory agent alpha-trinositol exerts its edema-preventing effects through modulation of beta 1 integrin function.

Edema formation in acute inflammation can be induced through lowering of interstitial fluid pressure (Pif) and seems to involve dynamic beta 1 integrin-mediated interactions between dermal cells and extracellular matrix fibers. The present experiments investigate the role of beta 1 integrins in the control of Pif. The anti-inflammatory drug alpha-trinositol (1,2,6-D-myo-inositol trisphosphate) stabilizes Pif in acute inflammation. Pretreatment with 5 mg IV alpha-trinositol in pentobarbital-anesthetized rats inhibited the lowering in Pif and the edema formation induced by subdermal injection of anti-beta 1 integrin IgG. This stabilization of the beta 1 integrin function in vivo was paralleled by effects of alpha-trinositol on contraction of fibroblast-populated three-dimensional collagen lattices in vitro. alpha-Trinositol was additive to the known stimulatory effect of platelet-derived growth factor-BB on the final gel size in the collagen gel contraction assay. Furthermore, alpha-trinositol counteracted the inhibitory effect of anti-beta 1 integrin Fab fragments on collagen gel contraction. Finally, subdermal injection of dibutyryl-cAMP (db-cAMP) induced increased negativity of Pif to the same extent as did anti-beta 1 integrin antibodies, and in vitro db-cAMP reduced the ability of fibroblasts to contract collagen gels. The latter effect was opposed by alpha-trinositol. The data demonstrate that alpha-trinositol modulates beta 1 integrin function and may do so via intracellular pathways in turn affecting the function and/or cell surface expression of beta 1 integrins and suggest that alpha-trinositol can serve as a tool to study integrin function. Furthermore, the data indicate that the collagen contraction assays may provide important information of the control of Pif in vivo.

Acute Disease↗