Capillary Leak Syndrome
Serum Albumin, Radio-Iodinated
Cell Membrane Permeability
Ovarian Hyperstimulation Syndrome
Potent mast cell degranulation and vascular permeability triggered by urocortin through activation of corticotropin-releasing hormone receptors. (1/3442)Urocortin (Ucn) is related to corticotropin-releasing hormone (CRH), and both are released in the brain under stress where they stimulate CRH 1 and 2 receptors (CRHR). Outside the brain, they may have proinflammatory actions through activation of mast cells, which are located perivascularly close to nerve endings and degranulate in response to acute psychological stress. Here, we report that a concentration of intradermal Ucn as low as 10 nM induced dose-dependent rat skin mast cell degranulation and increased vascular permeability. This effect appeared to be equipotent to that of calcitonin gene-related peptide and neurotensin. Ucn-induced skin vasodilation was inhibited by pretreatment with the mast cell stabilizer disodium cromoglycate (cromolyn) and was absent in the mast cell-deficient W/Wv mice. The selective nonpeptide CRH receptor 1 antagonist, antalarmin and the nonselective peptide antagonist astressin both reduced vascular permeability triggered by Ucn but not that by Substance P or histamine. In contrast, the peptide antagonist alpha-helical CRH-(9-41) reduced the effect of all three. The vasodilatory effect of Ucn was largely inhibited by pretreatment with H1 receptor antagonists, suggesting that histamine is the major mediator involved in vitro. Neuropeptide depletion of sensory neurons, treatment with the ganglionic blocker hexamethonium, or in situ skin infiltration with the local anesthetic lidocaine did not affect Ucn-induced vascular permeability, indicating that its in situ effect was not mediated through the peripheral nervous system. These results indicate that Ucn is one of the most potent triggers of rat mast cell degranulation and skin vascular permeability. This effect of Ucn may explain stress-induced disorders, such as atopic dermatitis or psoriasis, and may lead to new forms of treatment. (+info)
Reduction of sodium deoxycholic acid-induced scratching behaviour by bradykinin B2 receptor antagonists. (2/3442)1. Subcutaneous injection of sodium deoxycholic acid into the anterior of the back of male ddY mice elicited dose-dependent scratching of the injected site with the forepaws and hindpaws. 2. Up to 100 microg of sodium deoxycholic acid induced no significant increase in vascular permeability at the injection site as assessed by a dye leakage method. 3. Bradykinin (BK) B2 receptor antagonists, FR173657 and Hoe140, significantly decreased the frequency of scratching induced by sodium deoxycholic acid. 4. Treatment with aprotinin to inhibit tissue kallikrein reduced the scratching behaviour induced by sodium deoxycholic acid, whereas treatment with soybean trypsin inhibitor to inhibit plasma kallikrein did not. 5. Although injection of kininase II inhibitor, lisinopril together with sodium deoxycholic acid did not alter the scratching behaviour, phosphoramidon, a neutral endopeptidase inhibitor, significantly increased the frequency of scratching. 6. Homogenates of the skin excised from the backs of mice were subjected to gel-filtration column chromatography followed by an assay of kinin release by trypsin from each fraction separated. Less kinin release from the fractions containing kininogen of low molecular weight was observed in the skin injected with sodium deoxycholic acid than in normal skin. 7. The frequency of scratching after the injection of sodium deoxycholic acid in plasma kininogen-deficient Brown Norway Katholiek rats was significantly lower than that in normal rats of the same strain, Brown Norway Kitasato rats. 8. These results indicate that BK released from low-molecular-weight kininogen by tissue kallikrein, but not from high-molecular-weight kininogen by plasma kallikrein, may be involved in the scratching behaviour induced by the injection of sodium deoxycholic acid in the rodent. (+info)
Role for nitric oxide in the hyperpermeability and hemodynamic changes induced by intravenous VEGF. (3/3442)PURPOSE: To explore the effects of brief intravenous (IV) infusion of vascular endothelial growth factor (VEGF) on vascular albumin permeability, blood flow, and vascular conductance (blood flow normalized to arterial blood pressure) in ocular tissues and brain and to assess the role of nitric oxide in mediating these changes. METHODS: A quantitative, double-tracer, radiolabeled albumin permeation method was combined with radiolabeled microspheres for assessment of changes in vascular permeability and blood flow, respectively, induced in ocular tissues by IV infusion of recombinant human VEGF165 for 20 minutes (80-450 picomoles/kg body weight). An inhibitor of nitric oxide synthase (NOS), NG-monomethyl-L-arginine (L-NMMA; 50 micromoles/kg body weight infused simultaneously with VEGF), was used to explore the role of nitric oxide in mediating the vascular changes induced by VEGF. RESULTS: Infusion of VEGF165 in thiopental-anesthetized rats dose-dependently increased 125I albumin permeation in the retina, anterior uvea, and choroid/sclera and in brain, aorta, lung, kidney, small intestine, and peripheral nerve. Mean arterial blood pressure, cardiac output, and stroke volume were decreased only at the highest dose of VEGF, whereas heart rate remained unchanged. Blood flow was increased in the anterior uvea, and vascular conductance was increased in retina, anterior uvea, choroid/sclera, and brain at the highest dose of VEGF. The NOS inhibitor, L-NMMA, blocked VEGF-induced vascular hyperpermeability in all ocular and nonocular tissues, prevented the increase in vascular conductance in all ocular tissues, and blocked the decrease in mean arterial blood pressure, cardiac output, and stroke volume. Infusion of L-NMMA alone decreased vascular conductance in choroid/sclera and kidney, slightly increased mean arterial blood pressure, and in general, did not affect 125I-albumin permeation. (L-NMMA slightly decreased albumin permeation in the retina and increased it in the brain.) CONCLUSIONS: Intravenous infusion of VEGF can acutely impair endothelial cell barrier functional integrity and relax resistance arterioles in ocular tissues and brain through a mechanism involving activation of NOS. (+info)
Strain-dependent induction of allergic sensitization caused by peanut allergen DNA immunization in mice. (4/3442)To investigate the potential application of allergen gene immunization in the modulation of food allergy, C3H/HeSn (C3H) mice received i.m. injections of pAra h2 plasmid DNA encoding one of the major peanut allergens, Ara h2. Three weeks following pDNA immunization, serum Ara h2-specific IgG2a, IgG1, but not IgE, were increased significantly in a dose-dependent manner. IgG1 was 30-fold higher in multiply compared with singly immunized mice. Ara h2 or peanut protein injection of immunized mice induced anaphylactic reactions, which were more severe in multiply immunized mice. Heat-inactivated immune serum induced passive cutaneous anaphylaxis, suggesting that anaphylaxis in C3H mice was mediated by IgG1. IgG1 responses were also induced by intradermal injection of pAra h2, and by i.m. injection of pOMC, the plasmid DNA encoding the major egg allergen protein, ovomucoid. To elucidate whether the pDNA immunization-induced anaphylaxis was a strain-dependent phenomenon, AKR/J and BALB/c mice also received multiple i.m. pAra h2 immunizations. Injection of peanut protein into these strains at weeks 3 or 5 following immunization did not induce reactions. Although IgG2a was increased significantly from week 2 in AKR/J mice and from week 4 in BALB/c mice and remained elevated for at least 6 wk, no IgG1 or IgE was detected. These results indicate that the type of immune responses to pDNA immunization in mice is strain dependent. Consequently, models for studying human allergen gene immunization require careful selection of suitable strains. In addition, this suggests that similar interindividual variation is likely in humans. (+info)
Antipsoriatic, anti-inflammatory, and analgesic effects of an extract of red propolis. (5/3442)AIM: To study the antipsoriatic, anti-inflammatory, and analgesic effects of ethanolic extract of red propolis. METHODS AND RESULTS: This extract induced the formation of granular layer in the mouse tail test used as a model of psoriasis. Propolis 50 mg.kg-1 i.g. showed anti-inflammatory activity in the cotton-pellet granuloma assay in rats, in croton oil-induced edema in mice at a dose of 25% (2.5 microL), and in the peritoneal capillary permeability test in mice at a dose of 10 mg.kg-1. The extract (25 mg.kg-1 i.g.) showed analgesic effect in the model of acetic acid-induced writhings, whereas 40 mg.kg-1 was effective in the hot plate test in mice. CONCLUSION: Anti-inflammatory, analgesic, and antipsoriatric properties of Cuban red propolis were evident. (+info)
Endogenous nitric oxide in the maintenance of rat microvascular integrity against widespread plasma leakage following abdominal laparotomy. (6/3442)1. The role of nitric oxide (NO) in the maintenance of microvascular integrity during minor surgical manipulation has been evaluated in the rat. 2. The NO synthase inhibitors, NG-nitro-L-arginine methyl ester (L-NAME, 5 mg kg(-1), s.c.) and N(G)-monomethyl-L-arginine (L-NMMA, 50 mg kg(-1), s.c.) had no effect on microvascular leakage of radiolabelled albumin over 1 h in the stomach, duodenum, jejunum, colon, lung and kidney in the un-operated conscious or pentobarbitone-anaesthetized rat. 3. In contrast, in anaesthetized rats with a midline abdominal laparotomy (5 cm), L-NAME (1-5 mg kg(-1), s.c.) or L-NMMA (12.5-50 mg kg(-1), s.c.) dose-dependently increased gastrointestinal, renal and pulmonary vascular leakage, effects reversed by L-arginine pretreatment (300 mg kg(-1), s.c., 15 min). These actions were not observed in anaesthetized rats that had only received a midline abdominal skin incision (5 cm). 4. Pretreatment with a rabbit anti-rat neutrophil serum (0.4 ml kg(-1), i.p.), 4 h before laparotomy, abolished the plasma leakage induced by L-NAME in all the organs investigated. 5. These results indicate that the following abdominal laparotomy, inhibition of constitutive NO synthase provokes vascular leakage in the general microcirculation, by a process that may involve neutrophils. Such effects could thus confound studies on the microvascular actions of NO synthase inhibitors using acute surgically prepared in vivo models. The findings thus suggest that constitutively-formed NO has a crucial role in the maintenance of acute microvascular integrity following abdominal surgical intervention. (+info)
Neurogenic plasma leakage in mouse airways. (7/3442)1. This study sought to determine whether neurogenic inflammation occurs in the airways by examining the effects of capsaicin or substance P on microvascular plasma leakage in the trachea and lungs of male pathogen-free C57BL/6 mice. 2. Single bolus intravenous injections of capsaicin (0.5 and 1 micromol kg(-1), i.v.) or substance P (1, 10 and 37 nmol kg(-10, i.v.) failed to induce significant leakage in the trachea, assessed as extravasation of Evans blue dye, but did induce leakage in the urinary bladder and skin. 3. Pretreatment with captopril (2.5 mg kg(-1), i.v.), a selective inhibitor of angiotensin converting enzyme (ACE), either alone or in combination with phosphoramidon (2.5 mg kg(-1), i.v.), a selective inhibitor of neutral endopeptidase (NEP), increased baseline leakage of Evans blue in the absence of any exogenous inflammatory mediator. The increase was reversed by the bradykinin B2 receptor antagonist Hoe 140 (0.1 mg kg(-1), i.v.). 4. After pretreatment with phosphoramidon and captopril, capsaicin increased the Evans blue leakage above the baseline in the trachea, but not in the lung. This increase was reversed by the tachykinin (NK1) receptor antagonist SR 140333 (0.7 mg kg(-1), i.v.), but not by the NK2 receptor antagonist SR 48968 (1 mg kg(-1), i.v.). 5. Experiments using Monastral blue pigment as a tracer localized the leakage to postcapillary venules in the trachea and intrapulmonary bronchi, although the labelled vessels were less numerous in mice than in comparably treated rats. Blood vessels of the pulmonary circulation were not labelled. 6. We conclude that neurogenic inflammation can occur in airways of pathogen-free mice, but only after the inhibition of enzymes that normally degrade inflammatory peptides. Neurogenic inflammation does not involve the pulmonary microvasculature. (+info)
Enhancement of fluid filtration across tumor vessels: implication for delivery of macromolecules. (8/3442)Cancer therapies using genes and other macromolecules might realize their full clinical potential if they could be delivered to tumor tissue in optimal quantities. Unfortunately, the compromised circulation within tumors poses a formidable resistance to adequate and uniform penetration of these agents. Previously, we have proposed elevated interstitial fluid pressure (IFP) as a major physiological barrier to delivery of macromolecules. Here we postulate that modulation of tumor microvascular pressure (MVP) and associated changes in IFP would enhance macromolecular delivery into a solid tumor. To test our hypothesis, we altered tumor MVP by either periodic injection or continuous infusion of angiotensin II (AII) and measured the resulting changes in IFP and uptake of macromolecules. We used the nicotinyl hydrazine derivative of human polyclonal IgG (HYNIC-IgG) as a nonspecific macromolecule and CC49 antibody as a specific macromolecule. We found that both chronic and periodic modulation of tumor MVP enhances transvascular fluid filtration, leading to a 40% increase in total uptake of the specific antibody within 4 hr of its administration. Conversely, neither continuous nor periodic infusion of AII induced any increase in uptake of nonspecific antibodies. Strategies to improve delivery of macromolecules and limitations of this approach are identified. (+info)
Explain how Capillary Leak Syndrome (CLS) can cause severe fluid and electrolyte imbalances in the body, leading to potentially life-threatening complications.
Capillary Leak Syndrome (CLS) is a rare but potentially devastating condition that affects the blood vessels and can cause severe fluid and electrolyte imbalances in the body. These imbalances can lead to a range of symptoms, from mild discomfort to life-threatening complications. In this essay, we will explore how CLS can cause fluid and electrolyte imbalances and discuss the potential risks associated with this condition.
Fluid and Electrolyte Imbalances in CLS:
The hallmark of CLS is the leakage of fluid from the blood vessels into the surrounding tissues, leading to an excessive accumulation of fluid in the interstitial space. This can cause a range of symptoms, including swelling (edema), shortness of breath, and abdominal pain. However, the most severe complication of CLS is the development of electrolyte imbalances, which can lead to life-threatening complications if left untreated.
Electrolytes are essential minerals that regulate a range of bodily functions, including fluid balance, nerve function, and muscle contraction. When the blood vessels leak fluid into the interstitial space, they also lose electrolytes, leading to an imbalance in the body's electrolyte levels. This can cause a range of symptoms, including muscle weakness, heart arrhythmias, and seizures. In severe cases, electrolyte imbalances can lead to respiratory failure, cardiac arrest, and even death.
Potential Risks Associated with CLS:
The potential risks associated with CLS are numerous and can be severe. The most common complications of CLS include:
1. Respiratory failure: The excessive accumulation of fluid in the lungs can lead to respiratory failure, which can be life-threatening if left untreated.
2. Cardiac arrhythmias: Electrolyte imbalances can cause abnormal heart rhythms, which can lead to cardiac arrest and even death.
3. Seizures: The loss of electrolytes can cause seizures, which can be difficult to control and can lead to serious complications.
4. Kidney damage: Prolonged fluid accumulation in the body can put a strain on the kidneys, leading to permanent damage and even failure.
5. Infection: The presence of fluid in the body can provide a breeding ground for bacteria, leading to serious infections such as sepsis and meningitis.
6. Compartment syndrome: The accumulation of fluid in the muscles can cause compartment syndrome, a condition that can lead to permanent nerve and muscle damage if left untreated.
7. Gangrene: In severe cases, the lack of blood flow to the tissues can lead to gangrene, which is the death of body tissue due to lack of blood supply.
8. Amputations: In severe cases, the loss of blood flow and oxygen to the tissues can lead to the need for amputation of affected limbs.
It is important to note that these risks are not limited to CLS, but can also be associated with other conditions that cause fluid accumulation in the body. It is essential to seek medical attention immediately if any of these symptoms occur, as prompt treatment can help mitigate these risks and improve outcomes.
The symptoms of dermatitis, exfoliative include:
* Intense redness and scaling or blistering of the skin
* Itching, which can be severe
* Burning sensation on the skin
* Dry, rough skin that may flake off
* Small, raised bumps or hives on the skin
* Crusting or oozing of the skin
The diagnosis of dermatitis, exfoliative is based on the appearance of the skin and the patient's medical history. A skin biopsy may be performed to confirm the diagnosis and rule out other conditions. Treatment typically involves topical medications, such as corticosteroids or immunomodulators, and may also include oral medications or phototherapy.
In addition to these symptoms and treatments, it is important to note that dermatitis, exfoliative can be a chronic condition and may recur over time. It can also lead to complications such as skin infections or scarring. Therefore, it is important for individuals with this condition to work closely with their healthcare provider to manage their symptoms and prevent complications.
Symptoms of pulmonary edema may include:
* Shortness of breath (dyspnea)
* Coughing up frothy sputum
* Chest pain or tightness
* Confusion or disorientation
Pulmonary edema can be diagnosed through physical examination, chest x-rays, electrocardiogram (ECG), and blood tests. Treatment options include oxygen therapy, diuretics, and medications to manage underlying conditions such as heart failure or sepsis. In severe cases, hospitalization may be necessary to provide mechanical ventilation.
Prevention measures for pulmonary edema include managing underlying medical conditions, avoiding exposure to pollutants and allergens, and seeking prompt medical attention if symptoms persist or worsen over time.
In summary, pulmonary edema is a serious condition that can impair lung function and lead to shortness of breath, chest pain, and other respiratory symptoms. Prompt diagnosis and treatment are essential to prevent complications and improve outcomes for patients with this condition.
There are several types of edema, including:
1. Pitting edema: This type of edema occurs when the fluid accumulates in the tissues and leaves a pit or depression when it is pressed. It is commonly seen in the skin of the lower legs and feet.
2. Non-pitting edema: This type of edema does not leave a pit or depression when pressed. It is often seen in the face, hands, and arms.
3. Cytedema: This type of edema is caused by an accumulation of fluid in the tissues of the limbs, particularly in the hands and feet.
4. Edema nervorum: This type of edema affects the nerves and can cause pain, numbness, and tingling in the affected area.
5. Lymphedema: This is a condition where the lymphatic system is unable to properly drain fluid from the body, leading to swelling in the arms or legs.
Edema can be diagnosed through physical examination, medical history, and diagnostic tests such as imaging studies and blood tests. Treatment options for edema depend on the underlying cause, but may include medications, lifestyle changes, and compression garments. In some cases, surgery or other interventions may be necessary to remove excess fluid or tissue.
OHSS typically occurs when too many eggs are stimulated to mature during ovulation, leading to an imbalance in hormone levels. The syndrome is more common in women who undergo IVF with high-dose fertility medications, multiple embryo transfer, or those with polycystic ovary syndrome (PCOS).
Symptoms of OHSS may include:
1. Enlarged ovaries that are painful to the touch
2. Abdominal bloating and discomfort
3. Pelvic pain
4. Nausea and vomiting
5. Diarrhea or constipation
6. Abnormal vaginal bleeding
7. Elevated hormone levels (estradiol and/or LH)
OHSS can be diagnosed through ultrasound and blood tests. Treatment options for OHSS include:
1. Cancellation of further fertility treatment until symptoms resolve
2. Medications to reduce hormone levels and inflammation
3. Ultrasound-guided aspiration of fluid from the ovaries
4. Hospitalization for monitoring and supportive care
Prevention is key, and fertility specialists take several measures to minimize the risk of OHSS, such as:
1. Monitoring hormone levels and ultrasound assessment of ovarian response during treatment
2. Adjusting medication dosages based on individual patient needs
3. Limited embryo transfer to reduce the risk of multiple pregnancies
4. Avoiding the use of high-dose stimulation protocols in women with PCOS or other risk factors
Early detection and proper management are crucial to prevent complications and ensure a successful outcome for fertility treatment. If you suspect you may have OHSS, it is essential to consult a fertility specialist immediately.
Note: This definition is intended for informational purposes only and should not be used to diagnose or treat a medical condition. If you suspect that you or your child may have a hemangioma, it is important to consult with a qualified healthcare professional for proper evaluation and treatment.
George Emil Palade
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- To evaluate the role and the underlying mechanism of SchA in increase of pulmonary vascular permeability induced by sepsis . (bvsalud.org)
- The effect of SchA on pulmonary vascular permeability was examined in rat acute lung injury model. (bvsalud.org)
- The effect of SchA on skin vascular permeability of mice was investigated through Miles assay. (bvsalud.org)
- peritoneal fluid accumulation is a common finding in many children with abdominal disorders and its generation secondary to increased vascular permeability. (bvsalud.org)
- The purpose of the present study as to evaluate the effect of changes in intravascular pressure and the inflammatory mediator bradykinin on rat mesenteric arterial and venous vascular permeability. (bvsalud.org)
- Vascular permeability to dextran was determined at 100, 200 and 300 % of physiological pressures. (bvsalud.org)
- vascular permeability was present at all measurements for both vessels and its magnitude directly proportional to the intravascular pressure. (bvsalud.org)
- 1999 ) Glomerular permeability I. Ferritin transfer across the normal glomerular capillary wall. (academictree.org)
- Specifically, these studies have implicated transient renal ischemia, direct renal tubular toxicity and changes in glomerular capillary permeability as possible mediators of RCIN, and these pathophysiologic mechanisms are not mutually exclusive. (elsevier.com)
- Schisandrin A ameliorates increased pulmonary capillary endothelial permeability accompanied with sepsis through inhibition of RhoA/ROCK1/MLC pathways. (bvsalud.org)
- Dexamethasone decreases airway inflammation by inhibiting migration of phagocytes and reversing capillary permeability, thereby reducing the edema that occurs in croup. (medscape.com)
- Edema results from increased movement of fluid from the intravascular to the interstitial space or decreased movement of water from the interstitium into the capillaries or lymphatic vessels. (msdmanuals.com)
- Less often, edema results from decreased movement of fluid out of the interstitial space into the capillaries due to lack of adequate plasma oncotic pressure as in nephrotic syndrome, protein-losing enteropathy, liver failure, or starvation. (msdmanuals.com)
- It is predicted, that two-phase transport properties such as the evolution of effective permeability as well as capillary pressures during drainage depend both on transport directions, which should be considered for Opalinus Clay when assessing its suitability as host rock for nuclear waste. (ejp-eurad.eu)
- A central nervous system event produces a dramatic change in Starling forces, which govern the movement of fluid between capillaries and the interstitium. (medscape.com)
- The administration of SchA alleviated rat pulmonary endothelial dysfunction, relieved increased permeability in the mouse skin and HUVECs induced by lipopolysaccharide (LPS). (bvsalud.org)
- In summary, our results indicate that SchA ameliorates the increase of pulmonary endothelial permeability induced by sepsis through inhibition of RhoA/ROCK1/MLC pathway, providing a potentially effective therapeutic strategy for sepsis . (bvsalud.org)
- Systemic capillary leak syndrome (SCLS) is an ex- of Zika virus in Brazil and the Americas. (cdc.gov)
- Causes of rupture of the capillaries foremost to IVH shift and subsume fluctuations in systemic and cerebral blood go, increases in cerebral blood purl from hypertension, intravenous infusion, spasm activity, increases in cerebral venous pressurize due to vaginal delivery, hypoxia, and respiratory distress. (daubnet.com)
- Increased capilliary permeability occurs in infections or as the result of toxin or inflammatory damage to the capillary walls. (msdmanuals.com)
- Dr. Jacobs, in reply, suggested that Gene investigate the permeability of capillary walls using synthetic dyes. (nationalacademies.org)
- First, August Krogh had just published his Nobel prize-winning book, Anatomy and Physiology of the Capillaries , in which he emphasized the quantitative histology of the capillary network and pointed out how little was known about the permeability of capillary walls. (nationalacademies.org)
- The vaporization temperatures were measured experimentally in each rock type and compared with boiling points measured at bulk conditions to investigate the deviation between the phase-change temperatures in capillary media and bulk values. (nature.com)
- Previous studies have suggested that immune responses contribute to an increase in capillary permeability. (who.int)
- Histamine binds to the H1 receptor in target cells to contract gut and bronchus smooth muscle and to increase venular permeability and rheum ( 6 ). (spandidos-publications.com)
- Since, studies have confirmed that blueberries increase capillary resistance and thus decrease redness. (alchimie-forever.com)
- Prednisone may decrease inflammation by reversing increased capillary permeability and suppressing the activity of polymorphonuclear leukocytes (PMNs). (medscape.com)
- Histamine increases the permeability of capillaries to white blood cells and various proteins to allow them to engage pathogens in the infected tissue ( 6 ). (spandidos-publications.com)
- Prednisolone decreases inflammation by suppressing migration of PMNs and reducing capillary permeability. (medscape.com)
- Swedana Karma hastens this process by increasing the permeability of capillary and bringing the morbidities into an extracellular fluid by dilating and clearing the channels of the body. (who.int)
- year medical student-sent a long manuscript entitled "The Capillary Pressure in Frog Mesentery Determined by Microinjection Methods" to the editors of the American Journal of Physiology . (nationalacademies.org)
- Computer simulations were used to predict capillary pressure curves during drainage, which also agree with laboratory data. (ejp-eurad.eu)
- The dermal clearance model combined with existing models for stratum corneum permeability and appropriate measures of protein binding were used to analyze in vivo concentration data from the literature and compare it to predictions made by the current mathematical model. (cdc.gov)
- Blueberries play a role in the management of flushing symptoms: they tighten and protect fine capillaries thanks to anthocyanins ,  and are thus ideal in skin care products targeting redness-prone skin. (alchimie-forever.com)
- When combined with existing models for stratum corneum permeability and appropriate measures of tissue binding, the developed model has the potential to significantly improve tissue concentration estimates for large or highly protein bound permeants following dermal exposure. (cdc.gov)
- Previous studies have suggested that immune responses contribute to an increase in capillary permeability. (who.int)