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PubMed2006

Resolution of common dietary sugars from probe sugars for test of intestinal permeability using capillary column gas chromatography.

BACKGROUND: The most widely accepted method for the evaluation of intestinal barrier integrity is the measurement of the permeation of sugar probes following an oral test dose of sugars. The most-widely used sugar probes are sucrose, lactulose, mannitol and sucralose. Measuring these sugars using a sensitive gas chromatographic (GC) method, we noticed interference on the area of the lactulose and mannitol peaks. METHODS: We tested different sugars to detect the possible makeup of these interferences and finally detected that the lactose interferes with lactulose peak and fructose interferes with mannitol peak. On further developing of our method, we were able to reasonably separate these peaks using different columns and condition for our assay. Sample preparation was rapid and simple and included adding internal standard sugars, derivitization and silylation. We used two chromatographic methods. In the first method we used Megabore column and had a run time of 34 min. This resulted in partial separation of the peaks. In the second method we used thin capillary column and was able to reasonably separate the lactose and lactulose peaks and the mannitol and fructose peaks with run time of 22 min. RESULTS: The sugar probes including mannitol, sucrose, lactulose, sucralose, fructose and lactose were detected precisely, without interference. The assay was linear between lactulose concentrations of 0.5 and 40 g/L (r(2)=1.000, P<0.0001) and mannitol concentrations of 0.01 and 40 g/L (r(2)=1.000). The sensitivity of this method remained high using new column and assay condition. The minimum detectable concentration calculated for both methods was 0.5 mg/L for lactulose and 1 mg/L for mannitol. CONCLUSION: This is the first report of interference of commonly used sugars with test of intestinal permeability. These sugars are found in most of fruits and dairy products and could easily interfere with the result of permeability tests. Our new GC assay of urine sugar probes permits the simultaneous quantitation of sucralose, sucrose, mannitol and lactulose, without interference with lactose and fructose. This assay is a rapid, simple, sensitive and reproducible method to accurately measure intestinal permeability.

Chromatography, Gas↗
PubMed1989

The radiographic differentiation of pulmonary oedema.

A radiographic scoring system has been reported to have a high diagnostic accuracy in the differentiation of pulmonary oedema of renal, cardiac and capillary origin. In the present study, a similar scoring system was used in 51 patients with radiographic appearances of pulmonary oedema due to renal failure (n = 16), cardiac failure (n = 13) and to adult respiratory distress syndrome (ARDS) (n = 22). Evidence of increased pulmonary capillary permeability to transferrin was sought in all patients using a double-isotope method to derive a protein accumulation index (PAI). Using the clinical diagnosis of each type of pulmonary oedema as the "gold standard", sensitivity, specificity and accuracy for the chest radiographic scoring system in pulmonary oedema of cardiac origin were 46, 84 and 75%, respectively. For renal patients these values were 63, 86 and 78% and for ARDS, 89, 33 and 77%. For the PAI in ARDS, sensitivity was 85%, specificity 67% and accuracy 86%. The radiographic scoring system failed to distinguish between pulmonary oedema of renal and cardiac origin and cannot be considered of diagnostic value, but it was more successful in assessment of ARDS. Radiographic appearances suggestive of capillary injury and increased capillary permeability to transferrin occurred in all groups and such findings are not specific to ARDS as currently defined.

Acute Kidney Injury↗
PubMed1989

The role of thromboxane A2 (TxA2) in allergic cutaneous reactions and the effect of (E)-3-[p-(1H-imidazol-1-ylmethyl) phenyl]-2-propenoic acid hydrochloride (OKY-046), a TxA2 synthetase inhibitor.

To study the role of thromboxane A2 (TxA2) in cutaneous allergic reactions, the effect of (E)-3-[p-(1H-Imidazol-1-ylmethyl)phenyl]-2-propenoic acid hydrochloride (OKY-046), a selective TxA2 synthetase inhibitor, on cutaneous reactions in rats and mice was studied. Simultaneously, the effect of 9,11-methanoepoxy-prostaglandin H2 (U-46619), a stable analogue of TxA2, on capillary permeability in mouse and rat skin was investigated. Passive cutaneous anaphylaxis (PCA) in mouse ear was clearly inhibited by OKY-046 but not by indomethacin. The inhibitory action of OKY-046 was not influenced by pretreatment with indomethacin. Moreover, prostaglandin I2, which accumulated as a result of the inhibition of TxA2 synthetase, did not affect the PCA. But, the dye leakages caused by histamine, serotonin and leukotriene C4 in mouse ear were clearly inhibited by OKY-046. In addition, OKY-046 inhibited rat reversed cutaneous anaphylaxis, but its inhibitory action was not affected by pretreatment with indomethacin. Contrary to the above results, rat footpad passive Arthus reaction and mouse footpad tuberculin delayed hypersensitivity reaction were not affected by OKY-046. Additionally, U-46619 did not cause an increase of capillary permeability in either mouse and rat skin. These results suggest a slight role of TxA2 in cutaneous allergic reactions in mice and rats and the efficacy of OKY-046 on Type I and II reactions regardless of the inhibition of TxA2 synthetase activity.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1991

Salivary secretion of albumin in type 1 (insulin-dependent) diabetes.

The concentration of albumin in saliva is low in healthy humans. To determine whether alterations in capillary permeability in diabetes affects the salivary glands, the concentration of albumin in parotid saliva was measured in 26 Type 1 (insulin-dependent) diabetic patients, and compared to 32 non-diabetic control subjects. The diabetic patients were subdivided into 3 groups on the basis of the urinary excretion of albumin in timed overnight collections of urine: (1) normal albumin excretion (less than 30 micrograms/min) n = 13; (2) microalbuminuria (30-300 micrograms/min) n = 7, and (3) macroalbuminuria (greater than 300 micrograms/min) n = 6. Saliva was collected for one minute following stimulation with 1 ml 10% citric acid, and the concentration of albumin was measured by a sensitive ELISA method. No significant difference in salivary albumin concentration was found between the control group and any of the diabetic groups. Thus, although urinary albumin excretion was increased, suggesting altered capillary permeability, simultaneous leakage of albumin into saliva was not observed. Measurement of salivary albumin concentration does not, therefore, provide a marker of occult microvascular disease in diabetes.

Adult↗
PubMed1997

Salivary excretion of endogenous proteins in nephrotic syndrome in children.

Size and charge selectivity of capillary permeability in the salivary glands of nephrotic children were investigated by measuring salivary excretion of endogenous plasma proteins of different size and charge. We examined 10 children with steroid-sensitive nephrotic syndrome (SSNS) in relapse and subsequent remission, 11 with steroid-resistant nephrotic syndrome, and 11 healthy children (controls). Albumin [mol. wt. 66 kilodaltons (kDa), isoelectric point (pI) 4.9] was measured by radio-immunoassay, transferrin (mol. wt. 77 kDa, pI 5.9) and immunoglobulins IgG1 (mol. wt. 150 kDa, pI 7-9) and IgG4 (mol. wt. 150 kDa, pI < 6) by enzyme-linked immunoabsorbent assay. In saliva, no significant differences were found between the four groups of children for any of the four proteins. Also, the saliva/plasma ratios of the four proteins were not different among the four groups. From these data, we conclude that in subjects with SSNS in relapse, neither size nor charge selectivity of salivary gland capillary permeability are affected.

Adolescent↗
PubMed1988

Angiotensin converting enzyme inhibition with a low dose of enalapril in normotensive diabetics with persistent proteinuria.

Angiotensin II is the main regulator of both glomerular haemodynamics and glomerular capillary permeability. An alteration in the function of intrarenal angiotensin II seems to be the cause of diabetic glomerulopathy in animals and humans. In order to investigate the renal effects of the angiotensin converting enzyme (ACE) inhibitor enalapril (5 mg once a day), 24 normotensive diabetic patients with persistent proteinuria, after a 3-month run-in period, were randomly allocated to receive the active drug (12 patients) or the corresponding placebo, for the 6 months. Effective renal plasma flow, glomerular filtration rate, renal vascular resistance and filtration fraction were measured at the end of the run-in and the treatment periods. Blood pressure, heart rate, urinary albumin excretion, plasma renin activity and aldosterone, blood glucose, serum fructosamine and body weight were checked monthly during the run-in and every 2 months during the treatment period. Enalapril decreased urinary albumin excretion in the normotensive diabetic patients without any changes in systemic blood pressure or glomerular haemodynamics. These results indicate that ACE inhibition interferes with the glomerular capillary permeability induced by angiotensin II.

Adult↗
PubMed1966

Increased permeability of the capillaries of the rat heart to plasma albumin with asphyxiation and with perfusion.

1. Studies on the rate of efflux from the isolated perfused rat heart of plasma albumin conjugated with Evans Blue showed the conjugate to have penetrated extensively the extravascular compartment of the organ during a period of 2 min. This was confirmed by direct analysis of hearts for Evans Blue after perfusion.2. Exposure of the hearts to Evans Blue-albumin conjugate for 8 min in vivo showed no significant penetration of the interstitial space.3. With the isolated preparation inclusion of promethazine in the perfusing medium significantly diminished the rate of penetration of the extravascular compartment by the conjugate as did injection of the animals with either reserpine 2 days before, or bretylium immediately before the experiment.4. Penetration of the interstitial compartment in vivo could be induced by repeated asphyxiation. This penetration could also be diminished by promethazine but was not influenced by mepyramine maleate. The increased permeability of capillaries to plasma proteins can be readily demonstrated in the whole animal by detecting the leakage from the vasculature of the plasma proteins conjugated with a dye (Menkin & Menkin, 1930; Miles & Miles, 1952). Evans Blue, which has been widely used as a vascular marker because of the stability of its conjugate with plasma albumin, is the most suitable dye for this purpose. In the present work this method has been applied to the isolated rat heart, to determine if changes in capillary permeability occur in the perfused tissue. When plasma albumin conjugated with Evans Blue was used as a vascular marker in this preparation, its rate of clearance was very much less than that of erythrocytes, and the amount contained in the heart corresponded to a space approaching that occupied by extracellular markers such as raffinose and inulin. It was concluded, therefore, that there was a failure of a considerable number of the cardiac capillaries to retain the plasma albumin, and subsequent work was directed towards the identification of the condition that gives rise to these changes and the possible involvement of a permeability factor.A preliminary account of part of this work was given to the Physiologcal Society (Sutherland & Young, 1961).

Animals↗
PubMed1993

von Willebrand factor: an endothelial marker to monitor in-vitro fertilization patients with ovarian hyperstimulation syndrome.

A retrospective study was conducted to evaluate the possible role of endothelial and extracellular factors in the pathophysiology of ovarian hyperstimulation syndrome (OHSS). Plasma changes in von Willebrand-Jürgen factor were correlated with the clinical condition of hyperstimulated patients, since the rise of capillary permeability is the central event in all subsequent morbidity. The corresponding oestradiol levels and ultrasound parameters were assessed. In-vitro fertilization patients designated as 'high responders' and with oestradiol values > 2500 pg/ml and > 8 pre-ovulatory follicles at the time of human chorionic gonadotrophin (HCG) injection were assessed. Among 62 patients, 37 fulfilled these criteria and 18 developed OHSS, indicating the low predictive ability of ultrasound and oestradiol values alone. The remaining 19 patients served as control group. von Willebrand factor-associated antigen in plasma was measured using enzyme-linked immunosorbent assay and ristocetin co-factor activity by an aggregatometric test. Basal values of the two groups of patients did not differ but there were large inter-individual variations. A slight increase occurred in the control group until the day of HCG although individual cycles showed 'no change of pattern' or a 'decreasing tendency' from the start. Some patients allocated to the non-hyperstimulated type showed a steep increase of values followed by a decline. A consistent increase in the OHSS group lasted after embryo transfer even to the late corpus luteum phase. These subtle changes of capillary permeability or damage always preceded the clinical signs, such as ascites, haemoconcentration, hypoproteinaemia and pleural effusion. Mean values differed in the two groups from the day preceding ovum retrieval.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Histamine, leukotriene C4 and interleukin-2 increase antibody uptake into a human carcinoma xenograft model.

Systemically administered radiolabelled anti-tumour antibody is ineffective in treating the majority of patients with liver metastasis from colorectal carcinoma. We have assessed whether agents which increase capillary permeability can increase tumour uptake of antibody isotope conjugate. We developed a xenograft model of colorectal carcinoma using an antibody directed against carcinoembryonic antigen (CEA). Tumours were grown subcutaneously in the hind limbs of athymic rats to derive their circulation from the femoral artery. Cannulae were placed in the common iliac artery and iliolumbar vein. Antibody was delivered systemically, regionally and regionally with histamine, leukotriene C4 and interleukin-2. Regionally administered anti-CEA antibody resulted in a significantly greater (P = 0.004) tumour to normal tissue ratio (1.66, s.d. = 0.68) compared to systematically administered antibody (1.25, s.d. = 0.73). The addition of vasoactive drugs produced an approximately 3-fold increase with an increase to a mean tumour:liver ratio of 3.24 (s.d. = 1.39) for histamine (P less than 0.001 compared to systemic delivery), 3.21 (s.d. = 1.13, P less than 0.001) for leukotriene C4 and 3.80 (s.d. = 1.53, P less than 0.001) for interleukin-2. The addition of histamine significantly (P = 0.004) increased the mean tumour to liver ratio (1.73, s.d. = 0.44) of non-specific antibody uptake compared with either systemic (1.12, s.d. = 0.24) or regional delivery (1.25, s.d. = 0.54) of non-specific antibody alone. Increasing tumour capillary permeability can produce a significant clinically useful increase in tumour uptake of antibody-isotope conjugate.

Animals↗
PubMed2000

Measurement of ceruloplasmin in the lungs of patients with acute respiratory distress syndrome: is plasma or local production the major source?

BACKGROUND: Oxidant-induced tissue damage is thought to contribute to the lung injury seen in patients with acute respiratory distress syndrome (ARDS). Ceruloplasmin (CP) is a major circulating antioxidant, increased levels of which have been measured in bronchoalveolar lavage fluid (BALF) taken from such patients. Traditionally, CP detected in these circumstances was thought to be plasma-derived, moving into the alveolar spaces as a consequence of the increased alveolar-capillary permeability that characterises ARDS. However, recent studies in murine models suggest that CP may be synthesised in the airways and even alveoli under physiological conditions. OBJECTIVES: The aims of this investigation were therefore to identify the source of any increased levels of CP detectable in BALF taken from patients with established ARDS. METHODS: Matched BALF and plasma samples taken from patients with ARDS (n = 46) and from controls without lung disease (n = 11) were analysed for CP (132 kD) and plasma specific albumin (ALB, 68 kD) and (alpha(2)-macroglobulin (alpha(2)-M, 820 kD). RESULTS: All three proteins were increased in BALF taken from patients with ARDS compared to controls (p < 0.01, ALB and CP; p < 0.001, alpha(2)-M). When protein levels were expressed as the ratios of BALF: plasma (designated Q), Q(CP) and Q(alpha2)-M increased in parallel to Q(ALB) (p < 0.001), indicating that all increases were primarily plasma-derived. Their relative coefficients of excretion (RCE: Q(CP)/Q(ALB) and Q(alpha2)-M/Q(ALB)) demonstrated that the larger molecular weight protein, alpha(2)-M, gave the best discrimination between patients with ARDS and normal controls (0.85 vs. 0.04; p < 0. 01), indicating that this was the most sensitive marker of alveolar-capillary permeability. CONCLUSIONS: Increased levels of CP in BALF from patients with ARDS are mainly attributable to plasma exudation.

Adult↗
PubMed1991

Pathogenesis of pulmonary edema during interleukin-2 therapy: correlation of chest radiographic and clinical findings in 54 patients.

The pathogenesis of pulmonary edema that occurs during interleukin-2 therapy has often been attributed to an increase in pulmonary capillary permeability. However, renal insufficiency, fluid overload, and hypotension also develop in many patients. These manifestations of systemic toxicity may contribute to the development of pulmonary edema during therapy. Understanding the cause of pulmonary edema during interleukin-2 therapy could directly affect patients' care. Therefore, we reviewed the chest radiographs and clinical course of 54 patients who received high-dose interleukin-2 therapy and lymphokine-activated killer cells for advanced carcinoma. The type, frequency, and course over time of pulmonary abnormalities were recorded and correlated with clinical measures of renal function, fluid status, and blood pressure. Focal or diffuse parenchymal lung opacities were found on radiographs in 43 (80%) of 54 patients. Findings of interstitial pulmonary edema were most common, occurring in 76% of patients. Weight gain, hypotension, and elevation of the serum creatinine level were not associated statistically with interstitial edema. Diffuse air-space disease developed in 20% of patients. Focal consolidation, which was associated with positive central venous catheter cultures (p less than .03), developed in 28% of patients. Pleural effusion occurred in 48% of patients and was associated with all types of parenchymal disease. These data suggest that the frequent development of pulmonary edema during interleukin-2 therapy is not due to renal insufficiency, fluid overload, or hypotension, but is more likely the result of an interleukin-2-related increase in pulmonary capillary permeability.

Adult↗
PubMed1981

Ara-C lung: noncardiogenic pulmonary edema complicating cytosine arabinoside therapy of leukemia.

Unexplained fatal pulmonary edema observed at autopsy in leukemic patients treated with cytosine arabinoside (Ara-C) suggested a possible role of the drug in causing increased alveolar capillary permeability. We reviewed clinical and pathologic features of the 181 patients with leukemia who were examined at autopsy at The Johns Hopkins Hospital in the past 12 years, 93 (51 percent) of whom had received intravenous Ara-C in doses of 7.5 to 30 mg/kg/day (average dose, 16 mg/kg/day). Fifty-one patients had received their last treatment within 30 days, and 42 patients between 31 and 894 days, prior to death. Among the 181 patients examined at autopsy 43 (24 percent) had massive edema, 59 (33 percent) had moderate edema, and 79 (44 percent) had either slight edema or no pulmonary edema. The 51 patients who had received Ara-C within 30 days of their death, compared to the other 130, had a highly significant increase in the frequency of pulmonary edema (p less than 0.001), which was massive in 24 and moderate in 18. In these 42 patients, causative or contributing factors that explained the edema were present in 14 (33 percent) of them, but in 28 (67 percent) there was no apparent explanation. In contrast, 60 of the 130 patients who had no or remote Ara-C therapy had massive (19 patients) or moderate (41 patients) pulmonary edema, which was explained in 55 (92 percent) and unexplained in only five (8 percent) (p less than 0.001). The unexplained pulmonary edema, a highly proteinaceous interstitial and intra-alveolar infiltrate, correlated with gastrointestinal lesions typical of Ara-C toxicity (p less than 0.001). Multivariate regression analysis showed that unexplained pulmonary edema was predicted by the recent administration of Ara-C, but by no other chemotherapeutic agent, including daunomycin, a potential cardiotoxin frequently given in conjunction with Ara-C. The study suggests that increased alveolar capillary permeability may result from the intravenous administration of cytosine arabinoside and that this complication should be considered when pulmonary edema develops in leukemic patients treated with Ara-C.

Adolescent↗
PubMed1992

Morphology and function of capillary networks in subregions of the rat tuber cinereum.

The differentiated cytology, cytochemistry, and functions within subdivisions of the tuber cinereum prompted this morphometric and physiological investigation of capillaries in the medium eminence and arcuate nucleus of albino rats. Morphometric studies established that the external zone of the median eminence had 3-5 times the number and surface area of true and sinusoidal capillaries than the internal or subependymal median eminence zones, or either of two subdivisions examined in the arcuate nucleus. Type-I true capillaries, around which Virchow-Robin spaces comprise 1% of arcuate tissue area, were situated proximally to the median eminence border. This finding is consistent with a premise that confluent pericapillary spaces enable infiltration of arcuate neurons by factors from capillary blood from the median eminence or Virchow-Robin spaces. Physiologically, the rate of penetration across the median eminence capillaries by blood-borne [14C]alpha-amino-isobutyric acid (a neutral amino acid used as a capillary permeability tracer) was 142 times greater than for capillaries in the distal arcuate nucleus within 12 s of tracer administration. A new finding was that the proximal arcuate nucleus had a permeability x surface area product of 69 microliters g-1 min-1, 34 times greater than that in more distal aspects of the tuber where blood-brain barrier properties exist. We also found that the microcirculatory transit time of a plasma space marker, [14C]sucrose, was considerably longer (1.2 s) in the median eminence and proximal arcuate nucleus than in the distal arcuate or ventromedial nucleus (0.4 s). By virtue of its high capillary permeability and extensive blood-tissue surface area, including the wide Virchow-Robin spaces, the median eminence external zone could be a gateway for flooding other tuberal compartments with blood-borne factors. This effect may be compounded by capillary bed specializations in the proximal arcuate nucleus where Type-I true capillaries, Type-III sinusoids, and pericapillary spaces are confluent with those in the median eminence. The results indicate that the proximal arcuate parenchyma could be exposed to circulating neuroactive substances on a moment-to-moment basis.

Animals↗
PubMed1983

Microvascular exchange of albumin.

The transcapillary exchange of albumin was examined in seven rabbits using plasma disappearance curves and black box kinetic analysis. From the experimental data and the Renkin and Kedem-Katchalsky equations it was found that the average whole body diffusional capillary permeability coefficient for albumin was 24 X 10(-8) cm/sec as the total whole body capillary permeability-surface area product was 0.0739 ml/100 g X min (surface area estimate 50 cm2/g). The convective components of the net albumin tracer flux was found to be 15%, and the pure permeation ratio of influx to outflux (R = 0.61) of systemic albumin was reduced to 0.57. The solvent drag component of either unidirectional flux relative to the permeative component was 0.037. The Casley-Smith hypothesis of solvent drag convection up a gradient across the capillary membrane could not be verified as possible. It is emphasized that the so-called transcapillary escape rate is an arbitrary rate constant which cannot be attributed to reflect any physiological process, especially not the transcapillary exchange of albumin.

Animals↗
PubMed1991

In situ pulmonary vascular perfusion for improved recovery of pulmonary intravascular macrophages.

The microcirculation contains mononuclear phagocytes, with features characteristic of macrophages, adhered to luminal capillary surfaces by intercellular adhesion plaques. These pulmonary intravascular macrophages may play an important role in regulating lung vascular tone and capillary permeability, and may modulate capillary endothelial cell growth and replication by the secretion of soluble mediators (i.e., arachidonate metabolites, cytokines). This study describes a technique which utilizes in situ lung perfusion to remove intravascular macrophages in large numbers from the microcirculation of porcine lung (n = 26). This technique yielded 3.8 +/- 0.5 x 10(8) (mean +/- SEM) mononuclear cells which were highly phagocytic toward particulate carbon (phagocytic index, 80 +/- 6%). Harvested mononuclear phagocytes reestablished intercellular adhesion plaques when placed on small vessel porcine pulmonary artery endothelial cell monolayers and exhibited histochemical characteristics typical of monocyte/macrophage lineage cells. Mononuclear cells obtained from lung microcirculation displayed size heterogeneity varying from 10.4 to 16.5 microns in diameter. Both large and small cell populations phagocytosed particulate carbon. Morphometric studies performed on collagenase-treated lung demonstrated that in situ perfusion removed significant numbers of intravascular macrophages in lung capillaries. The technique described permits the rapid removal of anchored mononuclear phagocytes from lung capillaries with minimal postmortem delay.

Animals↗
PubMed1997

High altitude pulmonary edema: hemodynamic aspects.

Over 30 years ago hemodynamic studies on patients with high altitude pulmonary edema (HAPE) excluded the prior contention that the basic cause was left ventricular failure and correctly implicated the pulmonary circulation as the culprit. Physiological studies during the acute stage have revealed a normal pulmonary artery wedge pressure, marked elevation of pulmonary artery pressure, severe arterial unsaturation, and usually a low cardiac output. Pulmonary arteriolar (pre-capillary) resistance was elevated. A working hypothesis of the etiology of HAPE suggests that hypoxic pulmonary vasoconstriction is extensive but not uniform. The result is overperfusion of the remaining patent vessels with transmission of the high pulmonary artery pressure to capillaries. Dilatation of the capillaries and high flow results in capillary injury with leakage of protein and red cells into the alveoli. While hypoxic vasoconstriction appears to be the major cause of patchy vascular obstruction the occurrence of thrombi in the pulmonary vessels may also play a role in more severe and advanced cases. The above concept of the mechanism of HAPE has been further supported by animal studies showing pulmonary edema occurring when increased pressure and flow is produced in a portion of the pulmonary vascular bed. Clinical studies which have supported this concept include the susceptibility to HAPE of patients with an absent pulmonary artery, pulmonary edema occurring in pulmonary embolism, following removal of pulmonary arterial thrombi and following balloon dilatation of stenoses of branches of the pulmonary artery. In addition to those hemodynamic factors an increase in capillary permeability due to cell derived products resulting from capillary wall injury is an important aspect of edema formation.

Altitude Sickness↗
PubMedDate not supplied

Biological mediators of acute inflammation.

Inflammation may be defined as the normal response of living tissue to injury or infection. It is important to emphasize two components of this definition. First, that inflammation is a normal response and, as such, is expected to occur when tissue is damaged. Indeed, if injured tissue did not exhibit signs of inflammation this would be considered abnormal. Secondly, inflammation occurs in living tissue, hence the need for an adequate blood supply to the tissues in order for an inflammatory response to be exhibited. The inflammatory response may be triggered by mechanical injury, chemical toxins, invasion by microorganisms, and hypersensitivity reactions. Three major events occur during the inflammatory response: the blood supply to the affected area is increased substantially, capillary permeability is increased, and leucocytes migrate from the capillary vessels into the surrounding interstitial spaces to the site of inflammation or injury. The inflammatory response represents a complex biological and biochemical process involving cells of the immune system and a plethora of biological mediators. Cell-to-cell communication molecules known collectively as cytokines play an extremely important role in mediating the process of inflammation. An extensive exposition of this complex phenomenon is beyond the scope of this article. Rather, the author provides a review of inflammation, an overview of the role of certain biological mediators in inflammation, and a discussion of the implications of certain biological response modifiers in clinical practice.

Acute Disease↗