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PubMed1999

Transperitoneal transport in diabetic and non-diabetic patients on peritoneal dialysis.

To investigate differences in the transport characteristics of the peritoneal membrane between diabetic and non-diabetic patients on chronic peritoneal dialysis, a study was conducted in 21 non-diabetic and 18 diabetic patients. Transperitoneal transport of small solutes was evaluated in terms of the mass transfer area coefficients (urea, creatinine and glucose), ultra-filtration sieving coefficients (urea and creatinine) and by peritoneal equilibration test results. The capacity of the peritoneal membrane to transport macromolecules was evaluated by albumin mass transfer rates and clearances of albumin. Transperitoneal water transport was evaluated by the ultra-filtration properties and the lymphatic flow rates. Finally, the whole-body capillary permeability was estimated by measuring the unidirectional flux of albumin across the capillary wall, i.e. the transcapillary escape rate of 125I-labelled human albumin. Despite a significantly increased transcapillary escape rate of albumin in the diabetic patients, no differences in peritoneal membrane characteristics could be demonstrated between diabetic and non-diabetic patients on peritoneal dialysis.

Adult↗
PubMed1994

Vascular permeability factor in brain metastases: correlation with vasogenic brain edema and tumor angiogenesis.

Metastatic brain tumors are almost always associated with vasogenic brain edema, which in turn plays a pivotal role in the evolution of neurological morbidity associated with these lesions. Attention has recently focused on a group of proteinaceous vascular permeability factors (VPF's) that are capable of inducing angiogenesis and promoting increased capillary permeability. To test the hypothesis that metastatic brain tumors expressing VPF's are associated with peritumoral cerebral edema, a rabbit polyclonal immunoglobulin (Ig) G anti-VPF was used to immunostain pathological specimens of metastatic cerebral tumors obtained from 22 patients who underwent surgery at Yale-New Haven Hospital. Magnetic resonance (MR) imaging was used to correlate VPF staining in tumor tissue with the occurrence of peritumoral brain edema. A histological study of the microvasculature was then conducted by immunostaining the specimens for endothelial cell factor VIII surface antigen, using two gliosis specimens as controls. Results revealed 21 of 22 tumors stained positively for VPF's; the negative-VPF tumor was a melanoma that exhibited no peritumoral edema. Twenty of 22 tumors had MR imaging-evident vasogenic edema. The presence and intensity of VPF immunostaining of microvascular features were noted and compared. Factor VIII staining demonstrated tumor vascularity to be most abundant in VPF-rich regions of tumor. The authors therefore report a high correlation between the presence of VPF's and the occurrence of peritumoral brain edema associated with cerebral metastases.

Brain Edema↗
PubMed1996

Drug-induced alteration of endothelial permeability in the rat aorta. Potential consequences on the vessel wall.

UNLABELLED: We recently reported that some diuretics affect capillary permeability in the normotensive rat. In the present study, we explore the effect of selected antihypertensive drugs administered orally during 10 days, on Evans blue (EB) extravasation within the wall of the thoracic (TA) and abdominal aorta (AA) obtained from spontaneously hypertensive rats (SHR). Description of the EB method has been previously reported. Daily doses (mg/kg) of captopril (CAP: 3.0), perindopril (PER: 0.3), nifedipine (NIF: 1.0), clentiazem (CLE: 0.1), hydralazine (HYD: 0.5), furosemide (FUR: 0.5), cicletanine (CIC: 2.0), hydrochlorothiazide (HCZ: 0.5), and indapamide (IND: 0.04) resulted in comparable blood pressure reduction. Percent changes in EB tissue concentration (measured in ug/g dry tissue) was increased by 24% in both the TA and AA in the untreated SHR. CAP reduced by half EB leakage in the TA, while PER decreased EB extravasation 16% below baseline values. Both angiotensin converting enzyme inhibitors failed to normalize EB leakage in the AA. The calcium channel blockers also normalized EB extravasation in the two segments of the aorta, except that CLE was without effect in the AA. HYD normalized EB leakage in the TA, but not in the AA. All diuretics tested reduced EB extravasation by 48 to 58% below baseline values in the TA, whereas CIC only normalized EB leakage. None of the diuretics affected EB extravasation in the AA of the SHR. IN CONCLUSION: 1-the two segments of the aorta were similarly affected in the SHR; 2-despite comparable effect on blood pressure, treatment of the SHR was associated with different responses in the TA and AA; 3-within a given class of drugs, different effects are observed on EB.

Animals↗
PubMed2002

Pathogenesis of high-altitude pulmonary edema: inflammation is not an etiologic factor.

CONTEXT: The pathogenesis of high-altitude pulmonary edema (HAPE) is considered an altered permeability of the alveolar-capillary barrier secondary to intense pulmonary vasoconstriction and high capillary pressure, but previous bronchoalveolar lavage (BAL) findings in well-established HAPE are also consistent with inflammatory etiologic characteristics. OBJECTIVES: To determine whether inflammation is a primary event in HAPE and to define the temporal sequence of events in HAPE. DESIGN, SETTING, AND PARTICIPANTS: Case study from July through August 1999 of 10 subjects with susceptibility to HAPE and 6 subjects resistant to HAPE, all of whom are nonprofessional alpinists with previous mountaineering experience above 3000 m. MAIN OUTCOME MEASURES: Pulmonary artery pressure measurements and BAL findings at low altitude (490 m) and shortly before or at the onset of HAPE at an altitude of 4559 m. RESULTS: Subjects who were HAPE susceptible had higher mean (SD) pulmonary artery systolic blood pressures at 4559 m compared with HAPE-resistant subjects (66 vs 37 mm Hg; P =.004). Despite development of HAPE in the majority of HAPE-susceptible subjects, there were no differences in BAL fluid total leukocyte counts between resistant and susceptible subjects or between counts taken at low and high altitudes. Subjects who developed HAPE had BAL fluid with high concentrations of plasma-derived proteins and erythrocytes, but there was no increase in plasma concentrations of surfactant protein A and Clara cell protein. The chest radiograph score was 12.7 for the 3 HAPE-susceptible subjects who developed HAPE before BAL was performed; they were lavaged within 3 to 5 hours. The remainder of the HAPE-susceptible group was lavaged before edema was apparent on radiographs. However, 6 subjects from the HAPE-susceptible group who developed HAPE on the following day had a score on bronchoscopy of 1.5, which increased to 4.6, reflective of mild pulmonary edema. In HAPE cases, there were no elevations in a number of proinflammatory cytokines and eicosanoid and nitric oxide metabolites. CONCLUSIONS: Early HAPE is characterized by high pulmonary artery pressures that lead to a protein-rich and mildly hemorrhagic edema, with normal levels of leukocytes, cytokines, and eicosanoids. HAPE is a form of hydrostatic pulmonary edema with altered alveolar-capillary permeability.

Adult↗
PubMed2006

Fluorescent labeling of renal cells in vivo.

In vivo fluorescence imaging, using confocal or multiphoton microscopes, provides a powerful method to analyze kidney function in experimental animals. In this review, the preparation used for physiological studies in rats is described. A variety of fluorescent probes are available to study glomerular permeability, renal blood flow, peritubular capillary permeability, cell ion concentrations, tubule transport properties, and the functional status of renal cells. We have recently used micropuncture techniques and an adenovirus vector to accomplish gene transfer into kidney tubule and endothelial cells; this new methodology will allow the dynamic study of fluorescently-labeled proteins. Two examples of the use of two-photon fluorescence microscopy to study renal pathophysiology, namely polycystic kidney disease and renal ischemia, are presented. Software is available to quantify data collected from in vivo imaging experiments and to construct 3-dimensional images of renal structures. Two-photon or confocal microscopy offers many opportunities for a better understanding of kidney function in health and disease.

Animals↗
PubMed1983

Role of angiotensin II-induced renal functional changes in mesangial deposition of exogenous ferritin in rats.

The relationship between acute angiotensin II (AII)-induced functional changes of the kidney and mesangial localization of macromolecules was investigated in rats utilizing native horse spleen ferritin as an exogenous tracer. One group of rats received a 30-minute infusion of a pressor dose of AII. Ten minutes before sacrifice they were injected with a single intravenous dose of ferritin. In the other group the injection of ferritin was followed by an 80-minute infusion of AII. Serial measurements of systolic blood pressure (BP), inulin clearance (CIN), p-aminohippuric acid (PAH) clearance (CPAH), filtration fraction (FF), and excretion of albumin (UAlb V) and ferritin (UFe V) were obtained. Although AII-treated rats showed significant increases of BP, FF, UAlb V and UFe V over controls, they were not different from controls with respect to plasma ferritin concentrations, renal delivery of ferritin, CPAH, and CIN. Semiquantitative evaluation of renal tissue by immunofluorescence and electron microscopy revealed that at 10 minutes no differences in the early and mild deposition of ferritin in the mesangium were appreciable. In contrast, at 80 minutes, AII-treated rats had markedly enhanced mesangial localization of ferritin when compared with controls. In the animals infused with AII for 80 minutes, the amount of glomerular ferritin deposition correlated strongly with UAlb V and UFe V. Combining the results of both, AII and controls at 80 minutes, these correlations were still present, in addition to weaker yet significant correlations of glomerular ferritin with BP and absolute changes of FF during the treatment period. The results show that, over a time interval of 80 minutes, AII augments the mesangial accumulation of ferritin in the presence of normal tracer delivery to the kidney. The enhanced mesangial localization of ferritin is observed under circumstances where overall increases in glomerular capillary permeability to albumin and ferritin are present. Although the precise mechanisms underlying these effects are not identified, AII-induced changes of glomerular microcirculatory forces and permeability properties of the glomerular capillary appear to be involved.

Albuminuria↗
PubMed1997

Failure of carbazochrome sodium sulfonate (AC-17) to prevent dengue vascular permeability or shock: a randomized, controlled trial.

OBJECTIVE: We studied the ability of carbazochrome sodium sulfonate (AC-17) to prevent capillary permeability in dengue hemorrhagic fever/dengue shock syndrome. METHOD: A randomized, placebo-controlled trial in 95 children stratified by age and sex was conducted in two hospitals during 1992. AC-17 (n = 45 cases) or B vitamins as placebo (n = 50) were given as a bolus infusion and then as a continuous drip for 24 hours; a total of 300 mg of AC-17 was administered on the first 2 days and 150 mg on the third day. RESULTS: The two groups were comparable in age, sex, duration of illness, and clinical manifestations. No significant difference in shock or pleural effusion was noted between the two groups. Shock developed in 8.9% (4/45) of patients in the AC-17 group and 6% (3/50) in the placebo group (p = 0.44). Pleural effusion was found at 0, 24, 48, and 72 hours after admission in 4.4%, 20%, 31.1%, and 20% in the AC-17 group and 2%, 14%, 28%, and 14% in the placebo group, respectively. CONCLUSION: Administration of AC-17 does not prevent plasma leakage or shock in dengue hemorrhagic fever/dengue shock syndrome.

Adrenochrome↗
PubMed1999

Transcapillary escape rate of albumin is increased and related to haemodynamic changes in normo-albuminuric type 1 diabetic patients.

OBJECTIVE: An increase in urinary albumin excretion (UAE) in type 1 diabetic patients might reflect changes in vascular permeability and/or local haemodynamic factors. Indeed, transcapillary escape of albumin (TERalb), a measure of systemic capillary efflux, is increased in diabetic patients, even in those with a modest increase of albuminuria. In normo-albuminuric type 1 diabetic patients, systemic capillary and glomerular flow is increased. We hypothesized that these haemodynamic changes contribute to an elevated TERalb, even in the phase preceding micro-albuminuria. METHODS: We measured TERalb in 39 normo-albuminuric type 1 diabetic patients and 46 healthy controls. TERalb was calculated from the disappearance curve of 125I-albumin. Renal and systemic haemodynamics were measured by standard techniques. Forearm blood flow (FBF) was measured by plethysmography. Endothelial function was assessed by intra-arterial infusion of acetylcholine. The structural integrity of the vessel wall was determined by the post-occlusive reactive hyperaemia test. RESULTS: TERalb was increased in diabetic patients (5.53+/-0.40 versus 4.39+/-0.21 %/h, P = 0.01). Patients were divided into tertiles with respect to their TERalb. There were no differences in UAE, blood pressure, metabolic parameters, endothelial function or maximal vasodilatation after occlusion between the groups. However, filtration fraction and FBF were significantly increased in the group of diabetic patients with the highest levels of TERalb. Overall, in diabetic patients, FBF was significantly correlated with TERalb. CONCLUSIONS: TERalb is increased in normo-albuminuric type 1 diabetic patients. In these patients with an increased capillary permeability, there is no evidence of endothelial dysfunction or vessel wall damage. However, both FBF and filtration fraction are increased. Therefore, the increased vascular permeability in the early phase of type 1 diabetes is associated with general haemodynamic alterations. Notably, such an increase in vascular permeability is not necessarily reflected by abnormal UAE. This could be due to either a lack of change in glomerular permeability or due to the fact that the threshold for tubular reabsorption of albumin has not been exceeded.

Adult↗
PubMed2000

Pulmonary edema in fatal heroin overdose: immunohistological investigations with IgE, collagen IV and laminin - no increase of defects of alveolar-capillary membranes.

Pulmonary edema complicating heroin overdosage is a well recognized entity and regarded as the major mechanism contributing to death in heroin addicts. It's pathogenesis is unknown, several mechanisms are discussed: hypoxia-induced increase of pulmonary capillary permeability, depressed myocardial contractility, centrally induced respiratory depression, primary toxic effects on the alveolar capillaries and acute anaphylactic shock. The present study included opiate-related deaths (n=23) and a control group of sudden cardiovascular deaths (n=12) to verify the hypothesis, that defects of the alveolar capillary membranes and/or an acute anaphylactic reaction leads to pulmonary congestion, edema and hemorrhages. Lung specimens were obtained from these 35 autopsies of persons autopsied in the Institute of Forensic Medicine, University of Bonn, in 1997 and 1998. All specimens were examined with hematoxylin-eosin, prussian blue and investigated with immunohistological methods using primary antibodies against collagen IV, laminin and IgE. Defects of the basal laminae of the alveoli were found, demonstrated by laminin and collagen IV, and the number of IgE-positive cells was counted in both groups. There was an increased but not significant number of IgE-positive cells in the heroin-group and defects of the epithelial and endothelial basal laminae were found in both groups without significant differences.

Anaphylaxis↗
PubMed1993

Etiology of venous ulceration.

The etiology of venous ulceration is far more complex than Homans' theory of stagnation and hypo-oxygenation. Indeed, studies have shown that flow in lipodermatosclerotic limbs is actually faster than normal. We suggest, therefore, that the terms "stasis dermatitis" and "stasis ulcer" be dropped from medical parlance. The term "lipodermatosclerosis with ulceration" as used by the British, or simply "venous ulcer," would seem more appropriate. Venous hypertension, produced by incompetence of deep and communicating vein valves and thrombosis of segments of the deep system, is closely correlated with the development of venous ulcers. Precisely how this venous hypertension translates into ulceration is unclear. Burnand et al showed that fibrin cuffs are deposited around the capillaries in lipodermatosclerotic limbs. These cuffs may serve as barriers to the diffusion of oxygen, leading to local ischemia and epidermal necrosis. Others suggest that trapped leukocytes in the microcirculation alter capillary permeability by releasing various inflammatory mediators that hasten the flow of fibrinogen across the capillary membrane and promote the formation of fibrin cuffs. Proof of this hypothesis is still lacking, but may eventually come from using radioactive WBC tagging procedures. A synthesis of these two theories may in fact explain the etiology of venous ulceration.

Capillary Permeability↗
PubMed1984

Transcapillary passage of albumin in mammary tumours and in normal lactating mammary glands of the rat.

A triple-isotope technique was used to obtain albumin clearances and blood flow in DMBA induced mammary tumours, normal lactating mammary glands and various other tissues of the rat. Albumin clearance was high both in tumours (0.0337 ml/min/100 g) and in lactating mammary glands (0.0414 ml/min/100 g). Albumin extraction (defined as the ratio of clearance over plasma flow) was exceptionally high in tumours (23 X 10(-4)) and lactating glands (18 X 10(-4)) as compared to all other tissues (1-7 X 10(-4)). This probably reflects an increased capillary permeability to macromolecules and/or a change in the relation between blood flow and available capillary surface area, both in the physiological, hormonally induced gland and in the abnormal neoplasia derived from the same tissue. Increased extravasation of albumin, together with other changes (e.g. impaired lymph formation) may be important factors behind the production of increased tumour interstitial pressure, which tend to reduce nutritional blood flow in tumours.

Albumins↗
PubMed2003

Role of p38 mitogen-activated protein kinase in lung injury after burn trauma.

This study was undertaken to evaluate the effect of SB203580, a specific p38 mitogen-activated protein (MAP) kinase inhibitor, on burn-induced lung injury as well as the release of tumor necrosis factor (TNF)-alpha and interleukin (IL)-1beta in rats to characterize the role of p38 MAP kinase in lung injury after burn trauma. Sprague-Dawley rats were divided into three groups: 1) sham group, or rats who underwent sham burn; 2) control group, or rats given third-degree burns over 30% total body surface area (TBSA) and lactated Ringer solution for resuscitation; and 3) SB203580 group, or rats given burn injury and lactated Ringers solution with SB203580 inside for resuscitation. Pulmonary injury was assessed at 24 h by pulmonary capillary permeability determined with fluorescein isothiocyanate-labeled albumin and lung histologic analysis. TNF-alpha and IL-1beta protein in bronchoalveolar lavage fluid and serum were measured by enzyme-linked immunosorbent assay and p38 MAP kinase was activity determined in lung by Western blot analysis. These studies showed that significant activation of p38 MAP kinase at 24 h postburn compared with control. Burn trauma resulted in increased pulmonary capillary leakage permeability, elevated levels of TNF-alpha and IL-1beta in bronchoalveolar lavage fluid and serum, and worsened histologic condition. SB203580 inhibited the activation of p38 MAP kinase, reduced the levels of TNF-alpha and IL-1beta, and prevented burn-mediated lung injury. These data suggest that p38 MAP kinase activation is one important aspect of the signaling event that may mediate the release of TNF-alpha and IL-1beta and contributes to burn-induced lung injury.

Animals↗
PubMed2001

Radioisotope albumin flux measurement of microvascular lung permeability: an independent parameter in acute respiratory failure?

AIM: To evaluate the extent to which single measurements of microvascular lung permeability may be relevant as an additional parameter in a heterogenous clinical patient collective with Acute Lung Injury (ALI) and Acute Respiratory Distress Syndrome (ARDS). METHODS: In 36 patients with pneumonia (13), non pneumogenic sepsis (9) or trauma (14) meeting the consensus conference criteria of ALI or ARDS double-isotope protein flux measurements (51Cr erythrocytes as intravascular tracer, Tc-99m human albumin as diffusible tracer) of microvascular lung permeability were performed using the Normalized Slope Index (NSI). The examination was to determine whether there is a relationship between the clinical diagnosis of ALI/ARDS, impaired permeability and clinical parameters, that is the underlying disease, oxygenation, duration of mechanical ventilation and mean pulmonary-artery pressure (PAP). RESULTS: At the time of study, 25 patients presented with increased permeability (NSI > 1 x 10(-3) min-1) indicating on exudative stage of disease, and 11 patients with normal permeability. The permeability impairment correlated with the underlying disease (p > 0.05). With respect to survival, there was a negative correlation to PAP (p < 0.01). Apart from that no correlations between the individual parameters were found. Especially no correlation was found between permeability impairment and oxygenation, duration of disease or PAP. CONCLUSION: In ALI and ARDS, pulmonary capillary permeability is a diagnostic parameter which is independent from clinical variables. Permeability measurement makes a stage classification (exudative versus non exudative phase) of ALI/ARDS possible based on a measurable pathophysiological correlate.

Adult↗
PubMed1981

[Effect of drugs on the permeability of the histohematic barriers in a complicated course of myocardial infarct].

The investigations have shown the pathogenetic role of enhanced capillary permeability on the development of myocardial infarction and its complications. To a definite degree the above disorders are conditioned by the activation of the kallikrein-kinin system. This made us try contrykal with heparin in the comprehensive system of treatment of these patients. A clear-cut clinical and laboratory effect has been obtained which justifies recommending the use of protease inhibitors in complicated myocardial infarction.

Adult↗
PubMed1988

High permeability pulmonary edema (ARDS) during tocolytic therapy--a case report.

A 26 year old previously healthy woman who was treated with fenoterol for premature labor at 30 gestational weeks developed pulmonary edema requiring intubation and mechanical ventilation. Vaginal delivery was accomplished with forceps after tocolytic therapy had been stopped. Right heart catheterization with measurement of pulmonary wedge pressure did not reveal left ventricular failure. Protein determination in lung edema fluid provided evidence of increased pulmonary capillary permeability. Recovery was rapid and ventilatory support was stopped after 36 hours. It is suggested that the infusion of beta-sympathomimetic drugs may alter the permeability of the alveolar-capillary membranes which together with triggering factors such as fluid overload might lead to clinically manifest pulmonary edema.

Adult↗
PubMed1963

On the nature of the chemical mediators involved in anaphylactic reactions in mice.

The effects of mepyramine, promethazine, chlorpromazine and lysergic acid diethylamide have been compared on the capillary permeability changes of the skin, produced by histamine, by 5-hydroxytryptamine and by passive cutaneous anaphylaxis in mice. Promethazine, mepyramine and chlorpromazine can inhibit, in decreasing order of activity, the effect of histamine, whilst lysergic acid diethylamide is inactive. Lysergic acid diethylamide and chlorpromazine are equally potent inhibitors of the action of 5-hydroxytryptamine on the peripheral vascular bed, whilst mepyramine is inactive. Promethazine has intermediate activity. Passive cutaneous anaphylaxis is strongly inhibited by chlorpromazine and by promethazine. Mepyramine and lysergic acid diethylamide, each injected alone, affect only weakly the anaphylactic reaction. However, passive cutaneous anaphylaxis is almost completely abolished by the simultaneous injection of the two last antagonists. It is suggested that the anaphylactic reaction in mice is the result of simultaneous release of both mediators, histamine and 5-hydroxytryptamine, each of them strengthening the effect of the other.

Anaphylaxis↗
PubMed1997

Actions of serum and plasma albumin on intracellular Ca2+ in human endothelial cells.

1. The effects of serum and plasma albumin on [Ca2+]i in human endothelial cells were examined using single-cell Ca2+ imaging. Two types of endothelial cell were used: human umbilical vein endothelial cells (HUVEC) in primary culture, and the endothelial-derived cell line ECV304. 2. Serum albumin caused a large and transient rise in [Ca2+]i, due to Ca2+ release from an IP3-sensitive internal store, followed by a maintained elevation in [Ca2+]i attributable to Ca2+ influx from the external medium. A half-maximal rise in [Ca2+]i was produced by a concentration of serum albumin of about 1 microgram ml-1. 3. The Ca(2+)-releasing action of serum albumin is abolished by methanol extraction and is therefore attributable to an attached polar lipid. A possible candidate is lysophosphatidic acid, known to be released from platelets during blood coagulation, which produced similar effects to those of serum albumin. 4. In HUVEC, plasma albumin caused a sustained decrease in [Ca2+]i from the mean resting level of 114 nM to 58 nM. No effect of plasma albumin was observed in ECV304 cells. 5. The decrease in [Ca2+]i caused by plasma albumin is due to an uptake into intracellular stores. The store loading substantially potentiates the action of Ca(2+)-releasing agonists such as histamine. 6. The results show that normal plasma albumin, which carries few lipids, lowers [Ca2+]i and potentiates the actions of Ca(2+)-releasing agonists by promoting Ca2+ uptake into intracellular stores. When converted to the serum form, by binding lysophosphatidic acid released during blood coagulation, albumin has a potent effect in elevating [Ca2+]i. Blood coagulation may therefore play a role in regulating vascular tone and capillary permeability.

Calcium↗