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PubMed1980

Lung water changes after thermal injury. The effects of crystalloid resuscitation and sepsis.

Respiratory failure after thermal injury is common, but the etiologic roles of high volume crystalloid resuscitation, hypoproteinemia, inhalation injury, or sepsis have not been specifically defined in human studies. We used the thermal-green dye double indicator dilution measurement of extravascular lung water (EVLW) to follow daily lung water changes in seven severly burned adult patients, resuscitated with only crystalloid solutions. An average weight gain of 21.3 kg, a 30% increase (p < 0.001), was present two to three days after admission. Admission EVLW for all patients was 7.9 +/- 1.2 ml/kg, (means +/- SD), and EVLW at the time of maximal weight gain was 5.9 +/- 1.4 ml/kg, a 25% decrease (p < 0.05). Admission pulmonary artery wedge pressure (PAWP) was 8 +/- 3 mmHG, which was not significantly different from PAWP of 13 +/- 4 mmHg at the time of maximal weight gain. In the three patients who died of sepsis, their terminal weight averaged 17.8 kg (27%) above their admitting weight (p < 0.01) and EVLW was 26.4 +/- 4.4 ml/kg, a 200% increase (p < 0.02) from admission. Their terminal PAWP averaged 22 +/- 2 mmHg, a 170% increase (p < 0.005). None of these patients had an increase in EVLW until clinical signs of sepsis occurred and the rise in EVLW preceded the rise in PAWP. Calculated mean plasma colloid osmotic pressure (PCOP) on admission was 20.7 +/- 4.9 mmHg; at the time of maximal weight gain, it was 8.6 +/- 1.7 mmHg (p < 0.001). The PCOP-PAWP gradient fell to -4 +/- 4 mmHg (p < 0.001) at the time of maximal weight gain and remained less than +4 mmHg throughout the study period in all patients. We conclude that massive crystalloid resuscitation while maintaining PAWP below 15 mmHg does not cause an increase in EVLW during the first four days after thermal injury. EVLW actually decreases slightly in all patients despite marked weight gain, hypoproteinemia and a negative PCOP-PAWP gradient. EVLW does not correlate with the PCOP-PAWP gradient in either septic or nonseptic periods. Three patients had severe inhalational injury and normal EVLW for the first four postburn days. It therefore appears that significant interstitial edema does not result from inhalational injury. There is also no evidence that thermal injury causes an early increase in pulmonary capillary permeability. The occurrence of sepsis, however, results in rapid accumulation of lung water, without any change in hydrostatic or osmotic forces. This study supports the primary role of sepsis in altering pulmonary capillary permeability with resulting pulmonary edema.

Adult↗

PubMed1998

Ovarian hyperstimulation syndrome: facts and fallacies.

Severe or critical ovarian hyperstimulation syndrome (OHSS) is a serious complication of ovarian hyperstimulation for assisted reproduction techniques (ART). The syndrome is characterized by cystic enlargement of the ovaries and fluid shifts from the intravascular to the third space. The morbidity in OHSS is mainly determined by the hemodynamic changes caused by increased capillary permeability. The incidence of OHSS depends on definitions, risk factors, ovarian stimulation protocols, luteal support and conception. Currently, research on the pathogenesis of OHSS is focused on increased capillary permeability. Several theories are reviewed. Until the pathogenesis of OHSS becomes clear, treatment is restricted to supportive therapy. The various proposals for management of OHSS are discussed and, based on the available data, directions for the management of various grades of OHSS are summarized. However, prevention and early recognition are still the most important tools to handle OHSS. A flowchart with preventive measures for OHSS is presented derived from the available literature.

Algorithms↗

PubMed1997

The anti-inflammatory effects of ketoprofen in animal experiments.

The authors investigated the anti-inflammatory actions of ketoprofen using a battery of tests: in the rat paw oedema test induced by five different inciters, in the capillary permeability test, and in measuring the interleukin-8 (IL-8) production and superoxide dismutase (SOD) activity. The findings in these studies show that ketoprofen inhibits rat paw oedema, suppresses capillary permeability, reduces IL-8 production and increases SOD activity in the acetic-acid-induced inflammatory state. These results would seem to provide a clear rationale for exploring the usefulness of ketoprofen in the treatment of acute and chronic inflammatory diseases.

Acetic Acid↗

PubMed1994

Active immunization by a dengue virus-induced cytokine.

Dengue type 2 virus (DV)-induced cytotoxic factor (CF) is capable of reproducing various pathological lesions in mice that are seen in human dengue. The present study was undertaken to investigate the protective effect of active immunization of mice with CF. Mice were immunized with 5 microgram of CF and prevention of CF-induced increase in capillary permeability and damage to the blood-brain barrier were studied at weekly intervals, up to 48 weeks, by challenging with 3 microgram of CF. Maximum protection against increase in capillary permeability and damage to the blood-brain barrier was observed in week 4 after immunization. A breakthrough in the protection occurred with higher doses of CF in a dose-dependent manner. Challenge with a lethal intracerebral (i.c.) dose of DV showed significantly prolonged mean survival time and delayed onset of symptoms of sickness in the immunized mice compared with the normal mice, but the titre of the virus in the brain was similar in the two groups. On i.p. challenge with the virus the protection against damage to the blood-brain barrier was 86 +/- 7% at week 4 and 17 +/- 4% at week 26 after immunization. Sera obtained from the immunized mice showed the presence of CF-specific antibodies by ELISA, Western blot, and by neutralization of the cytotoxic activity of CF in vitro. The present study describes successful prevention of a cytokine-induced pathology by specific active immunization.

Animals↗

PubMedDate not supplied

Comparison of albumin-(Gd-DTPA)30 and Gd-DTPA-24-cascade-polymer for measurements of normal and abnormal microvascular permeability.

The purpose of this study was to compare a new MR macromolecular contrast medium (MMCM), gadolinium-diethylenetriamine pentaacetic acid (Gd-DTPA)-24-cascade-polymer, to a well-studied prototype MMCM, for the potential of distinguishing tissues of varying endothelial permeability. Three tissue models of varying capillary permeability were studied in a total of 46 rats: normal myocardium (normal capillaries), subcutaneously implanted adenocarcinoma (mild capillary leak), and reperfused infarcted myocardium (high capillary leak). TI-weighted MRI was performed before and dynamically after injection of either albumin-(Gd-DTPA)30 or the cascade polymer (each .02 mmol gadolinium [Gd] per kg). Data analysis based on a two-compartment kinetic model yielded estimates of fractional blood volume (BV) (percentage) and fractional leak rate (FLR) (1 per hour). Permeability to the cascade polymer as reflected in FLR was considerable in normal myocardium (8.24 per hour), of similar value in tumors (8.55 per hour), but significantly greater in infarcted myocardium (39.17 per hour, P < .01) versus normal myocardium. The larger albumin-(Gd-DTPA)30 demonstrated minimal extravasation in normal myocardium (FLR .33 per hour); FLR in tumors was 100% higher (.66 per hour, P < .002) and FLR in reperfused capillaries was significantly greater (7.94 per hour, P < .001). Based on capillary permeability measurements, the cascade polymer may have limited utility for detection of mildly increased microvascular permeabilities. For severe tissue injury, the cascade polymer can resolve abnormal microvascular integrity.

Analysis of Variance↗

PubMed2002

Therapy of microcirculatory disorders in severe acute pancreatitis: what mediators should we block?

OBJECTIVE: To compare the effect of different vasoactive mediator antagonists in the same model of severe acute pancreatitis (AP) and to evaluate whether combinations of the agents exhibit synergistic effects. DESIGN: Prospective experimental study. SETTING: Microcirculation and pancreas research laboratory at an university hospital. PARTICIPANTS: Hundred eighty anesthetized male Sprague-Dawley rats. INTERVENTIONS: Six hours after inducing AP by intra-ductal bile salt infusion and i.v. cerulein in 168 rats, these were randomized for therapy with (1) saline, (2) endothelin receptor antagonist (ET-RA), (3) platelet activating factor receptor antagonist (PAF-RA), (4) intercellular adhesion molecule-1 antibody (ICAM-1-AB) or different combinations (5-7). After 24 h the animals underwent a second laparotomy for intra-vital microscopic determination of pancreatic and colonic capillary permeability, blood flow and leukocyte-endothelial interaction. RESULTS: AP induction decreased capillary blood flow and increased permeability and leukocyte rolling. ET-RA, PAF-RA and ICAM-1-AB decreased capillary permeability, increased blood flow and reduced leukocyte rolling. ET-RA was most effective in decreasing capillary permeability in both organs as well as in increasing pancreatic capillary blood flow. Combining vasoactive mediator blockers did not further improve target parameters. CONCLUSIONS: This study supports previous observations that ET-RA, PAF-RA and ICAM-1-AB improve microcirculation in AP and that ET-RA is more effective than PAF-RA or ICAM-1-AB, especially in counteracting capillary leakage. Although this may suggest that they act through different mechanisms, antagonist combinations failed to improve microcirculation further. We conclude that ET-RA is the most promising candidate for a clinical trial to reduce capillary leakage in patients with AP.

Acute Disease↗

PubMed1977

Systemic capillary leak syndrome and monoclonal IgG gammopathy; studies in a sixth patient and a review of the literature.

The clincical and laboratory features of a sixth patient with periodic systemic capillary leak syndrome are reported. During an attack metabolic studies demonstrated a marked shift of plasma (10 to 70%) from the intravascular to the extravascular space resulting in hemoconcentration (highest hematocrit of 82). At the termination of the attack there was a return of the electrolytes, water and proteins to the intravascular compartment. The cardiovascular, renal and endocrine compensation was appropriate to this insult and no underlying abnormalities were demonstrated in these systems. The effector pathways of coagulation, complement, bradykinin generation, prostaglandins and histamine metabolism did not appear to be responsible for the altered capillary permeability. The patient was not missing inhibitors of these same pathways. The only persistently abnormal finding was a monoclonal IgG gammopathy. However, further studies of this paraprotein did not uncover a link between it and the abnormal capillary permeability. Five similar cases are reviewed; at least four and possibly all of these patients also had an IgG paraprotein. Treatment of these attacks was unsuccessful. Attemps to prevent the episodes with a wide variety of therapeutic agents failed. Treatment of the acute attacks with administration of intravenous fluids, did not maintain an adequate intravascular volume and may lead to fluid overload upon return of normal capillary integrity. Pressor agents were of no apparent value and may cause increased cardiac irritability. Although the clinical features and pathophysiology of the capillary leak syndrome have been defined, the etiology remains unknown.

Adult↗

PubMed1995

Clinical implications of impaired microcirculation.

Various types of microcirculation disturbances have been described in the course of systemic diseases, hypertension, diabetes, obesity, and the so-called "idiopathic oedema" syndrome. This article summarizes the relevant microcirculatory disorders associated with diabetes and their pathophysiology. These functional disorders occur before or in association with anatomical lesions of diabetic microangiopathy. Increased capillary permeability to albumin is frequently observed in diabetes. In a placebo-controlled trial, Daflon 500 mg, a purified, micronized, flavonoidic fraction, significantly improved this disorder. Patients complaining of an oedematous syndrome almost always have an increased extracellular fluid volume, probably largely due to increased capillary permeability. Diabetes and "idiopathic oedema" therefore constitute two examples of the major clinical implications of impaired microcirculation.

Capillary Permeability↗

PubMed1975

A study of the plasma kinin-generating system in children with the minimal lesion, idiopathic nephrotic syndrome.

Although the precise etiologic incitant of the minimal lesion idiopathic nephrotic syndrome of childhood is not known, it is likely that a host mechanism mediates the permeability alterations of the glomerular capillary wall resulting in massive proteinuria. As a first step in examining the possibility that local kinin release may account for the proteinuria in this disorder, two parameters of the plasma kinin-generating system, plasma prekallikrein and kallikrein inhibitor, were assayed during 27 nephrotic episodes in 21 corticosteroid-responsive children. Plasma kallikrein was assayed by means of its esterase activity on a synthetic arginine ester substrate, N-alpha-tosyl-L-arginine methyl ester (TAMe), after activation of Hageman factor by kaolin. This activity, after subtraction of spontaneous arginine esterase activity (i.e., TAMe esterase activity measured in plasma not exposed to kaolin) is derived from prekallikrein. Plasma prekallikrein activity in 11 normal children was 99.6 +/- 2.9 mumol TAMe hydrolyzed/ml plasma/hr (mean +/- SEM). Kallikrein inhibitor was quantified in arbitrary units. Kallifrein inhibitor activity in 11 normal children was 0.94 +/- 0.04 units. During the overt nephrotic syndrome, before initiation of intensive daily corticosteroid treatment, mean values were: prekallikrein, 58.5 +/- 7.24 mumol/ml/hr; and kallikrein inhibitor, 0.35 +/- 0.06 units. After corticosteroid-induced remission occurred, mean values were: plasma prekallikrein, 118.6 +/- 3.2 mumol/ml/hr; and kallikrein inhitor, 0.78 +/- 0.03 mumol/ml/hr. Both parameters were again assayed in 14 of the 21 children after complete cessation of corticosteroid treatment. Plasma prekallikrein was normal, 99.6 +/- 4.8 mumol/ml/hr; but kallikrein inhibitor was still somewhat depressed, 0.84 +/- 0.03 units. A subset of 9 patients had marked depression of plasma prekallikrein to levels less than 20 mumol/ml/hr and essentially undetectable inhibitor activity. Serum alpha-2 macroglobulin was elevated in nephrotic patients: mean value during relapse, 862 +/- 29 mg/100 ml; during corticosteroid-maintaining remission, 615 +/- 29 mg/100 ml. After cessation of corticosteroids, mean serum level was 481 +/- 20 mg/100 ml. The proportional reduction of plasma prekallikrein and kallikrein inhibitor suggested that an enzyme-inhibitor complex formed in vivo, perhaps at a local site of activation in proximity to the glomerular basement membrane. These data suggest that the plasma kinin-generating system may be the host effector mechanism subserving the increased glomerular capillary permeability in the minimal lesion nephrotic syndrome of childhood.

Aprotinin↗

PubMed1990

Atrial natriuretic factor increases vascular permeability.

An increase in central blood volume in microgravity may result in increased plasma levels of atrial natriuretic factor (ANF). Since elevations in plasma ANF are found in clinical syndromes associated with edema, and since space motion sickness induced by microgravity is associated with an increase in central blood volume and facial edema, we determined whether ANF increases capillary permeability to plasma protein. Conscious, bilaterally nephrectomized male rats were infused with either saline, ANF + saline, or hexamethonium + saline over 2 h following bolus injections of 125I-albumin and 14C-dextran of similar molecular size. Blood pressure was monitored and serial determinations of hematocrits were made. Animals infused with 1.0 micrograms.kg-1.min-1 ANF had significantly higher hematocrits than animals infused with saline vehicle. Infusion of ANF increased the extravasation of 125I-albumin, but not 14C-dextran from the intravascular compartment. ANF also induced a depressor response in rats, but the change in blood pressure did not account for changes in capillary permeability to albumin; similar depressor responses induced by hexamethonium were not accompanied by increased extravasation of albumin from the intravascular compartment. ANF may decrease plasma volume by increasing permeability to albumin, and this effect of ANF may account for some of the signs and symptoms of space motion sickness.

Adaptation, Physiological↗

PubMed1985

Positron emission tomographic measurement of blood-to-brain and blood-to-tumor transport of 82Rb: the effect of dexamethasone and whole-brain radiation therapy.

Unidirectional blood-to-brain and blood-to-tumor transport rate constants for rubidium 82 were determined using dynamic positron emission tomography in patients with primary or metastatic brain tumors. Regional influx rate constants (K1) and plasma water volume (Vp) were estimated from the time course of blood and brain radioactivity following a bolus injection of tracer. Eight patients were studied before and 24 to 72 hours after treatment using pharmacological doses of dexamethasone, and 6 additional patients with metastatic brain tumors were studied before and within 60 to 90 minutes after 200- to 600-rad whole-brain radiation therapy. Steroid treatment was associated with a 9 to 48% decrease in tumor K1 and a 21% mean decrease in tumor Vp. No consistent changes in K1 or Vp were observed in control brain regions. Tumor K1 and Vp did not increase in patients undergoing whole-brain radiation therapy, all of whom were taking dexamethasone at the time of study. These data suggest that corticosteroids decrease the permeability of tumor capillaries to small hydrophilic molecules (including those of some chemotherapeutic agents) and that steroid pretreatment prevents acute, and potentially dangerous, increases in tumor capillary permeability following cranial irradiation.

Adult↗

PubMed2002