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PubMed2006

Capillary physiology of human medulloblastoma: impact on chemotherapy.

BACKGROUND: Advances in the treatment of medulloblastoma have largely been attributed to the introduction of chemotherapy, although Phase III trials have shown advantages for chemotherapy only in subgroups. Because the efficacy of chemotherapy depends on tumor vascularization, the vascular physiology of human medulloblastomas was evaluated. METHODS: Seven patients with histologically proven medulloblastomas underwent measurements of capillary permeability and vascular plasma volume using contrast-enhanced dynamic computer tomography. Regional blood flow was measured in 5 patients using xenon computed tomography (CT). RESULTS: The capillary permeability-surface product for water-soluble compounds ranged from 1.7 +/- 5.5 to 17.6 +/- 12.3 muL/g/min with a mean of 10.5 +/- 6.3 microL/g/min. The vascular plasma volume ranged from 0.02 +/- 0.021 to 0.045 +/- 0.049 mL/g with a mean of 0.03 +/- 0.01 mL/g. The efflux rate ranged from 0.012 +/- 0.007 to 0.065 +/- 0.064 1/min with a mean of 0.039 +/- 0.020 1/min. Regional tumoral blood flow showed a mean of 19.86 +/- 6.8 mL/100g/min as compared with normal cerebellum with 45.4 +/- 12.03 mL/100g/min (P < .005). CONCLUSIONS: The current study demonstrated a low capillary permeability and blood flow in medulloblastomas that could explain the limited response rates of partially resected tumors even after aggressive high-dose chemotherapy, as recently reported.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1998

Modulation of arachidonic acid release and membrane fluidity by albumin in vascular smooth muscle and endothelial cells.

Albumin is the major plasma protein circulating in blood. Albumin potently decreases capillary permeability, although the mechanisms are not understood completely. Albumin also effectively binds arachidonic acid (AA), which increases capillary permeability. To investigate the interactions of BSA and AA with the cell membrane, the effect of these substances on [3H]AA release and membrane fluidity was studied in vascular myocytes and endothelial cells. BSA (0.2 and 1 mg . mL-1) stimulated a significant release of [3H]AA from both intact rat aorta and cultured smooth muscle cells. This effect was not mimicked by gamma-globulin or myoglobin (both 1 mg . mL-1) in intact tissue. BSA, but not gamma-globulin and myoglobin, decreased the membrane fluidity (assessed as changes in the steady-state fluorescence anisotropy of 1,6-diphenyl-1,3, 5-hexatriene) in a concentration-dependent manner with a half-maximum concentration between 0.007 and 0.4 mg . mL-1 in both freshly isolated and cultured rat aortic myocytes and human umbilical vein endothelial cells. AA (1 to 200 micromol/L) caused the opposite effect, increasing membrane fluidity and antagonizing the effect of BSA. BSA modified at its arginine residues, which are thought to be important in AA binding, did not stimulate [3H]AA release and was significantly less potent than native BSA in altering the membrane fluidity. The effect of BSA can be explained by a high-affinity binding of AA to the protein and extraction of AA from the cell membrane. The interaction between BSA and AA could play a role in the regulation of vascular permeability.

Animals↗
PubMed1990

Regulation of binding proteins for insulin-like growth factors (IGF) in humans. Increased expression of IGF binding protein 2 during IGF I treatment of healthy adults and in patients with extrapancreatic tumor hypoglycemia.

UNLABELLED: Insulin-like growth factors (IGFs) in blood form two complexes with specific binding proteins (BPs): a large, growth hormone (GH)-dependent complex with restricted capillary permeability, and a smaller complex, inversely related to GH, with high turnover of its IGF pool and free capillary permeability. The distribution of BPs and of IGFs I and II between these complexes was studied in sera from healthy adults treated with IGF I or/and GH and from patients with extrapancreatic tumor hypoglycemia. Like GH, IGF I administration raises IGF I and two glycosylation variants of IGFBP-3 in the large complex, but unlike GH drastically reduces IGF II. During IGF I infusion, IGFBP-3 appears in the small complex whose IGFBP-2 and IGF I increase three- to fivefold and fivefold, respectively. GH treatment, associated with elevated insulin levels, suppresses IGFBP-2 and inhibits its increase owing to infused IGF I. The small complex of tumor sera contains increased amounts of IGFBP-2 and -3, and two- to threefold elevated IGF II. CONCLUSIONS: low GH and/or insulin during IGF I infusion and in extrapancreatic tumor hypoglycemia enhance expression of IGFBP-2 and favor partition of IGFBP-3 into the small complex. Free capillary passage and high turnover of its increased IGF I or II pools may contribute to compensate for suppressed insulin secretion during IGF I infusion or to development of tumor hypoglycemia.

Carrier Proteins↗
PubMed1998

Transvascular and urinary leakage of albumin in atherosclerotic and hypertensive men.

Increased urine albumin is associated with atherosclerotic disease and predicts cardiovascular morbidity and mortality in nondiabetic populations. This finding is frequently postulated to reflect the impact of atherosclerotic damage on glomerular and systemic capillary permeability, an interesting but as yet untested hypothesis. The transcapillary escape rate of albumin (TERalb, the 1-hour decline rate of intravenous 125I-albumin, a measure of capillary macromolecular permeability), albuminuria, lipid levels, echocardiographic wall thickness, and insulin responses to oral glucose were measured in 30 untreated dipstick-negative lean men and clinically stable atherosclerotic peripheral vascular disease; tolerance to oral glucose was a requirement for inclusion in the study. Because hypertension per se might influence TERalb, the sample included either normotensive (n=18, 118+/-6/72+/-7 mm Hg) or hypertensive (n=12, 141+/-7/84+/-6 mmHg by 24-hour blood pressure monitoring) arteriopathic patients; 11 normal age- and gender-matched subjects (121+/-7/76+/-5 mmHg) were used as control subjects. TERalb was higher in patients (10.7+/-3.2 versus 7.4+/-1.7%/h, P<0.013), a difference that persisted after postload glucose, insulin, and lipid levels were accounted for by covariance analysis; atherosclerosis and hypertension together did not further impair vascular permeation to albumin. In contrast with TERalb, albuminuria was elevated only in the hypertensive subgroup; the 2 variables showed no relationship, even when the data were analyzed separately in normotensive and hypertensive subgroups. Urine albumin correlated positively with 24-hour blood pressure and wall thickness. Thus, systemic capillary permeability is altered in nondiabetic atherosclerotic patients independently from blood pressure levels, but this abnormality is not reflected by proportionate changes in albuminuria.

Aged↗
PubMed1982

Influence of hypertonic bolus injection on capillary transport of water, urea and albumin in dog lung.

The influence of hypertonic bolus on dog lung capillary permeability was determine by the in vivo osmotic transient method associated with the multiple indicator dilution method. Three instantaneous injections were made (into the pulmonary artery) at 20 min intervals. The first was an isotonic bolus of 14C-Urea and 125I-Albumin tracers. The second was a hypertonic bolus of urea also with 14C-Urea and 125I-Albumin tracers. The third was identical to the first. Simultaneously, blood samples were withdrawn from the aorta and radioactive concentration of the tracers was measured. No difference between extraction of the test tracer (14C-Urea) was found between any of the three injections (=E1 = 0.108; -E2 = 0.096; -E3 = 0.096). Comparison of the permeability surface-area product values confirmed this absence of modification. It was concluded that the hypertonic bolus did not change capillary permeability to a small hydrophilic molecule and that the solvent drag induced by hyperosmotic transient was negligible.

Albumins↗
PubMed1983

Permeability of pancreatic capillaries to small molecules.

The permeability of capillaries in the isolated, blood-perfused canine pancreas was studied with the double-indicator dilution technique. The permeability-surface area products (PS) for inulin and beta-lactoglobulin A were determined at different plasma flows (attained by pump perfusion). The PS for inulin increased with increasing plasma flow, while the PS for beta-lactoglobulin A was relatively independent of plasma flow. At the highest plasma flow acquired, PS for inulin and beta-lactoglobulin A were approximately 23 and 3.5 ml X min-1 X 100 g-1, respectively. The ratio of the PS values for these two solutes was greater than the ratio of their free diffusion coefficients, indicating restricted diffusion of beta-lactoglobulin A relative to inulin. The degree of restriction was consistent with a maximum equivalent pore radius of 67 A for pancreatic capillaries. An ultrastructural analysis revealed that ductal as well as acinar and islet capillaries were fenestrated. The permeability characteristics of fenestrated pancreatic capillaries are similar to those previously reported for the small intestine.

Animals↗
PubMed1991

Colloid oncotic pressure and body water dynamics in septic and injured patients.

Colloid oncotic pressure (COP) and fluid shifts were studied in 43 septic (SS) patients and 33 injured (HS) patients (ISS = 48.2). During maximal postresuscitation fluid retention, plasma volume (PV/RISA), red cell volume (RBC/51Cr), inulin space (ECF), and COP were measured. Interstitial space (IFS), PV/IFS ratio, and correlation coefficients (r) were calculated. A subgroup of 22 SS patients and 22 HS patients of equal study weight were also compared. Septic patients had greater IFS expansion (17.6 L vs. 11.5 L) than HS patients who, by inference, had more intracellular expansion. Expansion of IFS in SS patients correlated (r = -0.76, p less than 0.02) with reduced plasma COP; this was not seen in HS patients (r = -0.09, p less than 0.35). In contrast, plasma COP correlated (r = 0.72, p less than 0.001) with PV/RISA in HS patients but not in SS patients (r = 0.09, p greater than 0.35). We conclude: (1) SS patients with greater IFS expansion that correlates with reduced plasma COP likely have increased capillary permeability; and (2) HS patients with less IFS expansion that does not correlate with reduced plasma COP likely have maintained capillary permeability with altered IFS matrix configuration causing reduced protein exclusion.

Blood Proteins↗
PubMed1992

Limiting edema in neonatal cardiopulmonary bypass with narrow-range molecular weight hydroxyethyl starch.

The marked edema observed in neonatal cardiopulmonary bypass is thought to result from pathologic increases in capillary permeability. Pentafraction is a subfraction of hydroxyethyl starch that is thought to be of appropriate size and shape to be retained by leaking capillaries and seal endothelial gaps in capillary basement membranes. To test the hypothesis that pentafraction would reduce edema in neonatal cardiopulmonary bypass, we established a model of edema formation in neonatal bypass in which neonatal piglets underwent 2 hours of normothermic cardiopulmonary bypass with crystalloid prime and no myocardial ischemia. Before initiation of bypass, experimental animals (n = 11) received intravenous pentafraction, 3 gm/kg. Control animals (n = 10) received an equivalent volume of saline. Hemodynamic parameters, animal weight, fluid redistribution, and percent tissue water of individual organs were assessed during and after bypass. Pentafraction treatment resulted in significant differences in (1) lowered percent body weight gain from baseline (11% versus 48%), (2) lowered volume requirement to maintain venous reservoir during cardiopulmonary bypass (148 ml/kg versus 581 ml/kg), (3) less fluid loss from the peritoneum (11 ml/kg versus 115 ml/kg), and (4) lowered percent tissue water of kidney, pancreas, stomach, jejunum, colon, and skeletal muscle (p less than 0.05 by unpaired t test). Pentafraction had no effect on hemodynamic parameters during bypass nor in percent tissue water of heart, lung, liver, spleen, skin, or brain. In summary, pentafraction lessened weight gain and fluid requirements during cardiopulmonary bypass, favorably influencing the percent tissue water of certain organs. If pentafraction functions as proposed, it may have wide applicability not only in cardiopulmonary bypass (or extracorporeal membrane oxygenation) but also in other clinical scenarios with altered capillary permeability.

Animals↗
PubMed1981

Does reduced colloid oncotic pressure increase pulmonary dysfunction in sepsis?

Starling's hypothesis of forces governing fluid movement across capillary membranes suggests that any unopposed decrease in intracapillary colloid oncotic pressure (COP) or increase in capillary permeability should result in increased interstitial fluid. Iso-oncotic increase in pulmonary artery wedge (PAW) causes pulmonary dysfunction. Isobaric reduction of COP with normal capillary permeability does not result in pulmonary interstitial edema. Because sepsis is a frequent antecedent of clinical pulmonary dysfunction, the question was asked: does reduction in the COP-PAW gradient in the presence of sepsis result in increased pulmonary dysfunction? Twenty baboons were studied: group 1--control, group 2--4-h constant infusion of E. coli, group 3--plasmapheresis alone, group 4--plasmapheresis followed by sepsis. Ringer's lactate was infused to keep PAW constant. Arterial and mixed venous blood gases were drawn and the intrapulmonary shunt (QS/QT) was calculated. The data were compared using Tukey's HSD test and one way analysis of variance. Plasmapheresis alone resulted in a 68% reduction in COP (15 +/- 2.9 (SD) torr to 4.6 +/- 0.6 in group 3 and 16.5 +/- 4.3 to 5.7 +/- 0.9 in group 4, p less than 0.05). Sepsis resulted in an increase in QS/QT in all septic animals. There was no increased QS/QT in those animals that had sepsis added to plasmapheresis, group 4 (p less than 0.05). These data indicate that sepsis leads to pulmonary dysfunction but that this dysfunction appears to be independent of colloid oncotic forces.

Animals↗
PubMed1986

[Intrathecal ACNU against malignant leptomeningeal tumors--toxicity and therapeutic effect in experimental animals].

Leptomeningeal dissemination is one of the major causes which increase the morbidity and mortality of the patients with malignant brain tumors. The incidence of this complication is increasing, however, no sufficient treatment is available at present. Therefore, in an attempt to establish a new treatment, we studied toxicity and therapeutic effect of intrathecal ACNU (nimustine hydrochloride) using experimental animals. Systemic and local toxicity was tested in normal rats that received ACNU intracisternally. The animals given ACNU more than 3.0 mg/kg progressively lost their body weight, and ACNU 6.0 mg/kg was fatal in 80% of animals. Animals given ACNU less than 1.5 mg/kg gained weight in the same rate as in control animals. Increased capillary permeability to intravenous Evans blue was observed in the subpial region of the brain in the rats given ACNU 6.0 mg/kg intracisternally. The increase of capillary permeability was dominant along the ambient cistern, hypocampal fissure, and at the base of the brain. Demyelinization and loss of neurons were seen in the same areas as well. These changes were not observed in the animal given ACNU less than 1.5 mg/kg. Therapeutic effect of intrathecal ACNU against the leptomeningeal tumor was studied in rats with meningeal carcinomatosis which was induced by intracisternal inoculation of 1 X 10(4) cells of Walker 256 carcinosarcoma. The median survival times of the animal given ACNU 1.5 mg/kg intrathecally on day 2 or 5 after tumor inoculation were prolonged by 55 to 64%, and 64 to 145%, respectively, as compared to those of untreated control animals (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2005

Pathogenesis of stroke-like episodes in MELAS: analysis of neurovascular cellular mechanisms.

The pathogenesis of stroke-like episodes in mitochondrial encephalopathy, myopathy, lactic acidosis and stroke-like episodes (MELAS) is not fully understood although two main theories have been proposed; ischemic vascular hypothesis caused by "mitochondrial angiopathy" and generalized cytopathic hypothesis caused by "mitochondrial cytopathy". Crucial molecular mechanism includes the lack of taurine modification at the wobble uridine of mutant transfer RNAsLeu(UUR) resulting in defective translation of cognate codons due to a defect in codon-anticodon interaction. Whereas recent clinical studies have shed light on the neuronal hyperexcitability, which may potentially initiate a cascade of stroke-like events. Stroke-like episodes are characterized by neuronal hyperexcitability, neuronal vulnerability, increased capillary permeability, and focal hyperaemia. It is recognized that stroke-like lesions not only evolve in the area incongruent to a vascular territory, but also potentially spread into the surrounding cortex with concomitant vasogenic edema presumably provoked by prolonged epileptic activities. Based on the clinical observations, we speculate that stroke-like episodes appear to be non-ischemic neurovascular events; once neuronal hyperexcitability developed in a localized brain region as a result from either mitochondrial dysfunction in the capillary endothelial cells, or in neurons or astrocytes, epileptic activities may depolarize the adjacent neurons leading to propagation of epileptic activities in the surrounding cortex. Increased capillary permeability provoked by epileptic activities in the presence of mitochondrial capillary angiopathy may cause unique edematous brain lesions predominantly involving the cortex. As a consequence, susceptible neuronal population in the cortex may result in neuronal loss with a laminar or pseudo-laminar distribution.

Blood Vessels↗
PubMed1980

[Assessment of treatment of retinal angiopathies (author's transl)].

Angiopathies of the retina are the most common cause of blindness. Since it is difficult to assess the success of treatment by measuring visual acuity, not only because of restriction to the central area, today's trend is increasingly towards determination of capillary resistance, capillary permeability and platelet aggregation as objective criteria. The principles and relation to underlying diseases are discussed. As an example of variation of these parameters under the influence of capillary-active substances, the effects of hydroxy-ethylated rutosides are discussed.

Capillary Permeability↗
PubMed1998

Matrix metalloproteinases in cerebrovascular disease.

Cerebral ischemia and intracerebral hemorrhage cause extensive damage to neurons, disrupt the extracellular matrix, and increase capillary permeability. Multiple substrates participate in the cellular damage, including free radicals and proteases. Matrix metalloproteinases and serine proteases are two classes of proteases that are normally present in brain in latent forms, but once activated, contribute to the injury process. These enzymes have a unique role in the remodeling of the extracellular matrix and in the modulation of the capillary permeability. Intracerebral injection of the matrix metalloproteinase, type IV collagenase, attacks the basal lamina around the capillary and opens the blood-brain barrier. Extracellular matrix-degrading proteases are induced by immediate early genes and cytokines, and regulated by growth factors. Activity of the matrix metalloproteinases is tightly controlled by activation mechanisms and tissue inhibitors of metalloproteinases. During ischemia and hemorrhage, multiple matrix metalloproteinases and serine proteases are produced along with their inhibitors. These proteolytic enzymes are involved in the delayed injury that accompanies the neuroinflammatory response. Synthetic inhibitors to metalloproteinases reduce proteolytic tissue damage, and may limit secondary neuroinflammation.

Animals↗
PubMed1971

Mechanism of Action of the Enteropathogenic Factor of Clostridium perfringens Type A.

Cell extract of an enteropathogenic strain of Clostridium perfringens type A was administered intravenously to lambs, rabbits, and guinea pigs. Lambs developed transitory diarrhea, lacrimation, salivation, nasal discharge, lassitude, and dyspnea in 1 to 5 hr after inoculation. Large doses of the inoculum caused rapid onset of the clinical signs and subsequent death. Examination of dead animals revealed intensely hyperemic small intestinal mucosa and some congestion in the liver, lungs, spleen, and kidneys. Rabbits showed excessive salivation, frequent defecation, tranquility, and dyspnea, followed by death. Guinea pigs became weak and died in 15 min to 7 hr. Congestion was evident in lungs, liver, spleen, and in the small intestine. In lambs and guinea pigs tested, atropine and epinephrine alleviated the clinical signs. Intradermally injected cell extract caused an immediate increase in capillary permeability and subsequent erythematous reaction without necrosis in the skin of guinea pigs. It is hypothesized that in the enteric infection C. perfringens enteropathogenic factor acts on the small intestine causing increased capillary permeability, vasodilation, and increased intestinal motility.

Journal Article↗
PubMedDate not supplied

[Importance of the qualitative composition of dietary proteins in the dietotherapy of ischemic heart disease patients].

The effects of two isocaloric antiatherosclerotic diets (containing 120 g protein) differing in the amino acid composition of protein sources introduced were studied and compared in patients with coronary heart disease. Conventional protein sources were used in the first diet, whereas in the second diet, 15% of protein (by weight) was replaced by soybean protein isolate. A study was also made of the effect of dietetic management on lipid metabolism in blood serum. Hemocoagulation, capillary permeability, the kallikrein-kinin system, and immune responsiveness. An increase in the hypolipidemic effect of the diet was noted together with a decrease in the activity of the kallikrein-kinin system, capillary permeability, and body autosensitization upon introduction into the diet of soybean protein isolate. The increase of the protein quota as well as that attained by means of introducing in the diet of soybean protein isolate reduces the therapeutic effect of the diet on hemostasis.

Adult↗
PubMed1995

A monoclonal antibody that blocks the complement regulatory activity of guinea pig erythrocytes and characterization of the antigen involved as guinea pig decay-accelerating factor.

MCA44 is a mAb with the capacity to sensitize neuraminidase-treated guinea pig E for hemolysis by homologous guinea pig C, and the Fab fragments of this mAb could also sensitize guinea pig E interfering with the function of a membrane inhibitor of C on guinea pig E. Using an immunosorbent column to which MCA44 was coupled, the antigenic molecule termed 44Ag was purified from the glycoprotein fraction extracted from E membranes. C intermediate sheep E treated with guinea pig C1 and C4 after sensitization with Ab (EAC14b cells) lost the ability to generate C3 convertase with C2 after incubation with 44Ag. Treatment of guinea pig E and PBL with phosphatidyl-inositol specific phospholipase C (PIPLC) partially removed 44Ag, as determined by flow cytometric analysis after immunofluorescence staining with MCA44. However, 125I-labeled 44Ag adsorbed to human E was efficiently removed by PIPLC treatment with a slight reduction in M(r). The 44Ag purified on an immunosorbent column showed three bands on SDS-PAGE. However, partial N-terminal amino acid sequences of the 55-kDa, 70-kDa, and 88-kDa bands under nonreducing conditions were identical and the sequence was 55% homologous to the N-terminal sequence of human decay accelerating factor (CD55). Intracutaneous administration of MCA44 or its F(ab')2 fragment resulted in increased capillary permeability, even after 3 days, as determined by the appearance of Evans blue spots after i.v. administration of the dye. Because control Abs including anti-class I-MHC did not cause such increased capillary permeability, the increase in permeability caused by MCA44 was likely induced by blocking the function of 44Ag in vivo, indicating a crucial role for these molecules in preventing over-activation of C at the site.

Amino Acid Sequence↗