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J van Gool

Publications and source records attributed to J van Gool.

At least 37 records · Page 2Linked to original sources
PubMed1986

The effects of alpha M-foetoprotein, an acute phase protein, and BaSO4-induced injury on IgE-mediated, systemic anaphylaxis in the rat.

A recently developed method for inducing fatal, IgE-mediated, bronchial and cardiovascular anaphylaxis in the rat was used to compare the effects of exogenously administered, purified alpha M-foetoprotein (alpha M FP) and BaSO4 pretreatment (as mean to induce an acute phase reaction with increased alpha M FP serum levels) with regard to mortality, bronchoconstriction and cardiovascular events. The BaSO4 pretreatment protected the rats almost completely against mortality, whereas exogenously administered alpha M FP offered no protection at all. With respect to the antigen-induced bronchoconstriction alpha M FP greatly inhibited the increase of the pulmonary resistance (RI), whereas the BaSO4 pretreatment suppressed either the dynamic lung compliance (Cdyn) or RI considerably. The cardiovascular events were only influenced by the BaSO4 pretreatment demonstrating a small but highly significant reduction of the initial fall in blood pressure together with a remarkable recovery within almost I h in the majority (91%) of the animals. Both exogenously administered alpha M FP and BaSO4 pretreatment increased the alpha M FP serum levels from a normal value of 59 +/- 4 micrograms/ml (n = 22), to 2732 +/- 252 micrograms/ml (n = 9) and 855 +/- 200 micrograms/ml (n = 22), respectively. From these data we conclude that the antianaphylactic activity of alpha M FP is limited to bronchoprotection of the more central parts of the lungs, whereas BaSO4 pretreatment covers a much broader antianaphylactic profile. This implies that BaSO4 pretreatment does not only induce alpha M FP but also other endogenous antianaphylactic factors.

Anaphylaxis↗
PubMed1984

Glucocorticoids and catecholamines as mediators of acute-phase proteins, especially rat alpha-macrofoetoprotein.

Adrenal hormones were studied as possible triggering substances of the synthesis of acute-phase reactants in rats. alpha-Macrofoetoprotein, which rises sharply in concentration during inflammation, was used to monitor the acute-phase reaction. In normal rats glucocorticoids and catecholamines induce alpha-macrofoetoprotein synthesis; glucocorticoids only increase alpha-macrofoetoprotein to moderate levels in plasma, but catecholamines enhance alpha-macrofoetoprotein synthesis to very high levels, comparable with those observed in the post-injury phase. However, catecholamines in vivo also activate the adrenal cortex, suggesting a synergistic effect of both kinds of adrenal hormones. Our study showed that in adrenalectomized rats, the effect of catecholamines on alpha-macrofoetoprotein synthesis is greatly diminished, whereas the moderate effect of glucocorticoids remains. Combination of glucocorticoids and catecholamines induces extremely high alpha-macrofoetoprotein levels in both adrenalectomized and normal rats. With crossed immunoelectrophoresis it was shown that other acute-phase reactants, such as haptoglobin and alpha 1-major acute-phase protein, are affected differently by the hormones. Contrary to glucocorticoids, catecholamines give a pattern comparable with that found after surgical injury.

Acute-Phase Proteins↗
PubMed1983

Inhibitory effects of BaSO4 on experimentally induced inflammation in the rat mediated by alpha M-foetoprotein.

The influence was studied of BaSO4 (i.p.) pretreatment on the mediator induced inflammatory responses: oedema formation, measured plethysmographically, increased vascular permeability to protein, measured by the extravascular accumulation of 125I-labeled albumin (125I-HSA) and vasodilatation, measured by the accumulation of 51Cr-labeled erythrocytes. Subplantar application of histamine, 5-hydroxytryptamine, bradykinin or prostaglandin E2 caused oedema formation, an enormous 125I-HSA accumulation and a relatively small 51Cr-labeled erythrocytes accumulation. BaSO4 pretreatment inhibited all these inflammatory responses to a high extent, while the alpha M-foetoprotein (alpha MFP) serum levels were increased from a normal value of 188 +/- 123 micrograms/ml up to 5200 +/- 2264 micrograms/ml (n = 29). From this study and previous data using purified alpha MFP it could be assumed that the anti-inflammatory effects induced by BaSO4 pretreatment are mediated by this enormous increase of the alpha MFP serum levels of alpha MFP are nonspecific and possibly caused by a coating and/or membrane stabilizing effect on cell membranes and/or endothelial junctions.

Albumins↗
PubMed1982

Inhibition of polymorphonuclear leukocyte chemotaxis by alpha-macrofetoprotein, an acute-phase reactant of the rat.

alpha-Macrofetoprotein (alpha M FP) is a normal fetal plasma constituent in the rat, with very low plasma levels in the adult phase but rising sharply after injury. This fetal acute-phase protein is a strong inhibitor of inflammatory edema. Fetal inflammatory reactions show diminished exudation, but also impaired emigration of polymorph nuclear cells (PMNs). Therefore we studied the effect of alpha M FP on chemotaxis of PMN in vitro and in vivo. In vitro experiments showed a strong inhibitory effect on casein-induced leukotaxis (Boyden technique) with a clear dose-effect relationship. In vivo with glycogen-induced pleurisy and peritonitis, high alpha M FP levels are accompanied by diminished PMN emigration and vice versa. The significance of these findings is discussed in relation to fetal pathology and also as a model showing the modulating effects of acute-phase proteins on the inflammatory reaction induced by tissue injury.

Acute-Phase Proteins↗
PubMed1982

Some aspects of iron metabolism during acute viral hepatitis.

In the acute phase of acute viral hepatitis high serum iron and serum ferritin levels were found in all patients. The normalisation of the serum ferritin concentration parallelled that of the serum glutamic pyruvic transaminase activity. However serum iron levels remained elevated for a long period of time. Chemical analysis of liver tissue showed a low total liver depot iron concentration during the first two weeks of the disease, indicating that the high serum iron levels are caused by iron liberation from disintegrated hepatocytes. Patients studied after two weeks showed higher liver iron concentrations, in particular the non-ferritin iron fraction, reflecting iron accumulation in the reticulo-endothelial system. Indeed, histological examination in the patients studied after two weeks showed sinusoidal lining cell siderosis in addition to "diffuse iron" in clusters lining cells which in electron microscopical studies proved to be macrophages. These cells showed a positive immunohistological reaction for ferritin protein. It is suggested that during acute viral hepatitis two mechanisms act together, i.e. changes in iron metabolism caused by damage of the main iron depot organ (specific liver pathology) and changes in iron metabolism common to all infectious processes.

Acute Disease↗
PubMed1979

Effect of human cord and postoperative serum on experimental inflammation in the rat.

Human cord and postoperative serum depressed the oedema provoked by mediators of the inflammatory reaction such as bradykinin, histamine, serotonin and prostaglandin E2 and also the experimental inflammation caused by carrageenin. Normal human and pregnancy serum did not have such an effect. In two cases of open neural tube defect, one of anencephaly and another of spina bifida, human amniotic fluid also had a strongly depressing effect on the experimental oedema provoked by serotonin. Human amniotic fluid from normal pregnancies did not inhibit this experimental inflammation. A protein-fraction of mol. wt 30,000--100,000 has been isolated from the inhibiting sera and shows the anti-inflammatory activity to be dose-related towards all the oedema-provoking substances used. Immunological studies showed that the inhibiting factor could be a protein in the pre-albuminic region, while alpha-foetoprotein did not appear to be responsible for the anti-inflammatory activity. Our conclusion is that human serum contains a protein of foetal origin with an acute-phase character and strong anti-inflammatory activities analogous to rat alpha 2-macrofoetoprotein.

Amniotic Fluid↗
PubMed1978

On the non-ferritin depot iron fraction in the rat liver.

Liver depot iron can be divided into two fractions: ferritin iron and non-ferritin depot iron. Three methods intended to measure the non-ferritin depot iron in the rat liver were compared using livers of normal rats and livers of rats loaded with iron by transfusion of erythrocytes. Liver depot iron varied between 75 and 850 microgram Fe/g liver. Non-ferritin depot iron, measured as the iron fraction sedimentable at 10 000 x g, was in the range 4--22 microgram Fe/g liver. This fraction did contain ferritin. When measured as the difference between total liver depot iron and heat-stable iron (ferritin iron), the range was 10--270 microgram Fe/g liver but this fraction also includes some ferritin iron. The values derived with both methods were linearly proportional to the total liver depot iron values. Non-ferritin depot iron, when measured as the difference between total liver depot iron and total ferritin iron, ranged from 0 to 190 microgram Fe/g liver. In this last method no ferritin iron is included. This method provides the best estimate of the non-ferritin depot iron fraction. The concentrations obtained with this method were not always linearly proportional to the total liver depot iron concentration. Intravenous injection of rat liver ferritin resulted in a rapid accumulation of ferritin iron in the liver, together with an increase of the non-ferritin depot iron fraction from 18 microgram Fe/g liver to 55 microgram Fe/g liver. This confirms a relationship between ferritin catabolism and the non-ferritin depot iron fraction.

Animals↗
PubMed1978

A method for measurement of liver iron fractions in needle biopsy specimens and some results in acute liver disease.

Methods are described for measurement of total tissue iron, ferritin iron, haem iron and ferritin protein in approx. 15 mg of tissue obtained by liver biopsy. The validity of these methods is examined by comparison with the values observed in larger samples of the same post-mortem derived liver tissue. Correlation coefficients vary between 0.80 and 0.99 (n = 11--16). It appears that in post-mortem liver tissue the haem iron concentration is higher than in biopsy specimens from patients. Analysis of liver biopsy specimens from patients with hepatitis showed a large variation in the mean iron content of the liver ferritin molecules. Also, the non-ferritin depot iron concentration and ferritin protein concentration is quite variable. It is suggested that in cases of advanced ferritin catabolism during hepatitis the mean percentage of iron in ferritin molecules often increases while at the same time the non-ferritin depot iron fraction decreases, probably because of iron release from the liver.

Acute Disease↗
PubMed1977

Hemosiderin. an EPR study of water-insoluble iron in human and rat liver.

EPR spectra of the water-insoluble iron fraction, hemosiderin of human and rat liver are described. The homogenate of freshly prepared perfused rat liver shows a non-heme iron signal at g=4.3 and a high-spin heme-iron signal around g=6, whereas the washed and sonicated sample of the insoluble iron fraction shows solely a non-heme iron signal at g=4.3. This indicates that hemosiderin from rat liver does not contain heme iron. Human-liver preparations from post mortem obtained material show in the homogenates as well as in the washed and sonicated samples an intense high-spin heme iron signal at g=6.0 and a non-heme iron signal at g=4.3. A comparative experiment, carried out with "aged" rat liver preparations, reveals the same spectra as with the human preparations. It is concluded that that the heme present in the insoluble iron fraction is caused by degradation of hemoglobin in the obduction material, and that heme is not a constituent of the insoluble depot iron.

Animals↗
PubMed1977

Inflammation inhibiting properties of rat alphaM foetoprotein (rat-alpha2 macroglobulin), an acute phase reactant.

alphaMFoetoprotein of the rat (rat alpha2macroglobulin) is present in serum during foetal development. After birth, alphaMFP declines rapidly, but the protein returns after injury. The injury we used consisted of skin and muscle incision, laparotomy, BaSO4 i.p. The protein occurs also during liverregeneration, livercardinogenesis en during infections. Therefore, alphaMFP can be considered as an acute phase reactant. We found that this protein strongly inhibits inflammatory exudation caused by carrageenin, histamin, prostaglandin E2, 5HT and bradykinin. Furthermore, we found that alphaMFP suppresses completely inflammatory reactions during Ga1.N-hepatitis. In this condition, the primary biochemical lesion, consisting of liver UDPG depletion, does occur in spite of the protective effect of alphaMFP. Thus, the inflammatory inhibiting effects of alphaMFP seem to be an important mechanism reducing inflammatory reaction patterns.

Animals↗
PubMed1977

Depot iron in the rat liver after hypertransfusion with rat erythrocytes.

In the rat liver the deposition of iron was measured after hypertransfusion with rat erythrocytes. The liver iron fractions were studied during four weeks after the hypertransfusions. In the first week the haemosiderin iron fraction increased together with the ferritin iron fraction. Most iron was deposited as ferritin iron. In the last week of the experiments, while the ferritin iron fraction still increased, the haemosiderin iron fraction decreased. At the same time plasma iron was utilized when erythropoiesis, which had been suppressed by the hypertransfusion, recommenced. It is suggest that, under these experimental conditions, liver haemosiderin iron is used in haemoglobin synthesis.

Animals↗