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B Urbaschek

Publications and source records attributed to B Urbaschek.

At least 37 records · Page 2Linked to original sources
PubMed1982

Aspects of beneficial endotoxin-mediated effects.

The status of hyperreactivity and hyporeactivity following the administration of endotoxin in a susceptible host represents phenomena which are of interest in an attempt to understand the role of endotoxins in pathophysiological events in general. Two experimental approaches designed to examine these events are reported herein; i.v. injection with minute concentrations of endotoxin (10 ng of a BOIVIN endotoxin from E. coli 0111) induces tolerance against lethal doses of endotoxin (0.5 microgram or 5.0 microgram) within 24 h in hyperreactive NMRI mice that were infected 14 days before with BCG. Transfer of post-endotoxin serum from BCG infected mice, which contains a myriad of macrophage mediators and which induces nonspecific resistance to X-irradiation, renders a strain of mice (C3H/HeJ) that is hyporeactive to endotoxins, susceptible to the lethal effect of endotoxin. Studies of the role of the macrophage and its mediators in the experimental models described here may contribute to a further understanding of the mechanisms underlying endotoxin-induced biological activities.

Animals↗
PubMed1982

In vivo microscopic studies of the responses of the liver to endotoxin.

In vivo microscopic methods concomitant with electron microscopic and histochemical procedures are being used to explore the sequelae of responses of Kupffer cells and the hepatic microvasculature to endotoxins. To gain further insight into the role of the liver in host defense and nonspecific resistance, the effects of endotoxin also are being studied in animals sensitized to endotoxin (BCG infection) or tolerant to endotoxin (pretreated with detoxified endotoxin, low doses of endotoxin, or in C3H/HeJ mice). The results to date, have demonstrated that endotoxin induces significant alterations in the hepatic microcirculation due to swelling of Kupffer and endothelial cells and the adhesion of leukocytes and platelets to the sinusoid wall. Lymphocytes frequently are associated with the Kupffer cells. Phagocytosis also is affected; following a brief period of stimulation, the rate of phagocytosis by Kupffer cells is depressed. In BCG infected animals all of these responses are exaggerated but can be minimized by pretreatment with detoxified endotoxin or minute concentrations of endotoxin 24 h prior to the challenge dose of endotoxin. The responses are not seen in the endotoxin low-responder, C3H/HeJ mouse which was found to have a deficiency in lysosomal enzymes and a paucity of functional Kupffer cells. The results provide some insight into the sequelae of cellular and microvascular events that occur in the liver during endotoxemia, endotoxin-related host defense mechanisms and non-specific resistance. In addition, support is provided for the central role of Kupffer cells in these events and that lysosomal enzymes participate in the toxic response elicited by endotoxin.

Animals↗
PubMed1979

The inflammatory response to endotoxins.

1. Endotoxins are very potent and widely spread inflammation-inducing substances. 2. In the course of local infections endotoxins represent one of the main principles of the pathogenicity of gram-negative bacteria by inducing acute nonspecific inflammation. 3. The pharmacological activities of endotoxins consist primarily in generating and liberating the classic mediators of acute nonspecific inflammation. 4. Endotoxins are able to enter into the circulation through their capicity to activate pharmacological mediators. 5. The endotoxic mediators which increase the permeability of the microcirculation of the intestinum enable endotoxins as components of the physiological intestinal flora to enter into the circulation; these induce systemic disease or shock depending on their concentration in the circulation. 6. In the course of chronic inflammation recidivism or recrudescence as trasient acute inflammatory outburst can be caused by local effects of endotoxins. 7. According to some recent observations the inflammation inducing capacity of endotoxins may promote the entry of aerobic bacteria into the blood stream which can result in mixed septicemia.

Animals↗
PubMed1978

[Microkymography--a method to measure the flow velocity in the microvascular bed after endotoxin administration (author's transl)].

In this paper the application of intravital microkymography on studies of the microcirculation of the hamster cheek pouch is presented. Flow velocity reduction which is one of the characteristic initial alterations in small blood vessels after injection of endotoxin is recorded in a direct way by the strip microkymography. The method of the recording system is described and some examples of the effects of endotoxin as well as of serotonin, one of the mediators of endotoxin, are given. The advantage of microkymography in quantitative and functional studies of endotoxic actions, e.g. flow velocity decreases and vessel diameter changes, is discussed.

Animals↗
PubMed1975

[Pathophysiological significance of endotoxins].

The biological activities of endotoxin are manifold. Besides the drop in platelets and the biphasic change in the number of leukocytes, severe disturbances in the capillary bed are among the first changes observed following the administration of endotoxin. It is well known that endotoxins cause the release of various vasoactive mediators. According to our results endotoxins enhance the activity of histamine and serotonin; these findings may contribute to a better understanding of the action of histamine and serotonin in the early post-endotoxin phase. The histamine-sensitizing effect of endotoxins is not prevented by antihistamines. Endotoxins and biogenic amines cause similar disturbances in the capillary bed. The changes that are observed in the content of the vessels, the vessel wall, and the perivascular region are the following: slowing down of the blood stream, degranulation of perivascular mast cells, granulocytosis, wall adhering granulocytes, plasma skimming, rouleaux-formation of erythrocytes, reduction in plasticity of many erythrocytes, acanthocytes, acanthocytosis, appearance of spherocytes and microcytes, and formation of massive aggregates of platelets and of microthrombi. Also, occasionally cell aggregates dissolve and as microemboli form new thrombi. Swelling of pericytes, endothelial, and periendothelial cells is observed, and dissociation and deformation of the endothelial cells occur. By means of contact of the vessel contents with the collagen, there is an additional activation of the coagulation system by factor XII possible. The changes of the epithelial lining and the wall adhering cells enhance the narrowing of the vessel lumen. Prestasis and occasionally stasis occur. One observes increased swelling of the endothelial and periendothelial cells, increased permeability of the vessel wall, passage of plasma and occasionally blood cells, especially erythrocytes, through the endothelium and massive microbleedings. While stasis is observed in the nutritive capillaries, in regions where arteriolar-venular shunts exist the flow continues. The systemic blood pressure may therefore remain unchanged during this phase, although the severe disturbances described occur in the capillary bed. Metabolic alterations, especially in the carbohydrate metabolism are mentioned.

Animals↗
PubMed1975

[Studies on the antigenicity of synthetic ACTH (beta1-24-corticotropin) in normal subjects (author's transl)].

9 healthy volunteers were subjected to a 3-week treatment with synthetic ACTH. Antibody response against beta1-24-corticotropin (Synacthen) was tested by passive transfer in the Prausnitz-Küstner reaction, complement fixation, passive hemagglutination and agar-gel diffusion. Failure of the healthy persons to produce reaginic or non-reaginic antibodies is compared titerature.

Adolescent↗