scholarly journals STUDIES ON THE GENERALIZED SHWARTZMAN REACTION

1952 ◽  
Vol 96 (6) ◽  
pp. 605-624 ◽  
Author(s):  
Lewis Thomas ◽  
Robert A. Good
Keyword(s):  
Nitrogen Mustard ◽  
Lethal Effect ◽  
Optimal Time ◽  
Time Interval ◽  
Renal Lesion ◽  
Protein Nitrogen ◽  
Local Skin ◽  
Cortical Necrosis ◽  
Before And After ◽  
Shwartzman Reaction

Certain factors involved in the production of the generalized Shwartzman reaction with meningococcal toxin in rabbits were investigated. The optimal amounts of toxin for the preparing and provoking injections, and the optimal time interval between injections were determined. Under suitable conditions of dosage and timing, bilateral cortical necrosis of the kidneys was produced in a high proportion of animals. When excessive amounts of toxin were used for preparation the incidence of the reaction was reduced. Animals undergoing the generalized Shwartzman reaction became severely prostrated within several hours after the provoking injection of toxin. The renal lesion became fully developed within 24 hours, and its occurrence was associated with a rise of the blood non-protein nitrogen. Edema and petechial hemorrhages in the ears were observed in rabbits with advanced renal lesions. The earliest change in the kidneys in the generalized Shwartzman reaction was the appearance of homogeneous, eosinophilic material, resembling fibrinoid, within the lumen of the glomerular capillaries. Occlusion of the capillaries by this material was regarded as the cause of subsequent tubular necrosis in the renal cortex. The material appeared to be derived from the blood, rather than from the capillary walls. Cortisone enhanced the lethal effect of a single, large dose of meningococcal toxin, as well as causing bilateral renal cortical necrosis. The generalized Shwartzman reaction produced by two injections of toxin was aggravated by cortisone and ACTH. Profound polymorphonuclear leukopenia was produced by both the preparing and provoking injections of toxin. When leukopenia was produced before the preparing injection of toxin, by treatment with nitrogen mustard, the generalized Shwartzman reaction was inhibited. During the intervals before and after leukopenia, and when leukopenia was prevented by shielding the femoral bone marrow from the action of nitrogen mustard, no inhibition of the generalized Shwartzman phenomenon was demonstrable. Various colloidal and particulate materials, which are capable of provoking the local skin Shwartzman reaction when injected intravenously, failed to provoke the generalized Shwartzman reaction. A working hypothesis was set up to account for certain events in the generalized Shwartzman reaction.

scholarly journals THE EFFECT OF CORTISONE ON THE SHWARTZMAN REACTION

1952 ◽  
Vol 95 (4) ◽  
pp. 409-428 ◽  
Author(s):  
Lewis Thomas ◽  
Robert A. Good ◽  
Keyword(s):  
Nitrogen Mustard ◽  
Intradermal Injection ◽  
Renal Lesion ◽  
Cortical Necrosis ◽  
Intravenous Injections ◽  
Pretreatment Period ◽  
Shwartzman Reaction ◽  
Systemic Symptoms ◽  
Schiff Reaction ◽  
Glomerular Capillaries

1. Cortisone, in a dose of 25 mg. daily and with a pretreatment period of 3 days, in rabbits weighing 1 to 1.5 kilos, did not inhibit the dermal Shwartzman reaction produced by meningococcal or S. marcescens toxin. 2. In cortisone-treated rabbits, a single intradermal injection of toxin produced a primary reaction of hemorrhage and necrosis in the skin at the injected site. This lesion resembled the Shwartzman reaction in its gross and histological appearance. 3. Like the Shwartzman reaction, the primary hemorrhagic reaction in cortisone-treated rabbits was prevented by nitrogen mustard, and the preventive effect of nitrogen mustard was partly eliminated when the femoral marrow was protected against the latter agent. 4. A single intravenous injection of meningococcal or S. marcescens toxin, in cortisone-treated rabbits, was followed by bilateral cortical necrosis of the kidneys in the majority of instances. The renal lesions, as well as hemorrhages in the lungs, spleen, liver, and gastrointestinal tract, resembled the lesions of the generalized Shwartzman reaction. Histologically, the glomerular capillaries in both types appeared to be occluded by homogeneous, eosinophilic material which showed a strongly positive Schiff reaction. 5. The renal lesion following a single injection of toxin in cortisone-treated animals, and that following two intravenous injections in the generalized Shwartzman reaction, were both completely prevented by nitrogen mustard. This effect of nitrogen mustard was inhibited when the femoral marrow was protected against the latter agent. 6. The injection of S. marcescens toxin into the skin of normal rabbits did not cause systemic symptoms, nor was it possible to provoke the generalized Shwartzman reaction by this route. In cortisone-treated rabbits, a similar intradermal injection was regularly followed by the development of bilateral cortical necrosis of the kidneys, indicating that absorption of toxin from the skin occurred in these animals. 7. Possible mechanisms to account for the observations are discussed. The authors are obliged to Professor James R. Dawson for many helpful suggestions during the course of this investigation.

scholarly journals STUDIES ON THE GENERALIZED SHWARTZMAN REACTION

1952 ◽  
Vol 96 (6) ◽  
pp. 625-641 ◽  
Author(s):  
Robert A. Good ◽  
Lewis Thomas
Keyword(s):  
Intravenous Injection ◽  
Trypan Blue ◽  
Nitrogen Mustard ◽  
Skin Lesions ◽  
Intradermal Injection ◽  
Cortical Necrosis ◽  
Single Intravenous Injection ◽  
Shwartzman Reaction ◽  
Kidney Lesions ◽  
Local Shwartzman Reaction

Intravenous injection of thorotrast or trypan blue rendered rabbits susceptible to the production of bilateral cortical necrosis of the kidneys by a single intravenous injection of small amounts of meningococcal or Serratia marcescens toxin. This reaction was not produced when thorotrast or trypan blue were injected after toxin had been given. A single intradermal injection of toxin produced hemorrhagic skin lesions resembling the local Shwartzman reaction in rabbits given thorotrast 6 hours previously. These animals also developed bilateral cortical necrosis of the kidneys. When the order of injection was reversed, and thorotrast given after toxin, neither skin nor kidney lesions occurred. The skin and kidney lesions in thorotrast-treated rabbits were, like the local and generalized Shwartzman reactions, completely prevented by treatment with nitrogen mustard, in doses sufficient to produce polymorphonuclear leukopenia. The significance of these reactions, and their relationship to the previously described response to toxin in cortisone-treated rabbits, are discussed.

scholarly journals STUDIES ON THE GENERALIZED SHWARTZMAN REACTION

1953 ◽  
Vol 97 (6) ◽  
pp. 871-888 ◽  
Author(s):  
Robert A. Good ◽  
Lewis Thomas
Keyword(s):  
Intravenous Injection ◽  
Essential Role ◽  
Vascular Occlusion ◽  
Lethal Effect ◽  
Intradermal Injection ◽  
Cortical Necrosis ◽  
Hemorrhagic Necrosis ◽  
Shwartzman Reaction ◽  
Previously Treated ◽  
Glomerular Capillaries

In order to explore the hypothesis that the occurrence of thrombosis of small blood vessels is an essential stage in the development of the local and generalized Shwartzman reactions, the effect of heparin was studied. Aqueous heparin, administered intravenously, and "depot" heparin, injected subcutaneously, prevented completely the occurrence of the local and generalized Shwartzman phenomena. The amounts of heparin required for protection were similar to the amounts required to produce sustained incoagulability of the blood of rabbits for a period of at least 4 hours. The local and generalized Shwartzman reactions were prevented when heparin was given at the time of provocation, but not when heparin was administered during the period of preparation. Heparin prevented the development of bilateral cortical necrosis of the kidneys following a single intravenous injection of meningococcal toxin in rabbits previously treated with cortisone or thorotrast. Hemorrhagic necrosis of the skin which follows an intradermal injection of toxin in thorotrast-treated rabbits was also prevented by heparin. Provocation of the dermal Shwartzman reaction with glycogen, saline suspension of rabbit liver, and human serum was prevented by treatment with heparin. Heparin itself, in the preparations and dosages used, had no consistent effect on either white blood cell or platelet counts. Heparin had no effect on the occurrence of polymorphonuclear leukopenia which follows an intravenous injection of meningococcal toxin. Treatment with heparin did not interfere with the lethal effect of single, large doses of meningococcus toxin. In animals in which bilateral cortical necrosis of the kidneys was prevented by heparin, occlusion of the glomerular capillaries by "fibrinoid" material did not occur. These observations support the concept that vascular occlusion plays an essential role in the development of the local and generalized Shwartzman reactions.

scholarly journals STUDIES ON THE GENERALIZED SHWARTZMAN REACTION

1953 ◽  
Vol 97 (5) ◽  
pp. 751-766 ◽  
Author(s):  
Lewis Thomas ◽  
Floyd W. Denny ◽  
Joan Floyd
Keyword(s):  
Time Interval ◽  
Time Of Death ◽  
Fibrinoid Necrosis ◽  
Optimal Conditions ◽  
Cortical Necrosis ◽  
Intravenous Injections ◽  
Hemorrhagic Necrosis ◽  
Group A ◽  
Shwartzman Reaction ◽  
Systemic Infections

Cutaneous and systemic infections of rabbits by Group A streptococci bring about a state of preparation for, respectively, the local and generalized Shwartzman reactions, produced by intravenous injection of meningococcal or S. marcescens toxin. With maximal systemic streptococcal infections, the lesions of the generalized Shwartzman reaction do not differ from those caused by two successive intravenous injections of Gram-negative bacterial toxins. The characteristic lesions of the reaction are bilateral cortical necrosis of the kidneys, hemorrhagic necrosis in the lungs, liver, and spleen, and myofiber necrosis in the myocardium. Under optimal conditions involving the dosages of streptococci and toxin, and the time interval between the injections, a new lesion consisting of necrosis and the accumulation of fibrinoid material in the walls of the coronary arteries occurred in approximately 50 per cent of animals within 48 hours after the injection of meningococcal toxin. Fibrinoid necrosis was not observed in the arteries of tissues other than the heart. It did not occur in control rabbits injected with streptococci alone or toxin alone, nor in animals with the generalized Shwartzman reaction produced by two intravenous injections of toxin. Streptococcal bacteriemia was present at the time of death in one-third of the animals with fibrinoid necrosis. In one animal, a group of bodies resembling cocci in chains was seen within the wall of a coronary artery with fibrinoid necrosis. A series of photomicrographs to illustrate the pathological changes in the hearts and kidneys of streptococcus-infected rabbits subjected to the Shwartzman reaction is presented.

Effect of Anticoagulating and Non-Anticoagulating Concentrations of Heparin on the Generalized Shwartzman Reaction

1970 ◽  
Vol 24 (01/02) ◽  
pp. 136-145 ◽  
Author(s):  
J. J Corrigan
Keyword(s):  
Dose Group ◽  
Blood Platelets ◽  
Coagulation Factors ◽  
Renal Lesion ◽  
Fibrin Deposition ◽  
Cortical Necrosis ◽  
Renal Cortical Necrosis ◽  
Intravenous Injections ◽  
Shwartzman Reaction

SummaryRabbits given 2 properly spaced intravenous injections of bacterial endotoxin develop bilateral renal cortical necrosis (generalized Shwartzman reaction - gSr). This renal lesion is the result of fibrin deposition secondary to diffuse intravascular clotting (DIC). Using this experimental model, the effect of anticoagulating (large) and non- anticoagulating (small) concentrations of heparin on the changes in blood platelets, plasma coagulation factors II, V, VIII and fibrinogen during the production of renal cortical necrosis was studied. The data demonstrate that all amounts of heparin given during, but not after, the period of intravascular clotting reduced the frequency of renal cortical necrosis. Anticoagulating concentrations completely prevented the renal lesion. Non-anticoagulating amounts could reduce the frequency of the renal lesions, but this effect was not predictable or consistent. Coagulation studies in the large dose group revealed thrombocytopenia reduced factors II, V, and VIII but no fibrinogen consumption. These findings suggest that heparin inhibits the formation of fibrin in vivo, thereby preventing the formation of renal cortical necrosis. The coagulation data in the small dose group differed in that fibrinogen consumption did occur. The possible explanations for the phenomenon were discussed.

Studies on the Pathogenesis of the Generalized Shwartzman Reaction

1964 ◽  
Vol 12 (02) ◽  
pp. 462-470 ◽  
Author(s):  
F Rodríguez-Erdmann
Keyword(s):  
Fibrinolytic System ◽  
Factor V ◽  
Morphological Pattern ◽  
Cortical Necrosis ◽  
G Factor ◽  
Conventional Form ◽  
Renal Cortical Necrosis ◽  
Shwartzman Reaction

SummaryAnimals treated in the conventional form to elicit the generalized Shwartzman reaction (gSr) by means of properly spaced injections of endotoxin develop an abrupt consumption of the plasmatic factors of the clotting mechanism, as demonstrated by the reduction of the activity of prothrombin and Ac-G (factor V). These animals show ultimatly characteristic morphological pattern: bilateral cortical necrosis of the kidney. Rabbits treated four hours after the second (‘‘provocative”) endotoxin injection with streptokinase (Varidase/Lederle) in order to activate the fibrinolytic system failed to develop the renal cortical necrosis, but their prothrombin and Ac-G (factor V) level decreased abruptly.Through indirect deduction the intravascular presence of thrombin-like activity is accepted four hours after the “provocative” endotoxin injection.

Temporal dynamics of encrusting communities during the Late Devonian: a case study from the Central Devonian Field, Russia

Paleobiology ◽  
2017 ◽  
Vol 43 (4) ◽  
pp. 550-568 ◽  
Author(s):  
Michał Zatoń ◽  
Tomasz Borszcz ◽  
Michał Rakociński
Keyword(s):  
Temporal Dynamics ◽  
Small Sample ◽  
Time Interval ◽  
Faunal Turnover ◽  
Central Devonian Field ◽  
Before And After ◽  
Substrate Size ◽  
Mass Extinction Event ◽  
Diversity Dynamics

AbstractIn this study we focused on the dynamics of encrusting assemblages preserved on brachiopod hosts collected from upper Frasnian and lower Famennian deposits of the Central Devonian Field, Russia. Because the encrusted brachiopods come from deposits bracketing the Frasnian/Famennian (F/F) boundary, the results also shed some light on ecological differences in encrusting communities before and after the Frasnian–Famennian (F-F) event. To explore the diversity dynamics of encrusting assemblages, we analyzed more than 1300 brachiopod valves (substrates) from two localities. Taxon accumulation plots and shareholder quorum subsampling (SQS) routines indicated that a reasonably small sample of brachiopod host valves (n=50) is sufficient to capture the majority of the encrusting genera recorded at a given site. The richness of encrusters per substrate declined simultaneously with the number of encrusting taxa in the lower Famennian, accompanied by a decrease in epibiont abundance, with a comparable decrease in mean encrustation intensity (percentage of bioclasts encrusted by one or more epibionts). Epibiont abundance and occupancy roughly mirror each other. Strikingly, few ecological characteristics are correlated with substrate size, possibly reflecting random settlement of larvae. Evenness, which is negatively correlated with substrate size, shows greater within-stage variability among samples than between Frasnian and Famennian intervals and may indicate the instability of early Famennian biocenoses following the faunal turnover. The occurrence distribution of encrusters points to nonrandom associations and exclusions among several encrusting taxa. However, abundance and occupancy of microconchids remained relatively stable throughout the sampled time interval. The notable decline in abundance (~60%) and relatively minor decline in diversity (~30%) suggest jointly that encrusting communities experienced ecological collapse rather than a major mass extinction event. The differences between the upper Frasnian and lower Famennian encrusting assemblages may thus record a turnover associated with the F-F event.

scholarly journals THE TOTAL NON-PROTEIN NITROGEN OF THE BLOOD IN NEPHRITIS AND ALLIED CONDITIONS

1913 ◽  
Vol 18 (3) ◽  
pp. 228-241 ◽  
Author(s):  
Clifford B. Farr ◽  
J. Harold Austin
Keyword(s):  
Cardiovascular Disease ◽  
Clinical Study ◽  
Clinical Improvement ◽  
Clinical Laboratory ◽  
Nitrogen Retention ◽  
Renal Lesion ◽  
Normal Range ◽  
Protein Nitrogen ◽  
Chronic Nephritis

1. In a series of non-nephritic individuals the total non-protein nitrogen of the blood, determined by Folin's method, was found to lie between 15 and 43 milligrams per 100 cubic centimeters. From 50 to 60 per cent. of this was in the ammonia-urea fraction. 2. In cardiovascular disease with renal congestion, but without other renal lesion, there was no evidence of increase of non-protein nitrogen in the blood, nor of alteration of the ammonia-urea percentage. 3. In chronic nephritis with marked albuminuria and edema there was very little, if any, increase or alteration. 4. In chronic nephritis with hypertension the non-protein nitrogen was definitely increased, ranging from 40 to 180 milligrams per 100 cubic centimeters of blood. The percentage of the ammonia-urea fraction was usually higher than in non-nephritic cases. 5. Cases showing high non-protein nitrogen values were subject to rapid fluctuations in these values in the course of a few days. As a rule, clinical improvement was associated with a fall of the non-protein nitrogen figures to nearer the normal range. 6. Uremia was almost always accompanied by an increase of non-protein nitrogen in the blood, but no constant relation could be established between the degree of increase and the tendency to uremia. 7. Our cases have not yet been followed for a long enough period to admit of conclusions as to the possible relation between the degree of non-protein nitrogen retention and ultimate prognosis. 8. We believe this method to be a valuable aid in the clinical study of nephritis and that it can be readily carried out in any well equipped clinical laboratory.

scholarly journals Evaluation of color stability of different temporary restorative materials

2015 ◽  
Vol 44 (5) ◽  
pp. 262-267 ◽  
Author(s):  
José Vitor Quinelli Mazaro ◽  
Luiz Miguel Minani ◽  
Adriana Cristina Zavanelli ◽  
Caroline Cantieri de Mello ◽  
Cleidiel Aparecido Araújo Lemos
Keyword(s):  
Storage Time ◽  
Color Change ◽  
Artificial Saliva ◽  
Color Stability ◽  
Time Interval ◽  
Acrylic Resins ◽  
Significant Difference ◽  
Restorative Materials ◽  
Before And After ◽  
Level Of Significance

AbstractIntroductionTemporary restorative materials are widely used, however, little is know about their color stability.Objectiveto evaluate the color stability of the following temporary restorative materials: acrylic and bis-acrylic resins after immersion in pigmenting solutions for different periods of storage.Material and methodFour materials were tested (Dêncor/Clássico, Protemp 4/3M ESPE; Structur 2 SC/Voco; Luxatemp AM Plus/DMG) and 30 test specimens (15 mm in diameter and 2 mm thick) per material were fabricated. They were divided according to the storage medium (artificial saliva, saliva + cola type soda, and saliva + coffee) and storage time intervals (2, 5, 7 and 15 days). Color measurements were made before and after immersions, with use of a spectrophotometer, by means of the CIE L*a*b* system. The data were analyzed by the analysis of variance and the Tukey Test, at a level of significance of 5%.ResultAcrylic resin presented greater color stability in comparison with bis-acrylic resins (p<0.001). When bis-acrylic resins were compared no significant difference was observed between the resins Structur and Luxatemp (p=0.767). As regards solutions tested, coffee showed the highest color change values (p<0.001), and the longer the storage time interval, the greater was the color change in all the temporary restorative materials analyzed (p<0.001).ConclusionAcrylic resin presented greater color stability in comparison with bis-acrylic resins (p<0.001). Coffee caused the greatest color change, and immersion time was determinant in color stability of the temporary materials analyzed.

scholarly journals Oral atorvastatin therapy increases nitric oxide-dependent cutaneous vasodilation in humans by decreasing ascorbate-sensitive oxidants

2011 ◽  
Vol 301 (3) ◽  
pp. R763-R768 ◽  
Author(s):  
Lacy A. Holowatz ◽  
W. Larry Kenney
Keyword(s):  
Nitric Oxide ◽  
Local Heating ◽  
Oxidant Stress ◽  
Microvascular Dysfunction ◽  
Local Skin ◽  
Cutaneous Vasodilation ◽  
Before And After ◽  
Atorvastatin Therapy ◽  
Oxide Synthase ◽  
Cutaneous Vascular Conductance

Elevated low-density lipoproteins (LDL) are associated with cutaneous microvascular dysfunction partially mediated by increased arginase activity, which is decreased following a systemic atorvastatin therapy. We hypothesized that increased ascorbate-sensitive oxidant stress, partially mediated through uncoupled nitric oxide synthase (NOS) induced by upregulated arginase, contributes to cutaneous microvascular dysfunction in hypercholesterolemic (HC) humans. Four microdialysis fibers were placed in the skin of nine HC (LDL = 177 ± 6 mg/dl) men and women before and after 3 mo of a systemic atorvastatin intervention and at baseline in nine normocholesterolemic (NC) (LDL = 95 ± 4 mg/dl) subjects. Sites served as control, NOS inhibited, L-ascorbate, and arginase-inhibited+L-ascorbate. Skin blood flow was measured while local skin heating (42°C) induced NO-dependent vasodilation. After the established plateau in all sites, 20 mM ≪ngname≫ was infused to quantify NO-dependent vasodilation. Data were normalized to maximum cutaneous vascular conductance (CVC) (sodium nitroprusside + 43°C). The plateau in vasodilation during local heating (HC: 78 ± 4 vs. NC: 96 ± 2% CVCmax, P < 0.01) and NO-dependent vasodilation (HC: 40 ± 4 vs. NC: 54 ± 4% CVCmax, P < 0.01) was reduced in the HC group. Acute L-ascorbate alone (91 ± 5% CVCmax, P < 0.001) or combined with arginase inhibition (96 ± 3% CVCmax, P < 0.001) augmented the plateau in vasodilation in the HC group but not the NC group (ascorbate: 96 ± 2; combo: 93 ± 4% CVCmax, both P > 0.05). After the atorvastatin intervention NO-dependent vasodilation was augmented in the HC group (HC postatorvastatin: 64 ± 4% CVCmax, P < 0.01), and there was no further effect of ascorbate alone (58 ± 4% CVCmax, P > 0.05) or combined with arginase inhibition (67 ± 4% CVCmax, P > 0.05). Increased ascorbate-sensitive oxidants contribute to hypercholesteromic associated cutaneous microvascular dysfunction which is partially reversed with atorvastatin therapy.

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