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Biomedical subjects

R Seelig

Publications and source records attributed to R Seelig.

At least 55 records · Page 3Linked to original sources
PubMed1980

[Endotoxinemia in acute pancreatitis (author's transl)].

In a clinical study the question was asked, whether endotoxinemia of intestinal origin accompanying acute pancreatitis would influence decisively the course of this disease. In 21 of 32 patients with acute pancreatitis endotoxinemia could be diagnosed by the Limulus test, in this group 9 patients died. In the group of patients without endotoxinemia however no patient died. Extrapancreatic complications as for instance coagulation defects, renal failure, and pulmonary changes were predominant in the patients with endotoxinemia. From these findings the conclusion is made, that endotoxinemia occurs frequently in acute pancreatitis and influences decisively the course of the disease.

Acute Disease↗
PubMed1978

Complement system in sodium taurocholate pancreatitis in the rat.

The role of the complement system was studied in Na-taurocholate pancreatitis in rats. Complement activity (CH 50) was determined at various times in the course of pancreatitis. Immediately after induction of acute pancreatitis, serum complement activity declined and massive C 3 deposits could be detected in the vicinity of acinar necroses and necrobioses. After a phase of recovery three to six hours postoperatively a second complement consumption occurred. Lethality rate increased as serum complement activity fell below 50% of preoperative values. The degree of C 3 deposition increased up to six hours. Decline of serum complement activity and deposition within the pancreas seemed to be correlated with histologically demonstrable tissue lesion. The first decline of complement activity in serum is thought to be caused by liberation of complement activating substances within the pancreas due to the detergent action of Na-taurocholate itself. The second decline, however, may be due to the liberation of complement activating and/or destroying enzymes into the blood stream.

Animals↗
PubMed1978

On the pathogenesis of galactosamine hepatitis. Indications of extrahepatocellular mechanisms responsible for liver cell death.

In order to evaluate the pathogenesis of galactosamine hepatitis, the action of galactosamine on mast cells, and alteration in the complement system suring the course of this experimental injury were studied. It has been previously demonstrated that rat livers after colectomy are refractory to galactosamine-induced liver cell necrosis and inflammation. For this reason colectomized animals were used to see whether the biochemical alterations produced by this aminosugar and thought to be responsible for cell death developed. Results showed: 1. galactosamine potently degranulates mast cells in vivo and in vitro, 2. the complement system is a) activated during the course of galactosamine hepatitis, probably by circulating endotoxins, and b) is essential for liver cell death in galactosamine hepatitis, and 3. colectomy does not prevent biochemical changes known to occur during galactosamine metabolism. It is concluded that death of galactosamine-injured liver cells is triggered by extrahepatocellular mechanisms, which lead ultimately to an activated complement system by endotoxins. It is postulated that related mechanism may also occur in viral hepatitis and in fulminant hepatic failure in man.

Animals↗
PubMed1978

Synergistic action of hepatocyte membrane defect and activated complement system in liver cell death--an experimental approach to fulminant hepatic failure.

The hypothesis was tested whether under the presence of a membrane defect of hepatocytes an activation of the complement system leads to massive liver cell necrosis. Low doses of galactosamine (50, 100, and 200 mg/kg) were administered to rats with and without an additional i.v. injection of sublethal doses of endotoxin (1.5 mg/kg). The latter was done in order to activate the complement system via the C3-bypath. Neither after doses of 50 mg/kg and 100 mg/kg nor after an additional administration endotoxin liver cell necrosis were observed. A dose of 200 mg/kg led to moderate liver cell necrosis, and when administered with endotoxin fulminant hepatic necrosis developed. The explanation was given that only after 200 mg/kg alterations of hepatocytes membranes were present, which prepare liver cells for complement mediated hepatocytolysis. In rats to which 1 g/kg galactosamine was given in addition to endotoxin it was demonstrated by immunohistology that the third component of complement was already fixed on hepatocyte plasma membranes at hour 3 and was accumulated within areas of necrotic liver parenchymal cells at hour 12. Thus, liver cell death is suggested as complement mediated if the membranes are altered. Clinical implications are given in concern of fulminant hepatic failure and an approach to effective treatment regims.

Animals↗
PubMed1977

[Immunohistological investigations and complement analysis in immunological diseases (author's transl)].

Immunohistological techniques and complement analysis are essential methods of investigation in the diagnosis of immunologically induced disease processes today. Immunopathogenesis or participation of immunological reactions in inflammatory processes such as glomerulonephritis, dermatitis, arthritis for example, can be detected through immunohistological demonstration of deposits of immunoglobulin and complement in biopsy material. Numerous antibodies against tissue and infection pathogens can be demonstrated in the serum by indirect immunofluorescence techniques.

Antibodies↗
PubMed1977

[Nephrotic syndrome presumable caused by an complex glomerulonephritis (author's transl)].

The nephrotic syndrome presumably caused by an immune complex glomerulonephritis constitutes a major side effect attendant upon chronic administration of penicillamine. The possible induction of an immune-complex glomerulonephritis by penicillamine and its further development after stopping the drug was investigated in rats. --60 rats were fed perorally 2000 mg D-Penicillamine/kg BW/die resp. for a period of 8--44 days. Following unilateral nephrectomy the animals were observed for further 5 weeks. --Dependent to the time of penicillamine application there was an increasing deposition of IgG and C3 in a granular pattern along the glomerular basement membrane and within the mesangium. The IgG deposits initially were focal and segmental later on diffuse and global in distribution. 5 weeks after stopping the penicillamine the immune globulin deposits had disappeared completely or at least in part as did the mild focal glomerulonephritis and the moderate proteinuria which developed in some animals after a 44 day treatment with penicillamine. --The results confirm the hitherto presumed immune complex pathogenesis of the penicillamine induced nephropathy. The disappearance of the immunoglobulins deposited and of proteinuria stopping penicillamine alludes the good prognosis of this kind of nephropathy.

Animals↗
PubMed1976

Complement-mediated acinar cell necroses in pancreatitis induced by basement membrane antibodies.

To study the role of the serum complement system in the early necrosis of acinar cells an acute pancreatitis was produced by injection of basement membrane antibodies into the pancreatic duct of mice and rats. In all animals deposition of complement (C3) and antibasement membrane IgG could be observed in an identical position within areas of acinar cell necrosis. The extent of parenchymal damage and the intensity of complement deposits corresponded to the injected dose of antibodies. The importance of cytolytically active complement components (C5-9) was demonstrated in congenitally C5-defective old line mice which did not show typical centrolobular necroses 1 hr after intraductal injection of antibodies. However, the normocomplementemic mice developed extensive necroses of acinar cells. The results support the hypothesis of a complement-induced acinar cell necrosis in acute pancreatitis.

Acute Disease↗
PubMed1976

Acute pancreatitis induced by intrapancreatic complement activation in the rat.

Acute necrotizing pancreatitis was introduced in rats by intrapancreatic complement activation. As an immunopathogenetic model for complement activation an intrapancreatic Arthus reaction was produced by intraductal injection of rabbit IgG into sensitized animals. Antibody independent complement activation was accomplished by intraductal injection of particulated inulin and cobra venom factor resp. As shwon by histological and immunohistological examination the development of acinar cell necroses and the consecutive inflammatory reaction followed an identical course in all three models. The generation of cytolytically active complement is suggested to be the common link in the formal pathogenesis of the initial membrane demage of the acinar cells which enables its autodigestion by pancreatic enzymes. The region of the initial complement activation within the pancreas but not the mode of its activation (by immunological or non-immunological processes) determine the topography of acinar cell necroses and connective tissue proliferation.

Acute Disease↗
PubMed1975

[Immunohistological findings in diffuse mesangial sclerosis associated with the nephrotic syndrome of infancy (author's transl)].

A 10-month-old infant developed a steroid resistant nephrotic syndrome. The renal biopsy revealed diffuse mesangial sclerosis of the glomerula. The child died from interstitial pneumonia 3 months after onset of the renal symptoms. Post mortem, the glomerular changes were diffuse but prominent in certain segments of the glomeruli. The immunohistological examination showed granular deposits of IgM and C3 in the mesangium and in the subendothelial region of the basement membrane. These findings are compatible with the hypothesis that diffuseal sclerosis is caused by glomerular deposition of immune complexes.

Autopsy↗
PubMed1975

[Influence of autolysis on the immunohistology of tissue-bound immunglobulins in the kidney (author's transl)].

The influence of autolysis on the immunhistological detectability and the immunological properties of tissue-bound basement membrane antibodies were investigated in the rat kidney. The immunhistological demonstration of antibodies was not affected up to 3 days post mortem. The disturbing autofluorescence of the autolytic tissue can be avoided by using peroxydase labeled antibodies. Basement-membrane antibodies that were eluted from the kidneys after an autolysis period of 2 days showed a homogenous linear deposition in kidney basement membrane after reinjection into normal rats. Their antibody properties were not affected.

Animals↗
PubMed1975

Antibodies reacting with the glomerular mesangium. Isolation and immunopathology.

Antigens of porcine lung were prepared by homogenization and ultrasonic treatment of lung tissue. The antigens were digested by collagenase and trypsin and chromatographed on Sephadex G 200. After immunization of rabbits with certain fractions of the chromatographed material, antibodies could be obtained in rabbits which fixed in vitro and in vivo in the glomerular mesangium of rats, hogs and the human, but not in the basement membrane of glomeruli of these species. Following intravenous injection into rats, the antibodies could be observed in the mesangial area without an apparent loss of antigenicity for 55 days. While 5 days after the application of 20 mg of the anti-mesangial IgG-preparation, there were no glomerular changes histologically demonstrable, after 55 days small amounts of rat-IgG could be demonstrated histochemically within the mesangium. Deposits of rat-complement (C3) could not be demonstrated with certainty. Severe morphological lesions were absent. Rats injected with the same doses of antibody and simultaneously immunized with rabbit-IgG showed a substantially greater deposit of autologous rat-IgG and rat-complement within the mesangial area after 55 days. By histological examination focal and segmental scleroses of the mesangium were determined. A significant pathological proteinuria did not occur. The present model constitutes a new possibility for studying the function of the glomerular mesangium.

Animals↗
PubMed1975

The serum complement system--a mediator of acute pancreatitis.

The role of the complement system in the initial membrane lesion of acute pancreatitis was investigated. In the experimental sodium-taurocholate pancreatitis of the rat a sudden and steady decline of serum complement was observed. The deposition of C3 component of complement in acute pancreatitis could be demonstrated by immunofluorescence. To rule out mere deposition or activation of complement in the interstitial exsudative fluid, single acinar cells of rat and rabbit pancreatic tissue were prepared and transfered to culture medium. In contrast to heat inactivated serum and C6 deficient serum these cells were lysed by trypsin activated fresh serum. Consequently, an acute pancreatitis could be induced by activating exclusively the complement system by injection of cobra venom factor into the pancreatic duct of rats. The activated complement system is thought to be responsible for initial membrane lesion in exsudative inflammation, as could be shown in acute pancreatitis.

Acute Disease↗