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Biomedical subjects

G Brandt

Publications and source records attributed to G Brandt.

At least 55 records · Page 3Linked to original sources
PubMed1978

[Minerals in normal and cirrhotic liver. The pathology of mineral dependent athrocytic liver cirrhosis].

Concentrations of iron, copper and zinc were measured in postmortem specimens of liver, muscle and brain tissue by atomic absorption spectrophotometry. Concentrations varied markedly in normal liver specimens from person to person, but not in other organ specimens. Copper concentrations in specimens from cirrhotic livers were normal in most cases, however at the upper limit of normal in about 20% of the cases evaluated. Concentrations of zinc and iron were lower than normal in cirrhotic livers. Mineral concentrations were higher by a factor of 10-20 in liver specimens of patients with hemochromatosis or M. Wilson than in normals. Iron overloading as a consequence of therapy (secondary hemochromatosis) and liver changes due to longtime artificially elevated plasma copper levels may imitate the adult form of the "classic" mineral storage diseases mentioned. Thus "athrocytotic" liver cirrhosis, being caused or accompanied by metal excess has to be considered as a polyetiological syndrome.

Adult↗
PubMed1977

Morphologic differential diagnosis of idiopathic cardiomyopathies.

Scanning electron microscopic examination of the myocardium in cardiomyopathies is a valuable complementary method beside light and transmissionelectron microscopy for the differential diagnosis of this rare disease. In two cases of congestive cardiomyopathy no marked alterations of the myocardial architecture could be found whereas in one case of nonobstructive hypertrophic cardiomyopathy myocardial cell alterations and structure disorders could be demonstrated in an almost stereologic view. The pathogenesis of heart failure in this disease was clearly shown. Similar changes were not observed in hearts without cardiomyopathy or in other forms of cardiac hypertrophy.

Autopsy↗
PubMed1977

[Mineral content of various organs in experimentally induced water-electrolyte imbalance].

Experimentally induced disorders of mineral metabolism are caused in rats in order to examine differences of electrolyte concentrations in several organs (heart muscle, skeletal muscle, liver, brain). Specimens are taken immediately after death or 24 hours after death. Water overload causes pointed deviations in mineral content of tissue in relation to the control group, deficiency of water results in only minimal changes. Hypotonic hydration increases the water content of skeletal muscle, the "cationic osmolality" is decreased in all organs. Overload with hypertonic solutions decreases water content of tissues, the concentrations of potassium and sodium are increased. Arrest of water intake for a few days leads to minimal changes in mineral concentrations in tissue although the organs seem to be "dry". In relation to specimen taken immediately after death the mineral content of tissues shows increased sodium and decreased potassium concentrations after 24 hours of death. The experimentally induced deviations of the organ mineral concentrations are preserved.

Animals↗
PubMed1976

[Diseases due to opportunist organisms as the cause of death in autopsy material (author's transl)].

Opportunist organisms become pathogenic as a result of reduced resistance of the host. In 1000 unselected autopsies, a "purulent" infectious disease was found to be the cause of death in 15.7% of the cases, an opportunist pathogenic organism being frequently demonstrated on culture. Morphologically, with a suitable histological technique, only opportunist fungi showed a characteristic substrate. Visceral mycoses with considerable significance for the cause of death were found in 1% of all cases. This emphasizes the opportunist pathogenic fungus as a potentially fatal causative organism which, however, cannot possibly cause an infection if the reservoir of pathogens is cleared prophylactically.

Adolescent↗
PubMed1976

[Myocardosis - myocardia - cardiomyopathy (author's transl)].

"Cardiomyopathy", a term formerly used for heart muscle disease of unknown aetiology, is at present applied to all myocardial diseases other than coronary-heart disease. This definition includes many different forms of metabolic disorders of heart muscle. Four manifestations of metabolic myocardial disease, differing in their aetiology and pathogenesis are distinguished: (1) "transport" myocardosis, (2) "arthrocytotic" myocardosis, (3) myocardia, and (4) idiopathic cardiomyopathy. They are differentiated by combined morphological and quantitative mineral examination. "Transport" myocardosis is the most common form and its particular aetiology can be further specified. Cause of death in patients with metabolic disorders often remains undiscovered even at autopsy. Combination of histological and quantitative mineral analysis of myocardium can further define the particular form.

Adolescent↗
PubMed1976

[Mineral content and morphology of heart muscle in different causes of death (author's transl)].

Mineral and water content of the right and left heart muscle were analyzed by atomic absorption spectrophotometry in 93 autopsy cases. Sodium, potassium, magnesium, and calcium concentrations were measured after acid digestion of tissues. Marked differences of the element distribution of both ventricles are seen constantly, although a significant correlation between water content and sodium as well as potassium and magnesium concentrations in both ventricles in seen. Comparing multiple causes of death (cardiac and non-cardiac) there are no differences in the postmortem mineral contents of heart muscle. Age-dependent correlations of mineral concentrations (as seen by Burger, 1960) were not detectable in this investigation. Postmortem mineral analyses of human heart muscles are excessively influenced by modern intensive care. Most of our cases had several causes of death, one of which was to be declared as the main cause of death in the necropsy record. Postmortem chemical mineral analysis of heart muscle can give an exact description of local variations and-in special cases-signs of general disorders of mineral metabolism, which are not detected by exclusively histologic investigations.

Adult↗
PubMed1976

Thoracic epidural analgesia-II: prolongation in the early postoperative period by continuous injection of 1.0% bupivacaine.

Sixteen patients were given thoracic epidural analgesia at the T5-T6 level with 2 ml of 1.0% bupivacaine solution plain for pain relief after upper abdominal surgery. In 13 cases the analgesia was prolonged by continuous injection of 1.0% bupivacaine for 24 or 48 h. Onset time and segmental spread of the analgesia are presented as well as segmental spread, intensity of the blockade, and peak expiratory flow rates during prolongation. Signs of tachyphylaxis were noticed, and also signs of accumulation of bupivacaine in plasma. A high incidence of urinary retention occurred. The method is not considered to be ideal for pain relief after upper abdominal surgery.

Adolescent↗
PubMed1976

[Postmortem demonstration of portal vein collateral circulation (author's transl)].

INTRODUCTION: Postmortem investigation of esophageal varices and the portal system is difficult, because veins are collapsed at autopsy. The demonstration of varices is possible by illumination of the isolated mucous membrane or by puncturing esophageal varices and filing them with different materials. MATERIAL AND METHODS: We use a 15% aqueous gelatine solution (if needed with additional barium sulfate for x-ray examination) which is supplemented by 40% formaldehyde (40 ml in 1 1 gelatine solution). The superior mesenteric vein is catheterized and filled by a clyster-pump. RESULTS: The mixture of gelatine and formaldehyde hardens within a few minutes. The autopsy is delayed only about half an hour. Within this time the portal system is well outlined. This method can show exactly the drainage of the portal system into the inferior vena cava. In cases of portocaval shunt or of esophageal transsection the result of the operation can be verified. The localization of the bleeding source of esophageal varices can be demonstrated by escape of the filling mass.

Autopsy↗
PubMed1975

[Pancreatic islets, plasma glucagon and renal calcification in rats fed various diets. Results of a pilot study (author's transl)].

Rats fed abnormally composed isocaloric diets during 21 days (low magnesium, atherogenous, high in proteins or carbohydrates) develop a mean increase in total number of pancreatic A cells, a significant increase of A/B ratio (atherogenous), and hyperglucagonemia in most of the groups under study. Histologic examination reveals calcification most marked in animals under low magnesium and atherogenous diets. They are only scarce following high protein diet; a normal or carbohydrate rich diet nullifies this phenomenon. Independent of the morphologic and functional state of the islets, supplementation by argining and histidine of normal chow is followed by a certain degree of renal calcification. Lowered urinary magnesium and calcium and elevated urinary sodium and phosphate together with a tendency toward hypercalcemia point to stimulation of parathyroids during malnutrition. Absolute or relative hyperglucagonemia must be considered the main causstive factor.

Animals↗