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D D Reichenbach

Publications and source records attributed to D D Reichenbach.

At least 37 records · Page 2Linked to original sources

Infective endocarditis associated with cell wall-deficient bacteria. Electron microscopic findings in four cases.

Although cell wall-deficient bacteria have been isolated in vitro from cases of endocarditis, no pathogenic role has been established for these forms in human disease. One criterion difficult to satisfy is the demonstration of these variants in human tissue, and electron microscopic documentation has not been reported. Cardiac valvular vegetations from four cases of endocarditis were examined by electron microscopy because of unusual histologic features of minimal inflammation and organization and small organisms that stained poorly by Gram stain. Although cell wall-complete bacteria were identified in the specimens, each showed the presence of cell wall-deficient forms within the vegetations; these variants predominated in three cases. Since manifestations of infective endocarditis were present in three cases and conventional cultures were negative, the evidence indirectly suggests a pathogenic role for these aberrant bacteria in human disease.

Adult↗

Pathology of the heart in sudden cardiac death.

Clinical and pathologic changes in 87 patients who could not be resuscitated from an episode of sudden cardiovascular collapse are described and compared with observations from patients in the same community who were successfully resuscitated from ventricular fibrillation. Findings in patients who died suddenly generally did not differ when the patients were groups by electrocardiographic rhythm on arrival of the mobile coronary aid unit. The pathologic changes of acute thrombosis and recent myocardial infarction did not occur with sufficient frequency in the entire group to be considered causally related to the sudden collapse, occurring in 10 and 5 percent of cases, respectively. Although most patients had evidence of obstructive coronary disease and old myocardial infarction, 8 percent had no significant vascular disease, acute thrombosis, myocarditis or valve disease that might be implicated as a factor in sudden death. There was no relation between age and severity of obstructive coronary disease or frequency of old myocardial infarction in patients who died suddenly. Complete atherosclerotic occlusion in one or more coronary vessels occurred in 51 of 87 (59 percent) and old myocardial infarction in 48 of 87 (55 percent). Although the mean age of this autopsy population was similar to that of all patients in the community who have had ventricular fibrillation on arrival of the aid unit, the nonsurvivors had a greater incidence of myocardial infarction and symptomatic heart disease (73 of 87) than did survivors. Comparison of this autopsy group with persons from the community who were resuscitated from ventricular fibrillation and subsequently had coronary angiograms indicates that the severity of coronary stenosis does not distinguish between survivors and nonsurvivors of an episode of ventricular fibrillation and suggests that other factors influence the outcome of an episode of ventricular fibrillation.

Adult↗

Extraneuronal monoamine oxidase in rat heart: biochemical characterization and electron microscopic localization.

Monoamine oxidase (MAO) increases in an age-weight relationship in the hearts of male rats. Accumulation of MAO is not related to the activities of such mitochondrial enzymes as succinic dehydrogenase or cytochrome oxidase which do not change with age. Our previous experiments, utilizing serotonin as a substrate, have determined that cardiac MAO in the young rat does not change after chemical sympathetectomy with 6-hydroxydopamine. In this study, rats of different ages were treated with 6-hydroxy-dopamine to investigate the neuronal vs. non-neuronal distribution of MAO in the heart. After sympathetectomy, various parts of the hearts and fractions of the hearts isolated by differential centrifugation were tested for changes in MAO activity with two different substrates (kynuramine and 14C-tryptamine). It was not possible to detect any changes in MAO activity in any parts or subcellular fractions of the heart as a result of denervation. Studies with clorgyline, the MAO inhibitor, in control and sympathetecomized animals revealed that rat cardiac MAO is mostly of the type A enzyme, which was originally thought to be neuronal. A histochemical technique for the electron microscopic demonstration of MAO with osmiophilic thiocarbamyl nitro blue tetrazolium was used in the rat heart in order to determine the ultrastructural location of the enzyme. Histochemical localization of MAO with the electron microscope using tryptamine as the substrate indicates that a substantial portion of rat cardiac MAO is located near the outer membranes of mitochondria within myocardial cells. This histochemical technique provides no evidence to support differential centrifugation data which suggests the presence of a sarcoplasmic reticular (microsomal) MAO in rat heart.

Aging↗

Myocardial cell necrosis and sudden death in humans.

Using morphologic criteria to distinguish between myocardial infarction and lesions that selectively involve myocardial cells, the authors found evidence of ongoing selective myocardial necrosis in 88% of 50 individuals dying suddenly. Acute coronary thrombosis was rare. Since the morphological characteristics of the cell injury differ significantly from that seen in infarction and since the lesion may occur in individuals without significant epicardial coronary disease, factors other than permanent vascular obstruction are indicated as having a role in sudden cardiac death. Some other yet-unidentified process may alter susceptible myocardial cells.

Coronary Disease↗