Biomedical subjects
Publications and source records attributed to H Frenzel.
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Small blood vessels of human vocal cords were examined by electron microscopy. The endothelial cells contain a large number of filaments. Two kinds of filaments could be differentiated: Short intermediate filaments with a diameter of 10-12 nm, which were localized in the pericaryon, and bundles of thin filaments with a periodicity of 480 nm lying beneath the luminal cellular membrane. The basement membrane of capillaries, arteries, and veins was lamellate. Between the outermost, not fully closed lamellae, myocytes or pericytes could be seen. Both the lamellate basement membranes and the large number of intermediate filaments in the endothelial cells are discussed as stabilizing structures in blood vessels which are exposed to high mechanical forces. The bundles of cross-striated thin filaments may possibly increase the permeability of the vessel wall by their contraction, permitting the well-known fast development of edema in the vocal cords. The importance of Weibel-Palade bodies, which could be disclosed in the endothelial cells in large numbers, is not yet known.
Following oral intake or inhalation, halogenated hydrocarbons are metabolized to hepatotoxic intermediates in the liver to only a small extent, the major part being eliminated via the lungs without biochemical transformation. Following intoxication, increased pulmonary elimination of hydrocarbons can be achieved in patients by treatment with CO2-induced hyperventilation. To investigate the efficacy of this new therapy under exact experimental conditions, female Wistar rats received 2.5 ml CCl4/kg BW by gastric intubation and were then treated with CO2-induced hyperventilation. In comparison to untreated animals, hyperventilated rats showed only a few signs of hepatic injury by histological evaluation, whereas massive centrolobular necroses and fatty infiltrations were observed in non-hyperventilated animals. By biochemical assessment, significant decreases of GOT, GPT and GDH activity were observed in the serum, when hyperventilated rats were compared to untreated animals. Moreover, the LD50 for CCl4 was almost trebled after hyperventilation compared to the non-hyperventilated animals. The increased LD50, and the biochemical and histological results therefore substantiate the usefulness of CO2-induced hyperventilation therapy in the treatment of intoxications by hydrocarbons under standardized experimental conditions.
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Dissection of the three coronary vessels as a rare fatal complication after intraoperative cannulation is described. A 58-year-old man died from progressive cardiac failure 12 days after mitral and aortic valve replacement. The cause of death was a nearly 12-day-old anteroseptal myocardial infarction as a result of a dissection of all three coronary vessels including the septal arteries. Histologic examination revealed a tear of the left and right coronary artery at their ostia. Thrombi of different age in the dissection and satellite-like recent necroses surrounding the 12-day-old myocardial infarction indicate a gradual progression of the dissection.
Compared to controls receiving physiological saline, the i.p. administration of dimethylnitrosamine (DMN) on 5 consecutive days to rats fed a nutritionally adequate liquid diet resulted 24 hours after the last injection of significant increases in glutamic dehydrogenase (GDH), glutamic oxylacetate transaminase (GOT), and glutamic pyruvate transaminase (GPT) activities in the serum, indicating a striking hepatotoxic effect of this compound. This was confirmed by the histological demonstration of massive centrolobular necrosis. Conversely, following pretreatment of the rats with an ethanol containing liquid diet for 23 days and subsequent administration of DMN the increases of serum enzyme activities and massive centrolobular necrosis could not be observed. These results therefore suggest that chronic alcohol consumption protects from hepatotoxicity due to DMN, most probably due to an enhancement of detoxifying pathways of the parent component or one of its toxic metabolites.
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The report concerns 5 patients with straddling or overriding atrioventricular valves. The overriding phenomenon was found 4 times in tricuspid, once in mitral position. In addition to this malformation, 2 patients had congenitally corrected transposition of the great arteries (CTGA), one patient had transposition of the great arteries (TGA), and another a double outlet right ventricle (DORV). In 2 instances corrective surgery was done without compromising the anatomical and functional integrity of the straddling valve. Three patients with straddling degree B-C received palliative procedures, the ventricular septal defect (VSD) was left open in order to save the straddling atrioventricular valve and pulmonary artery banding was done for protection of the pulmonary vascularity. One corrected patient died in the early postoperative period.
The development of a cardiac hypertrophy depends on modulation of two parameters, such as the amount of increased work load imposed on the heart and the rapidity with which the work load is applied. A gradual development of cardiac hypertrophy is usually observed in humans; at variance, the induction of cardiac hypertrophy is quite a rapid process in animal experiments. The enlargement of cardiac muscle cells during hypertrophy is due not only to an increased synthesis of contractile proteins but also to an accumulation of other cell constituents parallelly involved in the hypertrophy process. The mechanism whereby new sarcomeres are formed during cardiac hypertrophy is not yet completely clarified. Once the stimulus producing overload is removed, cardiac hypertrophy can regress completely. The possible role of biological regulators in inducing cardiac hypertrophy was also discussed.
Groups of female rats were treated orally with 0.5, 2.0, 8.0, and 32 mg/kg hexachlorobenzene twice a week for 203 days. The liver content of hexachlorobenzene was found to be dose-dependent. In the animals treated with the highest dose the concentration was 273 mug/g hexachlorobenzene. In the fresh and fixed hepatic tissue of the treated animals pink fluorescence was observed. Electron microscopy revealed a dose dependent enlargement of all hepatocytes due to proliferation of the SER in the centrolobular area or to increased glycogen deposits (beta- or alpha-particles) and SER in the intermediary and periportal area. Numerous porphyrin deposits and siderosomes, intimate disorganisation and moderate dislocation of the RER and a moderate enlargement of bizarre-sharped mitochondria were recognized. The relationship between porphyrin crystals and mitochondria on the one hand and between SER and glycogen deposits on the other is discussed.
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Changes in liver sinusoids following fractionated irradiation were studied by use of TEM and SEM. Rats received telecobalt-irradiation of their liver regions in daily doses of 500 r for 9 days, a total dose of 4500 r. One day after the end of the irradiation series the fine structure of hepatocytes was almost intact. In SEM the liver sinusoids contained numerous corpuscles, which in TEM were recognized as cellular blebs separated from endothelial cells. 8 days after irradiation small foci of necrotic hepatocytes could be visualized. Instead of complexes of small fenestrations (sieve plates) the endothelial cells contained striking round or oval holes in their tenuous processes. After 120 days small groups of hepatocytes with alterated fine structure of their organelles and some necrotic parenchyma cells were still present. Away from these focal necroses the endothelial cells now resembled sinusoidal endothelium in control animals. Fat-storing cells appeared to have multiplied and were enlarged. There was distinct fibrosis only in perisinusoidal spaces. The formation and discharge of electron lucent blebs is discussed as a mechanism compensating for an enhanced uptake of fluid into irradiation injured endothelial cells. In order to form holes in the tenuos processes of endothelial cells a disordered synthetic pattern and the shearing forces of the circulating blood are thought to be necessary. Repair of these intracellular holes may be possible. In rats irradiation induced lesions of the small intrahepatic vessels can be excluded as a cause of the late changes in liver parenchyma cells.
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Ultrastructural alterations of the liver were examined on the 1st, 2nd, 3rd, 5th, 7th and 14th day after a standard burn in mice. Our results can be divided pathogenetically into two groups: 1. Alterations explained by the primary thermal injury including electron-optically empty vacuoles and sinusendothelium destruction. 2. Alteration due to the influence of a specific burn toxin including mitochondrial changes and the formation of autophagic vacuoles. Evidence of this distinction was produced by a second investigation. Burn toxin isolated from the serum of severely burned patients was injected intraperitoneally (15 mg) into 4 mice. The livers were examined by electron microscopy on the 2nd, 4th, 7th and 14th day. Alterations described in 2 above were not observed in any case of this investigation series. The nature and timing of liver alterations were similar to those described in 2 above. In none of the cases were changes similar to those in 1 above observed.
Out of a great number of hearts investigated post-mortem by coronary arteriography and quantitative histology, 437 coronary arteries of 202 hearts had severe stenoses with a lumen reduction to less than 50 per cent. Mainly these most severe obstructions lay between 2 and 5 cm behind the aortic ostium. In the right coronary artery the frequency curve showed a smaller peak, a smaller decrease, and an inconsiderable second peak in the periphery. Perhaps the slow calibre reduction of the right coronary artery is significant for these findings. The narrowed lumen mostly lay a little eccentric and had an oval shape. A slit-like shape was a rare finding. Only in 20 per cent of the severe stenoses a normal intima was preserved in parts of the circumference of the coronary artery. Among 113 patients the following risk factors were known: hypertony, diabetes mellitus, cigarette smoking and hypercholesterinemia. Significant differences in the localisation of the most severe stenoses were not recognizable under the influence of these risk factors.
The initial phase of pulmonary edema development following intracranial pressure elevation was studied by means of transmission electron microscopy. Using perfusion fixation and application of a blood tracer (HRP horseradish peroxidase) the time sequence and site of fluid leakage out of pulmonary vessels was demonstrated: - passage of edema fluid through intercellular clefts of alveolar capillary endothelium - edema accumulation in alveolar interstitial tissue - draining of edema fluid from the alveolar septum to the interstitium of terminal bronchioli and to lymphatic vessels. An early interepithelial fluid leakage out of the alveolar wall remains questionable.