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H David

Publications and source records attributed to H David.

At least 55 records · Page 3Linked to original sources
PubMed1993

Ultrastructural morphometric investigation of the heart of rabbits after a single administration of reserpine.

The ultrastructure of myocardial cells of chinchilla rabbits was morphometrically examined after administration of one dose of reserpine. The results show that 24 hours after administration of reserpine, there is a decrease in the number and an increase in the size of the mitochondria, a relaxation or narrowing and ramification of myofibrils, an increase in intracellular lipid content compared with control animals. These changes are the result of functional and chemical desympathization and they represent an ultrastructural-morphometric characteristic of the action on cardiomyocytes.

Animals↗
PubMed1992

Primary phase of hepatocytic autophagocytosis under ischaemic conditions.

Increased autophagocytosis in hepatocytes was found in response to conditions of ischaemia/hypoxia. Initial stages proved to be recordable. These were found to become manifest through the formation of phospholipid membrane structures, approximately 5 nm in width, coalescing in circular formations with vesicular extensions. They may further develop to form multilayer myelin structures. Enveloped cytoplasmic regions and organelles were unchanged, at the beginning, and subsequently coalesced typically into autophagolysosomes and autophagic vacuoles. Verification will be necessary to find out if these initial stages occur only in response to hypoxia or constitute a phenomenon of general validity.

Animals↗
PubMed1992

Ultrastructure and biochemistry of ischemic damages of small intestinal epithelial cells.

Ischemia (one hour) and following reperfusion (up to one hour) of the small intestine induce biochemical changes which are indices for the formation and action of oxygen free radicals and which occur predominantly during the reperfusion period. But the villi and the epithelial cells show different patterns of damage, occurring both at the end of the ischemic period and during the reperfusion period. Although the quantitative morphological changes are increased during the reperfusion in comparison with the ischemic phase the quality of the pattern of structural damage is the same in both periods of the experiment. This pattern of the damage includes: 1. the neighbourhood of groups of villi with total ischemic-lytic dissolution of the villi, of villi with damage of the epithelial cells at the tip and at the lateral area and of normal villi; 2. the different degree of structural damage of neighbouring epithelial cells within one villus whose cells are either of regular structural or damaged at subcellular organelles including the plasma membrane or of those being necrotically destroyed and on the way of release into the luminal space; 3. a differentiation of the structural changes of the microvilli and other organelles within single and neighbouring epithelial cells. The biochemical findings on purine nucleotide metabolism and on the formation of oxygen free radicals as "mean values" of a homogenate from a large group of cells cannot reflect the morphological-ultrastructural changes of single villi or even single epithelial cells. The possible reasons for the mosaicism of the morphological changes during ischemia and reperfusion are discussed.

Adenosine Triphosphate↗
PubMed1992

Electron microscopic and 31-P NMR studies of ischemic injured rat livers during preservation and reflow.

Ischemic injury induced during preservation and reperfusion contributes to post-operative failure in liver transplantation. Hepatic injury and recovery from preservation was studied in an isolated rat liver model reperfused with oxygenated erythrocytes. In order to correlate morphological and functional findings, 31-P nuclear magnetic resonance spectroscopy and electron microscopy were used to investigate metabolic and ultrastructural changes during 6 hours of reperfusion. Following cold preservation, EM's showed a primary sinusoidal cell injury, whereas the hepatocytes were well maintained. During reperfusion, hepatocytes displayed further damage. The simultaneous presence of vacuolarly degenerated mitochondria and mitochondria of increased activity was noted. 31-P NMP spectra demonstrated initially a partial ATP-recovery. The maximum level of 60% of the control ATP-value could not be further increased. EM and 31-P NMR indicate that the progressive injury to the liver is due to microcirculatory malfunction induced by an endothelial cell damage, followed by injured hepatocytes themselves, and the consequent intracellular energy crisis that is produced.

Animals↗
PubMed1992

[Ultrastructure of amitosis and mitosis of the liver].

Thousands of liver cells of several ultrastructural investigation programs of our laboratory have been evaluated in respect to amitosis and mitosis. Multiplication of hepatocytes by amitosis and mitosis often leads to bi-, tri- and multinucleated cells. No striking ultrastructural changes have been observed in the hepatocytes of human and animal livers. There are no indications of enhanced autophagocytosis or other signs of dedifferentiation. However, non-hepatocytes suffer ultrastructural changes during mitosis: endothelial cells reduce their organelles in number, round up their shape and form microvilli reaching between the microvilli of hepatocytic sinusoidal membrane. Mitotic Kupffer cells contain only small phagosomes and are separated from hepatocytes by endothelial cell processes.

Animals↗
PubMed1992

Adaptational increase of liver glutathione content during long-term application of cyclosporine A may attenuate toxic side effects.

The concentrations of reduced and oxidized glutathione and of adenine nucleotides were determined in liver, kidney and heart of rats during long-term (four weeks), high-dose therapy with cyclosporine A. In liver and kidney the concentration of oxidized glutathione increased following 4 weeks-therapy suggesting increased formation of free radicals and accelerated lipid peroxidation processes. These processes may be due to an increased activity of the cytochrome P-450 system. Compensatory levels of reduced glutathione were also increased. The adaptational increase of the tissue level of reduced glutathione, presumably the response to a chronic oxidative stress, was more distinct in the liver. The liver did not lose adenine nucleotides. In contrast the kidney, after 4 weeks of cyclosporine A therapy, lost 25% of the adenine nucleotides. These findings suggest that the liver is characterized by a greater potential for effective adaptation to oxidative stress conditions compared to the kidney. These adaptations may prevent distortions of energy and nucleotide metabolism in the liver which is in agreement with the minor ultrastructural changes we have observed.

Adaptation, Physiological↗
PubMed1992

[Nuclear ultrastructure of binuclear and trinuclear hepatocytes].

Binucleated and less frequently trinucleated hepatocytes appear in human and animal livers under normal conditions as well as in pathological cases. To provide further ultrastructural data hepatocyte nuclei were investigated in different pathological states. Important results of this study are: Size of the nuclei and structure of the karyoplasm as well as size and localization of the nucleolus are obviously, same in most of the binucleated hepatocytes. In a small percentage of hepatocytes the following findings have been made: One of the nuclei will be light microscopically overlooked due to its small size pretending mononucleated cells. The disappearance of one of the nuclei results in an increase of the number of mononucleated cells and should therefore be evaluated like a decrease of binucleated hepatocytes: a pathological incident. Functional differences between both nuclei become morphologically obvious during virus replication, e.g. HBc-particle production is restricted to one of the nuclei. These results seem to consist rather with amitotic than mitotic cell division.

Cell Nucleus↗
PubMed1991

Effect of pentoxiphylline on the recovery of the preserved rat liver: 31P NMR and ultrastructural studies.

Hepatic failure often occurs following transplantation. This is primarily due to cold ischemia during preservation, warm ischemia during implantation, and finally reperfusion damage after transplantation and reflow. The possibility that this ischemia and reperfusion-induced damage can be reduced by preischemic application of a xanthine derivative (pentoxiphylline) was examined using 31P NMR spectroscopy and electron microscopy (EM) studies of bioenergetic and ultrastructural changes in oxygenated erythrocyte-perfused rat livers. EM illustrated that the hepatocytes and the mitochondria appeared to be relatively unaffected by cold preservation of the liver, whereas the endothelial cells lining the sinusoids became disrupted. After reperfusion, NMR spectroscopy showed a partial recovery of ATP levels, and EM indicated progressive mitochondrial injury. This progressive injury to the liver was probably due to endothelial cell damage which resulted in microcirculatory malfunction and free radical formation during reperfusion. Pentoxiphylline pretreated livers showed better preservation of the cell morphology and exhibited better ATP recovery than untreated livers. Pentoxiphylline is known to prevent the loss of precursors of ATP resynthesis by inhibiting AMP dephosphorylation during ischemia and improves the microcirculation via vasodilatory properties following ischemia. Thus, it is concluded that pentoxiphylline may ameliorate ischemia-induced cell damage during transplantation.

Adenosine Monophosphate↗
PubMed1991

Electron microscopy of liver in patients with chronic haemodialysis.

Liver biopsies were performed on 18 haemodialysis patients with clinically as well as clinico-chemically altered liver values and partially positive HBV marker serology, with the view to comparing these values with ultrastructural findings in correlation with histological and immunohistological results. The following characteristic combination of findings was recorded at ultrastructural level: hypertrophy and hyperplasia of agranular endoplasmic reticulum of hepatocytes, haemosiderin deposits in Kupffer cells and hepatocytes, invasion of lymphocytes into Disse and intercellular spaces; megamitochondria in hepatocytes and perisinusoidal fibrosis established in some cases. The same findings proved to be recordable in histological diagnosis of hepatitis or toxico-metabolic liver damage. The study shows that inflammatory lesions are not all the only causes for haemodialysis-related changes in clinico-chemical values, so that liver biopsies together with ultrastructural investigations are indicated for differential diagnosis.

Adult↗
PubMed1991

Ultrastructure of the liver after hypoxia in the postnatal period.

Repeated phases of hypoxia (8 h daily for 2 to 5 days at pO2 11.33 kPa = 5.000 m in altitude) were induced to Sprague-Dawley rats in the postnatal period as well as up to the 64th day of age, and after different recovery phases the ultrastructure of hepatocytes was qualitatively and quantitatively analysed. Major results were as follows: 1. Increases in body and liver weights were delayed but were balanced off after 64 days. 2. Qualitative alterations are reversible spherical transformations of mitochondria, a degradation of lipids and a slight increase in autophagocytosis. 3. The quantitative mitochondrial parameters (volume density, number per unit area, average volume) were not even adjusted to control values after 64 days. Granular endoplasmic reticulum and ribosomes/polysomes were insignificantly reduced in comparison to control animals, structure and arrangement are regular. Lipids and glycogen were differently altered. 4. The findings of the hepatocytes after postnatal hypoxia were reversible, though the majority of parameters had not yet returned to normal after 2 months. An adaptation to repetitive hypoxic conditions is not provable.

Animals↗
PubMed1991

[Comparative studies on the cultivability and morphology of rat hepatocytes isolated by trypsin or collagenase].

In the present study rat hepatocytes isolated either by trypsin or by collagenase were investigated concerning its cultivability and its morphological properties. The cultivation was carried out as monolayer for 24 h. The yields of cells prepared by trypsin or collagenase amounted to 8 x 10(7) cells per liver and 15-30 x 10(7) cells per liver, respectively, with viabilities measured by trypan blue exclusion test of 70-80 and 90-95%, respectively. Nonhepatocytes were not taken into consideration. Using the electron microscopy it could be established that both freshly isolated and 24 h cultured hepatocytes were intact. There were no morphological differences between cells isolated by trypsin and cells isolated by collagenase. After 24 h cultivation hepatocytes prepared by trypsin showed a little tendency in forming a slightly flattened appearance and in forming intercellular contacts.

Animals↗
PubMed1991

Discrepancy between biochemical normalization and morphological recovery of jejunal mucosa during postischemic reperfusion in presence of the xanthine oxidase inhibitor oxypurinol.

An increased formation of oxygen free radicals in the reperfused rat small intestine is concluded from accumulations of oxidized glutathione, of thiobarbituric acid-reactive substances and of 4-hydroxynonenal. Xanthine oxidase inhibition prevented these biochemical changes. The histological and electronmicroscopic studies of intestinal sucosa showed significant structural deteriorations already at the end of the ischemic period obviously due to disturbances of cellular energy metabolism. The extent of dosage was increased during the reperfusion without qualitative changes of the pattern of structural dosage. The beneficial effects of oxypurinol on biochemical criteria which occurred already in the early phase of reperfusion were not reflected in significant morphological differences within the first hour of reperfusion. Differences of morphological findings between oxypurinol-treated and untreated animals could be observed after longer periods of reperfusion--during the regeneration of the tissue.

Animals↗
PubMed1990

Ultrastructure and quantitative composition of isolated endothelial cells of rat liver.

Isolated endothelial cells (n 110; 350-540 microns3 in volume) of the sinusoid of rat liver were found to differ from in situ endothelial cells by their rounded shape with the nucleus usually in the centre and fenestrae of the sieve plates across the entire cytoplasm. Their volume density is 0.2814 (SE 0.0085). Some of them tend to form complex, ramified structures as well as clefts and vacuoles up to 1 micron in size. Dense bodies are other structures quite often seen in endothelial cells (Vv 0.0189, SE 0.0085). Mitochondria, on the other hand, are extremely rare (Vv 0.0023, SE 0.0009). Both the preservation and relocation of sieve structure after isolation may probably be due to the cytoskeleton which in vivo causes changes of size and number of endothelial cell fenestrae under physiological and pathological conditions.

Animals↗
PubMed1990

[The concept of "organellopathies"--component of modern cellular pathology].

Review is made to an account of contemporary knowledge on cell organelles in an attempt to describe organellopathies known at present together with their relations with diseases and syndromes. Organellopathy is defined as a disease, with its primary effect and/or primary morphological and functional alterations being located in the organelle population of one or several cell types. Mitochondriopathies (mitochondrial disorders), lysosomopathies (lysosomal disease), peroxisomopathies (peroxisomal disorders), ciliopathies (ciliary diseases), and plasma membranopathies (brush border membrane diseases) have so far been most comprehensively characterised and are associated with distinctive clinical pictures. However, unambiguously characterised pathies are almost completely absent with regard to other organelles. With numerous ideas still being of speculative nature, the concept of organellopathies as such may be considered as an element of modern cellular pathology.

Cell Membrane↗