Prenatal development of coronary arteries in the rat: morphometric patterns.

The aim of this work was to address morphometric patterns of coronary artery (c.a.) development in the rat based on serial section analysis of hearts at different stages of prenatal development. Studies were performed on foetal hearts 15-21 days (ED) post-conception. Paraffin sections were stained with haematoxylin-eosin (H&E) and frozen sections were labelled with Griffonia simplicifolia I (GSI) lectin (endothelial cell marker). Coronary arteries' luminal diameters were measured at different distances from the aortic roots and the main c.a. branch lengths were calculated from serial sections. All measured values were compared to heart length and to foetal stages. On ED15 precursors of c.a. were distinguished as tubes running on both sides of the outflow tract. Below the aortic valves the tubes had the largest diameter. Formation and development of c.a. proceeded by elongation of vascular tubes distally, ramification and formation of the media and the adventitia. During the prenatal period the c.a. length increased approximately 14-fold, while heart length increased about 4-fold, and crown-rump length about 2.5-fold. The lumen of the proximal part of c.a. increased 4-fold during ED18-21. An increase in c.a. length is the fastest compared to the heart growth, and crown-rump growth during the foetal life.

[Index of histopathological changes in rapidly progressive glomerulonephritis: a preliminary report]. / Indeks zmian histopatologicznych w gwaltownie postepujacym klebuszkowym zapaleniu nerek--doniesienie wstepne.

We present the case of an 8-year-old girl with rapidly progressive glomerulonephritis. The activity and chronicity index of histopathological changes in this patient was determined in 2 renal biopsies performed in a 25-month interval. The determination of this index in renal biopsies may be useful in the choice of glomerulonephritis with bad prognosis therapy.

Comparative morphology of the hepatic and coronary artery walls. Part I. Differences in the distribution and intensity of non-atherosclerotic intimal thickening and atherosclerosis.

We compared the morphology of the hepatic artery intima which is free of atherosclerosis, with that of the typically atherosclerosis-prone coronary artery. The study group comprised material collected from 116 autopsies. Subjects were aged between 1 month and 90 years. Specimens were collected from grossly normal arterial segments. An already known fact was confirmed: the presence and remarkable intensity of non-atherosclerotic intimal thickening in the coronary arteries since the beginning of life. On the contrary, hepatic artery intimal thickening was incidental during the first 4 decades of life and regular later on. During all the decades intimal thickness was decreased in the hepatic artery in comparison to the coronary artery. Initial atherosclerosis was noted during the 4th decade of life in the coronary artery and during the 8th and 9th decades in the hepatic artery. Intimal thickness was always lower in women compared to men. These findings reveal a positive correlation between the intensity of intimal hyperplasia and the incidence of atherosclerosis. The intimal pattern is of limited value in the determination of an unidentified subject age who underwent an autopsy. The thickness of the hepatic artery intima, which surpasses 200 microns indicates that the subject is at least 40 years of age, while initial atherosclerosis--the 8th or 9th decades of life.

Comparative morphology of the hepatic and coronary artery walls. Part III. The insignificance of medial morphologic features in the determination of an autopsied unidentified subjects age.

Since hepatic arteries are free of atherosclerosis any possible wall structure change may be attributed to age. We determined the media of hepatic and coronary arteries in view of this assumption. We measured its thickness and myocytic density (per 1 mm2 of cross-section) from specimens collected from autopsied subjects, aged up to 90 years. The media gradually thickens with age, although values noted during particular decades remain statistically insignificant. The myocytic density (in 1 mm2) was almost constant throughout life. The latter observation is incompatible, in comparison with data reported by other authors (diminution was expected).

Prenatal development of coronary arteries in the rat: morphologic patterns.

The aim of this work was to address spatiotemporal and morphologic patterns of coronary artery development in rats, based on immunohistochemical and ultrastructural studies of hearts at different stages of prenatal development. Griffonia simplicifolia I lectin and alpha-smooth muscle antibody were used to demonstrate endothelial cells and/or their precursors and smooth muscle cells, respectively. Ultrastructural examination was performed on ED14-16 hearts to study the morphology of the developing coronary arteries in different regions of the truncus arteriosus and adjacent myocardium. On ED14 endothelial-like cells present within the mesenchyme surrounding the outflow tract penetrated the aortic wall and the truncoconal proximal myocardium. On ED15 these penetrating cells formed vascular clusters, which were the first signs of presumptive vascular channels. Development of the coronary artery proceeded by coalescence of discontinous vascular clusters, formation of the lumen (vascular channels) and establishing a connection of the proximal part with the aorta. The second layer of cells around vascular channels (embryonic media) consisted of mesenchymal cells that were attracted to the immature vessel and were first seen on ED15. At this time no lumenized connection of the coronary artery with the aorta has been seen. After the lumenized connection of the coronary artery with the aorta had been established perivascular cells of the media started to differentiate into vascular smooth muscle, as was shown by alpha-smooth muscle actin-staining. Further development and differentiation of the media and adventitia proceeded distally (towards the apex).

Light and electron microscopic picture of atherosclerotic plaque in stable and unstable angina.

By presenting this series of 127 cases of coronary atherectomy the authors join the workers who study morphological differences between the atherosclerotic plaques in stable and unstable angina. Routine staining of formalin-fixed, paraffin-embedded material was completed by the detection of T lymphocytes, macrophages, mast cells, smooth myocytes and grown-in capillaries using monoclonal antibodies (DAKO), as well as by the immunofluorescent demonstration of fibrinogen in the plaques. The plaques derived from patients with unstable angina showed a higher incidence of mast cells (significant) and macrophages (insignificant). These cells render the plaque more susceptible to rupture or fissuring. There was also significantly more frequent and quantitatively more abundant permeation of the plaque by fibrinogen that raises the chance of thrombosis. These findings support the view that unstable angina correlates with the phenomena that favour the rupture of the plaque and thrombosis. Electron microscopy has not been used so far to study coronary atherosclerotic plaques. This material includes 15 plaques from stable and 18 plaques from unstable angina. A cover of fibrin and blood platelets is a regular formation on the surface and in the superficial layer of the plaque from unstable angina. It contributes to the "thrombotic proneness" of the coronary artery. These plaques also show abundant elastic fibres. This pattern corresponds to myo-elastic intimal hyperplasia ("intimal thickening") where the production of intimal elastin constitutes an essential phenomenon. Intimal thickening is interpreted as a preatherosclerotic event. The presence of elastin reflects an early stage of the development of the plaque. The plaque from stable angina shows abundant collagen fibres, which aggravate the lesion.

Effect of aluminium hydroxide administration on normal mice: tissue distribution and ultrastructural localization of aluminium in liver.

In order to assess the risk of parenteral aluminium (Al) exposure, we evaluated the effects of intraperitoneal administration of aluminium hydroxide, a compound widely used in medicine. Mice (strain Pzh:SFIS) received intraperitoneally, every two weeks 1 mg Al or 0.1 mg Al for five days a week. Controls received injections of saline. Al concentrations in liver, bone and brain were evaluated by electrothermal atomic absorption spectrometry after exposure to 2 mg, 4 mg, and 6 mg Al. The concentration was the highest in liver and occurred after exposure to only 2 mg Al (265.1 +/- 27.7 mg/kg, 233.5 +/- 28.0 mg/kg). Generally further accumulation was not dose- and treatment-dependent. The only exception was a significant Al increase in the liver after exposure to 6 mg Al, injected 0.1 mg Al five days/week. Development of resorption granulomas was observed in the liver, Al being revealed by Morin fluorescence in constituent macrophages and giant cells. By electron probe X-ray microanalysis, Al was identified predominantly in lysosomes of macrophages and Kupffer cells. In tibia of mice, a dose-dependent Al accumulation was observed. The highest level of Al concentration after the 6 mg treatment was 23.5 +/- 3.82 mg/kg and 25.06 +/- 2.3 mg/kg. The Al concentration in the brain of mice had not changed significantly during Al treatment.

Tunnel capillaries in hypertrophied myocardium of rats with aorto-caval fistula.

Male inbred rats (Wag) with aorto-caval fistula were used as a model of volume-overloaded heart hypertrophy. Hearts were taken after 1, 2, and 6 months postoperatively for immunohistochemical, histological and ultrastructural investigations. Immunohistochemical staining with some anti-extracellular matrix antibodies and ultrastructural findings allowed us to recognize intracardiocytic tunnels which were intracellular invaginations of plasmalemma surrounded by basement membrane. Inside the tunnels endothelial cells forming well-developed capillaries were entrapped. Tunnel capillary formation is discussed as an adaptive response to increased cardiac work due to volume overload.

Some extracellular matrix elements as markers of 'capillary tunnels' in hypertrophied rat heart.

We studied the distribution of the extracellular matrix proteins fibronectin (FN) and laminin (LM) in the hypertrophied hearts of spontaneously hypertensive rats (SHR), using an immunofluorescence method with specific antibodies. The immunohistochemical reaction was positive in the cytoplasm of some hypertrophied cardiomyocytes. The results showed that FN and LM can be used as markers for tunnels, i.e. intracardiocytic invaginations of the sarcolemma. The tunnels observed contained capillaries.

[Schwannoma with granular cells. Indirect evidence of the closeness of schwannoma and Abrikosov's tumor]. / Shvannoma s zernistymi kletkami. Kosvennoe dokazatel'stvo blizosti shvannomy i opukholi Abrikosova.

A woman of 29 developed a slowly growing subcutaneous tumor (1.5 X 1 X 0.5 cm) of the forehead. This neoplasm showed the histological pattern of neurilemmoma with the presence of dispersed rectangular cells having acidophilic fine granular cytoplasm imitating those of Abrikosov's tumor. This case as well as a few others described in the literature seem to confirm the thesis of neurilemmal origin of the so-called Abrikosov's myoblastoma.

Activity of alkaline phosphatase in the healing rat liver after hepatectomy.

Changes of alkaline phosphatase activity in the process of healing liver injuries of rats on which partial hepatectomy was performed were the subject of our researches. Reaction on alkaline phosphatase was performed on cryostat sections according to the method of Gomori-Takamatsu. It has been found that granulated precipitate of cobalt sulphide was localized in the cytoplasm of granulocytes, macrophages and fibroblasts. A diffusive reaction comprized clusters of newly created collagen fibres. In early stages in the centres of necrosis, the activity of alkaline phosphatase increased, in later periods a lack of the activity was observed. Steatosis of liver tissue does not correlate with the intensity of the reaction. Lack of alkaline phosphatase activity is characteristic for old cicatrices. The authors discuss the effects of the histogenetical process during healing of liver injury on the results of the histoenzymatic reactions. The authors suggest that alkaline phosphatase is involved in the mechanism of re-building collagen fibres. It is stressed in the conclusion that the localization and intensity of alkaline phosphatase in the area of healing liver lesions are variable depending on the period of healing wound of the liver and the influence of other complications.