Cytosol levels of cytokines [interleukins 1b, 6, 8 (IL-1b, 6, 8), tumor necrosis factor-alpha (TNF-alpha)] in aneurysm walls were evaluated in a prospective non-randomized study of 57 patients. The group was divided into two subgroups: Subgroup I (ruptured aneurysms, n=11) and Subgroup II (asymptomatic aneurysms, n=32). A control group consisted of 14 kidney donors. Aortic walls were examined by immunohistochemistry and microscopy to detect inflammatory cells. More pronounced inflammatory changes and higher cytosol cytokine levels [IL6 (p<0.001), IL8 (p<0.0003) and TNFalpha (p<0.002)] were found in the walls of ruptured aneurysms than in the asymptomatic aneurysms. Immunohistochemically, most cells within the inflammatory infiltrates stained positively with the monoclonal antibody to the leucocyte common antigen (CD 45). The majority were of B-cell origin, which was demonstrated by positive staining with the monoclonal antibody L26 directed against the CD 20 antigen. These results show that an inflammatory process plays a significant role in patients with ruptured abdominal aortic aneurysms (AAA). A means of modifying the inflammatory process in the wall of AAAs might play an important role in preventing aneurysm rupture.

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Objective: Abdominal aortic aneurysm (AAA) is a serious disease due to its covert nature, relatively high prevalence and fatal prognosis in the case of rupture. To obtain new insights into AAA pathogenesis, we examined the relationships between histopathology, multiplex in vitro immunoassay data, diameter and symptomatology. Methods: In a prospective, non-randomised study, we evaluated samples from 6 normal infrarenal aortae and 65 AAA patients (65 walls, 55 thrombi). The AAA patients were either asymptomatic (n = 44), symptomatic (n = 7) or with ruptured AAA (n = 14). The AAA diameter was classified as small (<5 cm, n = 18), medium (5–7 cm, n = 26) and large (>7 cm, n = 21). We quantified the histopathology of the AAA wall and the adjacent thrombus. We assessed the expression of proteins in the same samples. Results: Asymptomatic AAAs had walls with more abundant inflammatory infiltrates, lower amounts of PAI-1, a higher number of tPA-positive elements, a tendency towards decreased collagen content, whereas the adjacent thrombi had a greater concentration of VCAM-1 and MMP-2 when compared with symptomatic AAAs. Compared with the aneurysmatic aorta, the normal aorta contained less collagen and more elastin, actin, desmin and PAI-1-positive elements; in addition, it was more vascular. Medium-sized AAAs were the most actin and vimentin rich, and large AAAs were the most vascular. Conclusion: Our results show that asymptomatic AAA walls often have more potentially deleterious histopathological alterations than symptomatic AAA walls. This result indicates that a progression from an asymptomatic AAA to rupture can be expected and screening patients who are at risk of rupture could be beneficial.

The aim of our work was to prepare part of the input data for a computational biomechanical model of both the active and passive elements of the tunica media of an aortic aneurysm. We analyzed tissue samples of the anterior wall of the normal, atherosclerotic and aneurysmatic subrenal abdominal aorta. We assessed the proportions of smooth muscle cells, elastin and collagen in histological sections of these samples and studied the morphological characteristics of the elastin network in the tunica media. Selected photomicrographs were studied, representing relatively well preserved areas without artifacts, ruptures, corrupted integrity of the tunica media or total elastinolysis. A new method was introduced for the assessment of structures formed by elastin membranes and fibres, using the fast Fourier transform (FFT) technique. The image was transformed into reciprocal (Fourier) space and the method made use of the fact that the FFT was very sensitive to the orientation distribution of thresholded elastin morphology. The results of this comparative study, obtained from selected samples from 24 patients, revealed that the percentage values of the constituents of the arterial wall can not distinguish between the preserved segments of normal, atherosclerotic or aneurysmatic aorta. The results of the Fourier analysis proved that the FFT provided an efficient method for evaluating cross sections of the elastin membranes and fibres, reflecting their anisotropy. The shape of the power spectrum of elastin was a simple pattern, whose description was quantified by the shape of its polar coordinates histogram. We discuss the methodological difficulties and biomechanical implications of our work as well compare it to other methods of elastin analysis.

Beranová M., P. Manìáková, P. ·íma, J. Slípka, F. VoÏeh, J. Koãová, M. âervinková, J. S˘kora: Morphology of Adrenal Gland and Lymph Organs is Impaired in Neurodeficient Lurcher Mutant Mice. Acta Vet. Brno 2002, 71: 23-28. There is a tight structural relation and functional co-operation between the nervous, endocrine and immune systems. A dense network of soluble neuro-endocrine and immune mediators exists to ensure close interactions. These hormones, cytokines and neurotransmitters all interact through positive and negative feed-forward and feedback loops. The mediators, once considered specific to the central nervous system (CNS), the endocrine system (ES) or the immune system (IS), do in fact act in all three systems, forming that way the united neuro-endocrine-immune system. The complex neuro-endocrine-immune networks operate under both physiological and pathological conditions.In the presented study microscopical analyses of selected immune organs (the thymus, spleen, inguinal and subscapular lymph nodes) and of the adrenal gland of the neurodeficient Lurcher mutant mice and control C3H mice were performed. In the neurodeficient mice the morphology of the immune organs was impaired. The changes followed in the spleen, especially the increased number of megakaryocytes, lead to the hypothesis of enhanced extramedullar hemopoiesis in the neurodeficient Lurcher mutant mice. Histopathological analysis of the adrenal gland showed the relative hypertrophy of the adrenal medulla. Regarding the adrenal cortex, the three cortical zones, zona glomerularis, fasciculata and reticularis, are difficult to be distinguished. It has been supposed that structural changes of adrenal medulla could document the increased secretion of catecholamines in the neurodeficient animals.Our observations confirm the idea of the tight cooperation of neuro-endocrine-immune structures and contribute to its better understanding, specifically in the conditions of postnatally progressing neurodeficiency. Lurcher mutant mice, homeostatic relatioships, neuro-endocrine-immune system, adrenal gland, megakaryocytesThe intrinsic condition for the individual survival is a balance of the internal enviromenthomeostasis. There are many proofs of the existence of a unified neuro-endocrine-immune regulatory system that is responsible for maintaining the homeostasis (Michael and Chapman 1990;Weigent and Blalock 1995;Besedovsky et al. 1983). The regulatory relations within that system are mutual and complex (Jankovic 1989;Csaba 1994; ·íma and Vûtviãka 1990;Provinciali and Fabris 1991;Pertseva 1991; Slípka 1961).To contribute to the explanation of these relations we used in our previous study "an experiment of the nature", gross-brain malformation -anencephaly -which eliminates the central nervous system and consequently the neuro-endocrine part of the homeostatic system (Slípka et al. 1997; B e ranová 1994). The spontaneously aborted human foetuses without any external malformation and human anencephalic foetuses were compared with