Vascular histopathologic reaction to pulmonary artery banding in an in vivo growing porcine model.

Pulmonary artery banding (PAB) is used as a surgical palliation to reduce excessive pulmonary blood flow caused by congenital heart defects. Due to the lack of microscopic studies dealing with the tissue remodeling caused by contemporary PAB materials, this study aimed to assess histologic changes associated with PAB surgery by analyzing local tissue reaction to the presence of Gore-Tex strips fixed around the pulmonary artery. Gore-Tex strips were used for PAB in a growing porcine model. After 5 weeks, histologic samples with PAB (n = 5) were compared with healthy pulmonary arterial segments distal to the PAB or from a sham-treated animal (n = 1). Stereology was used to quantify the density of the vasa vasorum and the area fraction of elastin, smooth muscle actin, macrophages, and nervi vasorum within the pulmonary arterial wall. The null hypothesis stated that samples did not differ histopathologically from adjacent vascular segments or sham-treated samples. The PAB samples had a greater area fraction of macrophages, a lower amount of nervi vasorum, and a tendency toward decreased smooth muscle content compared with samples that had no PAB strips. There was no destruction of elastic membranes, no medionecrosis, no pronounced inflammatory infiltration or foreign body reaction, and no vasa vasorum deficiency after the PAB. All the histopathologic changes were limited to the banded vascular segment and did not affect distal parts of the pulmonary artery. The study results show the tissue reaction of palliative PAB and suggest that Gore-Tex strips used contemporarily for PAB do not cause severe local histologic damage to the banded segment of the pulmonary arterial wall after 5 weeks in a porcine PAB model.

Asymptomatic abdominal aortic aneurysms show histological signs of progression: a quantitative histochemical analysis.

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.

Vasa vasorum quantification in human varicose great and small saphenous veins.

Recent research regarding saphenous vasa vasorum (VV) has focused on two main topics: the VV during varicogenesis in chronic venous insufficiency and the VV in saphenous grafts used in reconstructive vascular surgery. Our aim has been (i) to establish a technique for the histological quantification of the VV in human varicose great and small saphenous veins and (ii) to describe the density and distribution of the vasa vasorum within varicose veins. Great (n=11) and small (n=5) saphenous veins (length, 15-40cm) were collected from 12 patients who were undergoing venous stripping due to chronic venous insufficiency (Clinical-Etiology-Anatomy-Pathophysiology class 2-3). The veins were divided into 5-cm long segments. In total, 92 tissue blocks were collected to trace the variability of the density and distribution of the vasa vasorum in the proximo-distal direction. The endothelium was detected by immunohistochemistry using the von Willebrand factor. We quantified the number of microvessel profiles per section area and the relative distance of the microvessels from the outer border of the adventitia. The VV did not exhibit a preferential orientation in the varicose veins. VV density profiles were highest in the middle third of the venous wall and lowest in the inner third of the venous wall. Both the density and distribution of VV were uniform along the veins, and no differences were observed between the great and small saphenous veins. The VV density was statistically independent of the relative distance from the adventitia. The usability of this technique for perioperative frozen sections remains to be tested.

[Morphology and etiopathogenesis of the abdominal aortic aneurysm]. / Morfologie a etiopatogeneze aneuryzmatu brisní aorty.

The paper summarizes the latest research on the abdominal aorta aneurysm etiopathogenesis and compares normal aorta morphology with changes in the aortic aneurysm wall. The role of risk factors, especially hemodynamic and genetic, is discussed in detail. Special attention is paid to inflammatory processes including cytokines and matrix degrading proteases that contribute to the development of aneurysm. The role of thrombus and the current results of research into biomarkers indicating the risks and progression of the disease are analysed. Finally, a review of pharmacomodulation of the aortic aneurysm using statins, antibiotics, antihypertensive and nonsteroidal antiinflammatory drugs is presented.

Quantification of compact bone microporosities in the basal and alveolar portions of the human mandible using osteocyte lacunar density and area fraction of vascular canals.

Based on the orientation of the osteons, the basal portion and the alveolar portion of the body of the human mandible can be distinguished. In the compact bone, two types of microporosities can be quantified, the osteocyte lacunae and the vascular canals. Our aim was (i) to perform three-dimensional reconstruction of osteocyte lacunae to suggest an efficient means of sampling to estimate their numerical density and (ii) to compare bone microporosities in the basal and the alveolar portions of ten mandibles. Using optical disector, we estimated the density of osteocyte lacunae, and using a stereological point-counting technique, we quantified the area fraction of the vascular canals. The diameter of the lacunae was 14±3µm. While the fraction of vascular canals was comparable in both parts of the body of the mandible, the numerical density of osteocyte lacunae was higher (p=0.007) in the alveolar portion (17056±1264/mm(3)) than in the basal portion (14522±665/mm(3)). The lacunar and vascular microporosities were statistically independent of each other. As this is the first three-dimensional counting of osteocyte lacunae, we discuss the relation of this parameter to the biomechanics of the mandible, and we compare our data with previously used two-dimensional methods. We present an efficient sampling method that is useful for the histological description of bone microporosities. When taking into account the spatial characteristics of lacunae, the locally specific numerical density of lacunae can be easily assessed with the three-dimensional counting method, which is not biased by the variation in size and orientation of the lacunae.

Absence of microbiota (germ-free conditions) accelerates the atherosclerosis in ApoE-deficient mice fed standard low cholesterol diet.

AIM: The aim of our work was to determine the influence of intestinal bacteria on the development of atherosclerotic lesions using apolipoprotein E (ApoE)-deficient knockout mice. METHODS: The experiments were performed on ApoE-/--deficient mouse strain C57BL/6, bred under germ-free (GF) conditions for two generations or under conventional conditions with defined microflora (CV). The mice were fed a standard low cholesterol diet or cholesterol-rich diet for 3-4 months. We studied the development of advanced lesions in the thoracic and abdominal aorta by histological, morphometric and immunohistological methods. RESULTS: Conventionally reared ApoE-/- mice (containing no pathogenic intestinal microbiota) and fed a standard low cholesterol diet in contrast to a high cholesterol diet did not develop atherosclerotic aortic plaques. In contrast, ApoE-/- mice reared under germfree conditions for 2 generations and fed a low cholesterol diet exhibited atherosclerotic plaques in the aorta. Characteristic lipid deposition with foam cells and macrophages was found in their arterial walls. CONCLUSION: In contrast to the absence of atherosclerotic plaques in conventionally reared ApoE-deficient mice, germ-free ApoE-/- mice consuming the same low cholesterol standard diet developed atherosclerotic plaques in the aorta. Differences in atherosclerotic plaques between GF and CV ApoE-/- mice are not so apparent when mice are fed a high cholesterol diet. Our findings thus document the protective effect of microbiota (commensal bacteria) on atherosclerosis development.

Analysis of microcracks caused by drop shatter testing of porcine kidneys.

Although kidney trauma is a relatively common injury, its microscopic biomechanics are poorly understood. Experimental low-grade trauma in pig kidneys was studied using optical microscopy. We observed ruptures in the cortex as well as in the medulla. Both parts of the renal parenchyma were damaged, even in areas of the kidneys that were free of macroscopic cracks on the surface. To determine which constituents of the renal cortex and medulla, i.e. tubular parts of the nephron or the interstitial connective tissue, were less resistant to injury during the drop shatter test, we applied a simple stereological method to discriminate between random and tissue-specific rupture propagation. The ruptures propagated predominantly through the interstitial connective tissue of the renal cortex and medulla. The volume fraction of the tubules assessed by the Cavalieri principle was 90.4% within the renal cortex and 52.4% within the medulla. The most frequently affected blood vessels were the arcuate and interlobular veins, followed by the arcuate and interlobular arteries. No disruptions of the renal calyces were found.