Characteristics of pulmonary microvascular structure in postnatal yaks.

Yaks are typical plateau-adapted animals, however the microvascular changes and characteristics in their lungs after birth are still unclear. Pulmonary microvasculature characteristics and changes across age groups were analysed using morphological observation and molecular biology detection in yaks aged 1, 30 and 180 days old in addition to adults. Results: Our experiments demonstrated that yaks have fully developed pulmonary alveolar at birth but that interalveolar thickness increased with age. Immunofluorescence observations showed that microvessel density within the interalveolar septum in the yak gradually increased with age. In addition, transmission electron microscopy (TEM) results showed that the blood-air barrier of 1-day old and 30-days old yaks was significantly thicker than that observed at 180-days old and in adults (P < 0.05), which was caused by the thinning of the membrane of alveolar epithelial cells. Furthermore, Vegfa and Epas1 expression levels in 30-day old yaks were the highest in comparison to the other age groups (P < 0.05), whilst levels in adult yaks were the lowest (P < 0.05). The gradual increase in lung microvessel density can effectively satisfy the oxygen requirements of ageing yaks. In addition, these results suggest that the key period of yak lung development is from 30 to 180 days.

Danhong injection enhances the therapeutic effect of mannitol on hemispheric ischemic stroke by ameliorating blood-brain barrier disruption.

Mannitol, a representative of hyperosmolar therapy, is indispensable for the treatment of malignant cerebral infarction, but its therapeutic effect is limited by its exacerbation of blood-brain barrier (BBB) disruption. This study was to explore whether Danhong injection (DHI), a standardized product extracted from Salvia miltiorrhiza Bunge and Carthamus tinctorius L., inhibits the destructive effect of mannitol on BBB and thus enhancing the treatment of hemispheric ischemic stroke. SD rats were subjected to pMCAO followed by intravenous bolus injections of mannitol with/without DHI intervention. Neurological deficit score, brain edema, infarct volume at 24 h after MCAO and histopathology, microvascular ultrastructure, immunohistochemistry and immunofluorescence staining of endothelial cell junctions, energy metabolism in the ischemic penumbra were assessed. Intravenous mannitol after MCAO resulted in a decrease in 24 h mortality and cerebral edema, whereas no significant benefit on neurological deficits, infarct volume and microvascular ultrastructure. Moreover, mannitol led to the loss of endothelial integrity, manifested by the decreased expression of occludin, junctional adhesion molecule-1 (JAM-1) and zonula occluden-1 (ZO-1) and the discontinuity of occludin staining around the periphery of endothelial cells. Meanwhile, after mannitol treatment, energy-dependent vimentin and F-actin, ATP content, and ATP5D expression were down-regulated, while MMP2 and MMP9 expression increased in the ischemic penumbra. All the insults after mannitol treatment were attenuated by addition of intravenous DHI. The results suggest DHI as a potential remedy to attenuate mannitol-related BBB disruption, and the potential of DHI to upregulate energy metabolism and inhibit the activity of MMPs is likely attributable to its effects observed.

Assessing the impact of aging and blood pressure on dermal microvasculature by reactive hyperemia optical coherence tomography angiography.

Visualization and quantification of the skin microvasculature are important for studying the health of the human microcirculation. We correlated structural and pathophysiological changes of the dermal capillary-level microvasculature with age and blood pressure by using the reactive hyperemia optical coherence tomography angiography (RH-OCT-A) technique and evaluated both conventional OCT-A and the RH-OCT-A method as non-invasive imaging alternatives to histopathology. This observational pilot study acquired OCT-A and RH-OCT-A images of the dermal microvasculature of 13 young and 12 old healthy Caucasian female subjects. Two skin biopsies were collected per subject for histological analysis. The dermal microvasculature in OCT-A, RH-OCT-A, and histological images were automatically quantified and significant indications of vessel rarefaction in both old subjects and subjects with high blood pressure were observed by RH-OCT-A and histopathology. We showed that an increase in dermal microvasculature perfusion in response to reactive hyperemia was significantly lower in high blood pressure subjects compared to normal blood pressure subjects (117% vs. 229%). These results demonstrate that RH-OCT-A imaging holds functional information of the microvasculature with respect to physiological factors such as age and blood pressure that may help to monitor early disease progression and assess overall vascular health. Additionally, our results suggest that RH-OCT-A images may serve as a non-invasive alternative to histopathology for vascular analysis.

mTOR Attenuation with Rapamycin Reverses Neurovascular Uncoupling and Memory Deficits in Mice Modeling Alzheimer's Disease.

Vascular dysfunction is a universal feature of aging and decreased cerebral blood flow has been identified as an early event in the pathogenesis of Alzheimer's disease (AD). Cerebrovascular dysfunction in AD includes deficits in neurovascular coupling (NVC), a mechanism that ensures rapid delivery of energy substrates to active neurons through the blood supply. The mechanisms underlying NVC impairment in AD, however, are not well understood. We have previously shown that mechanistic/mammalian target of rapamycin (mTOR) drives cerebrovascular dysfunction in models of AD by reducing the activity of endothelial nitric oxide synthase (eNOS), and that attenuation of mTOR activity with rapamycin is sufficient to restore eNOS-dependent cerebrovascular function. Here we show mTOR drives NVC impairments in an AD model through the inhibition of neuronal NOS (nNOS)- and non-NOS-dependent components of NVC, and that mTOR attenuation with rapamycin is sufficient to restore NVC and even enhance it above WT responses. Restoration of NVC and concomitant reduction of cortical amyloid-ß levels effectively treated memory deficits in 12-month-old hAPP(J20) mice. These data indicate that mTOR is a critical driver of NVC dysfunction and underlies cognitive impairment in an AD model. Together with our previous findings, the present studies suggest that mTOR promotes cerebrovascular dysfunction in AD, which is associated with early disruption of nNOS activation, through its broad negative impact on nNOS as well as on non-NOS components of NVC. Our studies highlight the potential of mTOR attenuation as an efficacious treatment for AD and potentially other neurologic diseases of aging.SIGNIFICANCE STATEMENT Failure of the blood flow response to neuronal activation [neurovascular coupling (NVC)] in a model of AD precedes the onset of AD-like cognitive symptoms and is driven, to a large extent, by mammalian/mechanistic target of rapamycin (mTOR)-dependent inhibition of nitric oxide synthase activity. Our studies show that mTOR also drives AD-like failure of non-nitric oxide (NO)-mediated components of NVC. Thus, mTOR attenuation may serve to treat AD, where we find that neuronal NO synthase is profoundly reduced early in disease progression, and potentially other neurologic diseases of aging with cerebrovascular dysfunction as part of their etiology.

On P2X receptors in the brain: microvessels. Dedicated to the memory of the late Professor Geoffrey Burnstock (1929-2020).

This tribute article presents selected immunocytochemical and transmission electron microscope data on the location of ATP-gated P2X receptor in the rat brain, as studied in the 1990s in Prof G. Burnstock's laboratory at University College London. There are examples of immuno-ultrastructural findings and introductory information about pre- and post-synaptic location of P2X receptors in the rat cerebellum and endocrine hypothalamus to support the concept of purinergic transmission in the central nervous system. Then findings of diverse immunoreactivity for P2X1, P2X2, P2X4, and P2X6 receptors associated with brain microvessels are shown, including vascular endothelium and pericytes as well as perivascular astrocytes and neuronal components. These findings imply the involvement of P2X receptors and hence purinergic signalling in the neurovascular unit, at least in microvessels in the rat cerebellum and hypothalamic paraventricular and supraoptic nuclei examined here. Various aspects of P2X receptors in brain microvessels are discussed.

Microvasculature in hepatocellular carcinoma: An ultrastructural study.

BACKGROUND: Hepatocellular carcinoma (HCC) is one of the most vascularized tumor types, and is characterized by development of heterogeneous immature vessels with increased permeability. Here, we analyzed morphology and vascular permeability-related structures in endothelial cells of HCC microvessels. METHODS: Small (Type I) and large (Type II) peritumoral blood microvessels were assessed in HCC-bearing mice. By transmission electron microscopy, endothelial cell cytoplasm area, free transport vesicles, vesiculo-vacuolar organelles and clathrin-coated vesicles were measured. RESULTS: The phenotypic changes in the HCC microvessels included presence of sinusoidal capillarization, numerous luminal microprocesses and abnormal luminal channels, irregular dilatations of interendothelial junctions, local detachment of basement membranes and widened extracellular space. Endothelial cells Type I microvessels showed increased vesicular trafficking-related structures. CONCLUSION: Ultrastructural characteristics of microvessels Type I can associate with HCC new-formed microvessels. The morphological changes observed in HCC microvessels might explain the increased transcellular and paracellular permeability in HCC endothelial cells.

Microvascular anatomy of the urinary bladder in the adult African clawed toad, Xenopus laevis: A scanning electron microscope study of vascular casts.

We studied urinary bladders of adult male and female Xenopus laevis using light microscopy of stained tissue sections and scanning electron microscopy (SEM) of vascular corrosion casts (VCCs). Results showed that bilaterally a vesical artery branched off the femoral artery. At the dorso-lateral serosal surface of the body of the bladder each artery splitted within a short distance into up to five smaller arteries that supplied body and neck regions. Arteries gave off short and long terminal arterioles, which fed the mucosal capillary meshwork. Long terminal arterioles followed dimensional changes of the bladder, while short ones anchored the capillary network to the arterial system. Capillary mesh sizes and shapes varied according to the filling state of the urinary bladder. In the highly to moderately distended (filled) bladder, capillaries were rather straight or undulated only slightly, in the contracted (emptied) bladder they undulated strongly and lay side by side. Postcapillary venules formed by two equally sized capillaries or from capillaries, which serially drained into a small postcapillary venule. Vesical venules formed a large dorsal vesical and a varying number of smaller lateral and ventral vesical veins. The dorsal vesical vein drained either directly or via the posterior hemorrhoidal vein into the common pelvic vein. Lateral and ventral vesical veins also drained into the latter. The vascular patterns found were discussed in respect to the bladder spatial movements during distention (filling) and relaxation (emptying). Furthermore, it was hypothesized that an extensively filled bladder could compress the overlaying abdominal vein forcing part of the blood otherwise drained towards the liver to be detoured via the renal portal veins to the kidneys.

Structural Investigation of Epididymal Microvasculature and Its Relation to Telocytes and Immune Cells in Camel.

The vascular and perivascular cells, including telocytes (TCs) and immune cells, play an important role in male fertility. The current study intended to describe in detail the microvascular structures harboring special regulatory devices in addition to the interstitial cellular components of the one-humped camel epididymis. The samples were collected from 10 clinically healthy mature camels (Camelus dromedarius). The distribution and characteristics of TCs, peripheral blood vessels of the epididymis, and immune cells were investigated using the light, immunohistochemistry, immunofluorescence, and transmission electron microscopy analyses. Frequent occlusive or throttle arterioles were demonstrated in the epididymal interstitium and their tunica media consisted of glomus cells. In addition, some vein walls consisted of one or two layers of glomus cells. TCs, fibroblasts, muscle cells, and tunica media of the blood vessels, that present in the loose connective tissue surrounding the intertubular interstitium of camel epididymis, showed a positive reaction with vimentin. The endothelium of blood vessels and veins showed positive immunoreactivity for CD34 and vascular endothelial growth factor (VEGF). Furthermore, VEGF, CD34, and S100 proteins were expressed in dendritic cells (DCs) as well as TCs. The current data suggest the involvement of DCs and TCs in angiogenesis and a possible role for the interstitial components in creating an appropriate milieu for the full maturation of sperms.

Insulin protects against type 1 diabetes mellitus-induced ultrastructural abnormalities of pancreatic islet microcirculation.

Pancreatic islet microcirculation, consisting of pancreatic islet microvascular endothelial cells (IMECs) and pericytes (IMPCs), provides crucial support for the physiological function of pancreatic islet. Emerging evidence suggests that pancreatic islet microcirculation is impaired in type 1 diabetes mellitus (T1DM). Here, we investigated the potential ultrastructural protective effects of insulin against streptozotocin (STZ)-induced ultrastructural abnormalities of the pancreatic islet microcirculation in T1DM mouse model. For this purpose, pancreatic tissues were collected from control, STZ-induced T1DM and insulin-treated mice, and a pancreatic IMECs cell line (MS1) was cultured under control, 35 mM glucose with or without 10-8 M insulin conditions. Transmission and scanning electron microscopies were employed to evaluate the ultrastructure of the pancreatic islet microcirculation. We observed ultrastructural damage to IMECs and IMPCs in the type 1 diabetic group, as demonstrated by destruction of the cytoplasmic membrane and organelles (mainly mitochondria), and this damage was substantially reversed by insulin treatment. Furthermore, insulin inhibited collagenous fiber proliferation and alleviated edema of the widened pancreatic islet exocrine interface in T1DM mice. We conclude that insulin protects against T1DM-induced ultrastructural abnormalities of the pancreatic islet microcirculation.

Renal microvasculature in the adult pipid frog, Xenopus laevis: A scanning electron microscope study of vascular corrosion casts.

We studied the opisthonephric (mesonephric) kidneys of adult male and female Xenopus laevis using scanning electron microscopy (SEM) of vascular corrosion casts and light microscopy of paraplast embedded tissue sections. Both techniques displayed glomeruli from ventral to mid-dorsal regions of the kidneys with single glomeruli located dorsally close beneath the renal capsule. Glomeruli in general were fed by a single afferent arteriole and drained via a single thinner efferent arteriole into peritubular vessels. Light microscopy and SEM of vascular corrosion casts revealed sphincters at the origins of afferent arterioles, which arose closely, spaced from their parent renal arteries. The second source of renal blood supply via renal portal veins varied interindividually in branching patterns with vessels showing up to five branching orders before they became peritubular vessels. Main trunks and their first- and second-order branches revealed clear longish endothelial cell nuclei imprint patterns oriented parallel to the vessels longitudinal axis, a pattern characteristic for arteries. Peritubular vessels had irregular contours and were never seen as clear cylindrical structures. They ran rather parallel, anastomosed with neighbors and changed into renal venules and veins, which finally emptied into the ventrally located posterior caval vein. A third source of blood supply of the peritubular vessels by straight terminal portions of renal arteries (vasa recta) was not found.

Microvascular anatomy of ovary and oviduct in the adult African Clawed Toad (Xenopus laevis DAUDIN, 1802)-Histomorphology and scanning electron microscopy of vascular corrosion casts.

Ovaries and oviducts of the adult African Clawed Toad (Xenopus laevis DAUDIN, 1802) were studied by light microscopy (LM) of paraplast embedded tissue sections and scanning electron microscopy (SEM) of vascular corrosion casts (VCCs). Histomorphology revealed that ovarian vessels located in the thecal layers. Ovarian and interlobar arteries displayed a horse-shoe shaped longitudinally running bundle of vascular smooth muscle cells. Follicular blood vessels showed flattened profiles, which were confirmed by scanning electron microscopy in vascular corrosion casts. The flattened profiles obviously led to high intravasal pressures, which locally prevented filling of the follicular capillary bed. Oviduct arteries pierced the fibrous stroma surrounding the oviduct mucosa. In the pars convoluta, the mucosa consisted of a ciliated simple columnar epithelium and tubular oviduct glands that opened between ciliated epithelial cells into the oviduct lumen. Oviduct arteries branched at the basolateral surfaces of tubular glands. After a short tangential course, arterioles branched into capillaries which ran radially between oviduct glands towards the subepithelium. Anastomoses at different heights connected capillaries of neighbouring glands. Subepithelially, capillaries ran longitudinally and undulated. Postcapillary venules radiated centrifugally towards the stroma to finally drain into oviduct veins located in the stroma. Oviduct vascular densities clearly reflected non-ovulatory and ovulatory states.

Serial block-face scanning electron microscopy reveals novel intercellular connections in human term placental microvasculature.

The placental microvasculature is a conduit for fetal blood allowing solute exchange between the mother and the fetus. Serial block-face scanning electron microscopy (SBF SEM) allows ultrastructure to be viewed in three dimensions and provides a new perspective on placental anatomy. This study used SBF SEM to study endothelial cells within the human placental microvasculature from uncomplicated pregnancies. Term human placental villi were aldehyde-fixed and processed for imaging by SBF SEM. Manual segmentation was carried out on a terminal villous capillary and an intermediate villous arteriole and venule. Twenty-seven SBF SEM stacks from terminal villi were analysed using stereological approaches to determine the volumes of microvascular components and the proportions of pericyte coverage. SBF SEM analysis of capillary endothelial cells revealed the presence of interendothelial protrusions (IEPs) originating from the donor cell at the endothelial junction and forming deep thin projections up to 7 µm into the adjacent endothelial cells. IEP density was estimated to be in the order of 35 million cm-3 placental tissue. Pericytes cover 15% of the fetal capillary surface area in terminal villi. In comparison, the cytotrophoblast covered 24% of the syncytiotrophoblast basal membrane. A trans-endothelial channel was observed in a region of the vasculo-syncytial capillary. Pericyte coverage was extensive in both arteriole and venule. Three-dimensional imaging of the placental microvasculature identified novel ultrastructural features and provided an insight into factors that may influence capillary permeability and placental function. We hypothesise that the IEPs may allow mechanosensing between adjacent endothelial cells to assist in the maintenance of vessel integrity. The numbers of endothelial junctions, the presence of trans-endothelial channels and the extent of pericyte coverage all provide an insight into the factors determining capillary permeability.

Endothelial-specific Crif1 deletion induces BBB maturation and disruption via the alteration of actin dynamics by impaired mitochondrial respiration.

Cerebral endothelial cells (ECs) require junctional proteins to maintain blood-brain barrier (BBB) integrity, restricting toxic substances and controlling peripheral immune cells with a higher concentration of mitochondria than ECs of peripheral capillaries. The mechanism underlying BBB disruption by defective mitochondrial oxidative phosphorylation (OxPhos) is unclear in a mitochondria-related gene-targeted animal model. To assess the role of EC mitochondrial OxPhos function in the maintenance of the BBB, we developed an EC-specific CR6-interactin factor1 (Crif1) deletion mouse. We clearly observed defects in motor behavior, uncompacted myelin and leukocyte infiltration caused by BBB maturation and disruption in this mice. Furthermore, we investigated the alteration in the actin cytoskeleton, which interacts with junctional proteins to support BBB integrity. Loss of Crif1 led to reorganization of the actin cytoskeleton and a decrease in tight junction-associated protein expression through an ATP production defect in vitro and in vivo. Based on these results, we suggest that mitochondrial OxPhos is important for the maturation and maintenance of BBB integrity by supplying ATP to cerebral ECs.

Downregulation of microRNA-103a reduces microvascular endothelial cell injury in a rat model of cerebral ischemia by targeting AXIN2.

Multiple microRNAs (miRNAs) have been found to be linked with cerebral ischemia. Thus, this study was employed to characterize the capabilities of miRNA-103a (miR-103a) on the brain microvascular endothelial cells (BMECs) injury in rat models of middle cerebral artery occlusion (MCAO) by regulating AXIN2. The MCAO rat model was developed by the suture method, where normal saline, miR-103a inhibitors, or its negative control were separately injected into the lateral ventricle to assess the function of miR-103a inhibitors in BMECs apoptosis, microvessel density, as well as angiogenesis. In addition, the oxygen-glucose deprivation model was induced in primarily cultured BMECs to unearth the functions of miR-103a inhibitors on cell viability and apoptosis, lactate dehydrogenase (LDH) release and tube formation ability. Furthermore, the relationship between miR-103a and AXIN2 was verified. The modeled rats of MCAO showed robustly expressed miR-103a, poorly expressed AXIN2, severe neurological deficits, accelerated apoptosis and reduced angiogenesis. miR-103a expression had a negative correlation with AXIN2 messenger RNA expression (r = -0.799; p < .05). In response to the treatment of miR-103a inhibitors, the BMECs apoptosis was suppressed and angiogenesis was restored, corresponding to upregulated Bcl-2, VEGF, and Ang-1, in addition to downregulated caspase-3 and Bax. Meanwhile, AXIN2 was verified to be the miR-103a's target gene. More important, miR-103a inhibitors led to promoted BMEC viability and tube formation and suppressed apoptosis and LDH release rate. This study highlights that miR-103a targets and negatively regulates AXIN2, whereby reducing BMEC injury in cerebral ischemia.

Brain microvascular pathology in Susac syndrome: an electron microscopic study of five cases.

Susac syndrome is a rare, immune-mediated disease characterized by encephalopathy, branch retinal artery occlusion, and hearing loss. Herein, we describe the electron microscopic findings of three brain biopsies and two brain autopsies performed on five patients whose working clinical diagnosis was Susac syndrome. In all five cases, the key findings were basement membrane thickening and collagen deposition in the perivascular space involving small vessels and leading to thickening of vessel walls, narrowing, and vascular occlusion. These findings indicate that Susac syndrome is a microvascular disease. Mononuclear cells were present in the perivascular space, underlining the inflammatory nature of the pathology. Though nonspecific, the changes can be distinguished from genetic and acquired small vessel diseases. The encephalopathy of Susac syndrome overlaps clinically with degenerative and infectious conditions, and brain biopsy may be used for its diagnosis. Its vascular etiology may not be obvious on light microscopy, and electron microscopy is important for its confirmation.

Isometrically Resolved Photoacoustic Microscopy Based on Broadband Surface Plasmon Resonance Ultrasound Sensing.

Photoacoustic microscopy (PAM) can measure optical absorption-based molecular specificities within tissues. Despite the diffraction-limited lateral resolution in optical-resolution photoacoustic microscopy (OR-PAM), the ongoing challenge is poor axial resolution because of an insufficient ultrasound detection bandwidth, which hampers PAM volumetric imaging. We propose polarization-differential surface plasmon resonance (SPR) sensing for broadband and high-sensitivity photoacoustic (PA) detection, allowing OR-PAM with comparable resolution along lateral and axial directions. This sensor possesses an estimated noise-equivalent-pressure sensitivity of ∼477 Pa over an approximately linear pressure response up to 107 kPa. Moreover, an improved PA detection bandwidth of ∼173 MHz permits an axial resolution (∼7.6 µm) that approaches the lateral resolution (∼4.5 µm) of our OR-PAM system. The capability in spatially isometric micrometer-scale resolution enables in vivo volumetric label-free imaging of the microvasculature of a mouse ear. The SPR sensing technology promises broader applications of PAM in biomedical studies such as microcirculation.

The ultrastructural anatomy of the nuclear envelope in the masseter muscle indicates its role in the metabolism of the intracellular Ca+.

Specific ultrastructural anatomy of masticatory muscles is commonly referred to a general pattern assigned to striated muscles. Junctional feet consisting of calcium channels of the sarcoplasmic reticulum (i.e. the ryanodine receptors, RyRs) physically connected to the calcium channels of the t-tubules build triads within striated muscles. Functional RyRs were demonstrated in the nuclear envelopes of pancreas and of a skeletal muscle derived cell line, but not in muscle in situ. It was hypothesized that ryanodine receptors (RyRs) could also exist in the nuclear envelope in the masseter muscle, thus aiming at studying this by transmission electron microscopy. There were identified paired and consistent subsarcolemmal clusters of mitochondria, appearing as outpockets of the muscle fibers, usually flanking an endomysial microvessel. It was observed on grazing longitudinal cuts that the I-band-limited mitochondria were not strictly located in a single intermyofibrillar space but continued transversally over the I-band to the next intermyofibrillar space. It appeared that the I-band-limited transverse mitochondria participate with the column-forming mitochondria in building a rather incomplete mitochondrial reticulum of the masseter muscle. Subsarcolemmal nuclei presented nuclear envelope-associated RyRs. Moreover, t-tubules were contacting the nuclear envelope and they were seemingly filled from the perinuclear space. This could suggest that nucleoplasmic calcium could contribute to balance the cytosolic concentration via pre-built anatomical routes: (i) indirectly, via the RyRs of the nuclear envelope and (ii) directly via the communication of t-tubules and sarcoplasmic reticulum through the perinuclear space.

Microvascular Dysfunction Related to Progressive Left Ventricular Remodeling due to Chronic Occlusion of the Left Anterior Descending Artery in an Adult Porcine Heart.

Occlusion of a major coronary artery induces myocardial infarction (MI), leading to left ventricle (LV) remodeling due to progressive microvasculature dysfunction. Irreversible impairment in microvascular function has been suggested to extend from the infarcted region into the infarct-border or remote regions, depending on the time to revascularization. Our aim was to determine whether the occlusion of a major coronary artery induces microvascular dysfunction in the adjacent area perfused by intact coronary arteries using a porcine model for chronic total occlusion of the left anterior descending artery (LAD). MI was induced via an ameroid constrictor ring around the LAD in adult Göttingen pigs (Sus scrofa domesticus, n = 5). Age-matched normal pigs were treated as controls (n = 3). Cardiac magnetic resonance showed reduced systolic regional wall motion in the left circumflex (LCx) and right coronary artery (RCA) territories, with a progressively worsening motion in the infarction-adjacent area over an eight-week period. On 13N-ammonia positron emission tomography (PET), myocardial blood flow (MBF) during hyperemia was significantly greater in the LCx and RCA territories (particularly in the infarction-adjacent area) compared to that in the LAD territory at four weeks after infarct induction. Subsequently, the flow significantly decreased, approaching that in the LAD territory at eight weeks after infarct induction. Fluoroscopy-guided pressure-wire studies showed significantly higher microvascular resistance in the LCx area at eight weeks compared to that in controls. Electron microscopy showed endothelium swelling and microvasculature disruption in areas adjacent to the LCx and RCA territories. Anterior MI caused coronary microvascular dysfunction in the adjacent area, associated with a reduced MBF and regional wall motion.

Heart ventricular histology and microvasculature together with aortic histology and elastic lamellar structure: A comparison of a novel dual-purpose to a broiler chicken line.

The use of dual-purpose chickens is a strategy to avoid killing one-day-old male chicks of egg laying lines. Lohmann Dual (LD) is a novel dual-purpose chicken line created by the crossbreeding of layer and broiler lines. However, many of the cardiovascular diseases of broilers are likely to be associated with intensive genetic selection for growth and feed conversion efficiency. This study aimed to compare the macroscopic and microscopic structure of the heart and the aorta of the LD chicken line with that of the broiler chicken line, Ross 308 (Ross) under typical husbandry conditions for meat production. Eighty, one-day-old male chicks of each line were housed for 5 weeks (Ross) and 9 weeks (LD). Six birds of each line were sampled weekly. Heart mass, thickness of ventricular walls, cardiomyocyte size and blood capillary density as well as aortic diameter and thickness, number of elastic lamellae and elastic fiber percentage in the aortic wall were determined. The growth patterns of the heart were the same in the two lines. Although LD chickens had a lower absolute heart mass than that of Ross chickens, the relative heart mass in both lines was similar. The cardiomyocytes of LD chickens were larger than those of Ross's of the same body weight (BW), nevertheless both lines had similar thicknesses of their ventricular walls. The blood capillary density was greater in the LD heart than in that of the Ross heart. The aorta of LD chickens had proportionally; a greater aortic lumen radius, larger numbers of elastic lamellae and more elastic fibers than in Ross chickens. Our results suggest that the heart and aorta of the LD chickens have not been disadvantaged by their intensive genetic selection; furthermore, LD chickens have a better myocardial capillary supply and better aortic mechanical properties than those of Ross chickens.