Large Arterioles Research Articles

Aging is associated with changes to the biomechanical properties of the posterior cerebral artery and parenchymal arterioles.

Artery remodeling, described as a change in artery structure, may be responsible for the increased risk of cardiovascular disease with aging. Although the risk for stroke is known to increase with age, relatively young animals have been used in most stroke studies. Therefore, more information is needed on how aging alters the biomechanical properties of cerebral arteries. Posterior cerebral arteries (PCAs) and parenchymal arterioles (PAs) are important in controlling brain perfusion. We hypothesized that aged (22-24 mo old) C57bl/6 mice would have stiffer PCAs and PAs than young (3-5 mo old) mice. The biomechanical properties of the PCAs and PAs were assessed by pressure myography. Data are presented as means ± SE of young vs. old. In the PCA, older mice had increased outer (155.6 ± 3.2 vs. 169.9 ± 3.2 μm) and lumen (116.4 ± 3.6 vs. 137.1 ± 4.7 μm) diameters. Wall stress (375.6 ± 35.4 vs. 504.7 ± 60.0 dyn/cm(2)) and artery stiffness (β-coefficient: 5.2 ± 0.3 vs. 7.6 ± 0.9) were also increased. However, wall strain (0.8 ± 0.1 vs. 0.6 ± 0.1) was reduced with age. In the PAs from old mice, wall thickness (3.9 ± 0.3 vs. 5.1 ± 0.2 μm) and area (591.1 ± 95.4 vs. 852.8 ± 100 μm(2)) were increased while stress (758.1 ± 100.0 vs. 587.2 ± 35.1 dyn/cm(2)) was reduced. Aging also increased mean arterial and pulse pressures. We conclude that age-associated remodeling occurs in large cerebral arteries and arterioles and may increase the risk of cerebrovascular disease.

A mathematical model for the vessel recruitment in coronary microcirculation in the absence of active autoregulation

This paper proposes a mathematical model for vessel recruitment in the microvascular coronary network. The model is based on microvascular network units (MVNUs), where we define a MVNU as a portion of the microvascular network comprising seven generations of identical, parallel-arranged vessels (upstream arteries, large and small arterioles, capillaries, small and large venules, and downstream veins). The model implements a new mechanism to describe the variation in the number of MVNU in response to sudden variations of the local input pressure. In particular, it describes a recruitment mechanism dependent on distal pressure which operates in the coronary microcirculatory network even in maximally dilated conditions. We apply the model to interpret data from 29 patients who underwent revascularization by percutaneous coronary intervention (PCI). Treated vessels were the left anterior descending coronary artery, the left circumflex and the right coronary artery in 26, 2 and 1 patients, respectively. Following intracoronary adenosine administration, distal coronary pressure and blood flow were 48±18mmHg and 45±30ml/min before PCI, respectively, and significantly increased afterwards to 80±17mmHg and 68±32ml/min (p<0.001). The model predicts an increase in MVNU number in patients with preserved wall motion in the myocardial region which underwent PCI. On the contrary, a decrease in MVNU number is predicted by the model in patients with regional dysfunction and implies a relatively lower response of maximal flow to revascularization.

Vasculitic Neuropathies.

From pathological standpoint, we divide vasculitic neuropathies in two categories: nerve large arteriole vasculitides and nerve microvasculitis. It is also important to determine whether a large arteriole vasculitis has an infectious etiology as it entails different treatment approach. Treatment of non-infectious large arteriole vasculitides consists initially of induction therapy with corticosteroids. Adding an immunosuppressant, mainly cyclophosphamide, is often needed. Treatment of infectious large arteriole vasculitides needs a multidisciplinary approach to target both the underlying infection and the vasculitis. Corticosteroids are the first-line therapy for classic non-systemic vasculitic neuropathy. Stable or improving patients without biopsy evidence of active vasculitis can be either observed or treated. Currently, adding an immunosuppressant is only indicated for patients who continue to progress on corticosteroids alone or patients with a rapidly progressive course. The treatment of the radiculoplexus neuropathies such as diabetic lumbosacral radiculoplexus neuropathy, lumbosacral radiculoplexus neuropathy (in non-diabetic patients), and diabetic cervical radiculoplexus neuropathy, as well as painless diabetic motor neuropathy, is not well established yet. We treat patients, if they present early on in the disease course or if they have severe disabling symptoms, with IV methylprednisolone 1g once a week for 12weeks.

Critical histologic appraisal of the pseudocapsule of small renal tumors

Small renal tumors are usually enwrapped in a pseudocapsule with well-confined borders, a feature that facilitates the performance of nephron-sparing surgeries (NSS). Our study was designed to evaluate the histologic features of the pseudocapsule of small renal tumors. One hundred seventy-eight renal tumors (≤4 cm), which were surgically removed by total nephrectomy, partial nephrectomy, or enucleation procedures during 2002-2013, were re-examined microscopically. Special attention was paid to the completeness and thickness of the pseudocapsule as well as the extra-pseudocapsular extension (EPE); components of the pseudocapsule and the intra-pseudocapsular vasculature (size/number) were evaluated. The data were analyzed according to the histological tumor types, Fuhrman grades, and sizes. Student's t test and chi-square tests were used for statistical analysis. Among 178 renal tumors, clear cell renal carcinomas (RCC) showed the thickest pseudocapsule (average 0.23 mm), while oncocytoma showed the thinnest (average thickness of 0.09 mm). Chromophobe RCC had the highest rate of EPE and the highest percentage of tumors with larger (≥0.2 mm) intra-pseudocapsular arteries. The EPE rate was also related to the nuclear grade (p = 0.001). Muscular differentiation, reticulin, and collagen components were present in the fibrous stroma of the pseudocapsule. Our study suggests that clear cell RCC has the thickest pseudocapsule while oncocytoma has a poorly developed pseudocapsule, but shows the least infiltrative pattern. In small RCC (≤4.0 cm), the EPE rate is related to tumor grade but not to tumor size. Larger arterioles (≥0.2 mm) are encountered infrequently within the tumor pseudocapsule, with the highest percentage being found in chromophobe RCC and the lowest in papillary RCC.

(817) - Cardiac Allograft Vasculopathy Assessed By Quantitative Coronary Angiography: A Single Center Prospective Study

s S297 Methods: Retrospective data from 27 heart transplant patients who underwent endomyocardial biopsy, cardiac diastolic function evaluation by echocardiography at rest and maximum physical capacity evaluation by ergospirometry were collected and analysed in a double-blind trial. Also, it was obtained myocardial biopsy of 10 control patients from a previous study. No other data was obtained from them. In order to realize the histological analysis, slides were stained by picrosirius-polarization (quantitative analysis of collagen). The picrosirius-polarization stained slides were scanned and transferred to a software to quantify the area of fibrosis. It was determined these images would be obtained from 40x magnification and from well distributed and noncoincident microscopic fields, with over 50% of tissue area and without large arterioles, pericardium or endocardium. Five to ten photos per slide were obtained, totalizing an area between 0.46mm2 and 0.92mm2. Afterwards, a statistical data analysis was performed correlating the area of fibrosis with the other data of the transplanted patients. The results were considered significant at p-value inferior to 0.05. Results: It was observed a percentage of 7,43% of fibrosis from the transplanted patients, and a percentage of 1,99% of fibrosis in the control patients. The percentage of fibrosis was considered significant in the transplanted patients (p= 0,037 in Kolmogorov-Sminov test, and p= 0,000 in Shapiro-Wilk test), and considered significant in the control group by Shapiro-Wilk test (p= 0,001). The correlation of fibrosis area and data of diastolic cardiac function (E/E’) and physical capacity (mean VO2 after six minutes, max VO2) for each transplanted patient resulted in significance values all above 0,05. Conclusion: The presence of fibrosis in the myocardial tissue in heart transplant patients was considered significant in comparison with the control group. However, it was not possible to establish a correlation of the area of fibrosis and the diastolic heart dysfunction and physical capacity in transplanted patients.

(814) - Prognostic Value of Multislice Computed Tomography Coronary Angiography in Cardiac Transplant Recipients

s S297 Methods: Retrospective data from 27 heart transplant patients who underwent endomyocardial biopsy, cardiac diastolic function evaluation by echocardiography at rest and maximum physical capacity evaluation by ergospirometry were collected and analysed in a double-blind trial. Also, it was obtained myocardial biopsy of 10 control patients from a previous study. No other data was obtained from them. In order to realize the histological analysis, slides were stained by picrosirius-polarization (quantitative analysis of collagen). The picrosirius-polarization stained slides were scanned and transferred to a software to quantify the area of fibrosis. It was determined these images would be obtained from 40x magnification and from well distributed and noncoincident microscopic fields, with over 50% of tissue area and without large arterioles, pericardium or endocardium. Five to ten photos per slide were obtained, totalizing an area between 0.46mm2 and 0.92mm2. Afterwards, a statistical data analysis was performed correlating the area of fibrosis with the other data of the transplanted patients. The results were considered significant at p-value inferior to 0.05. Results: It was observed a percentage of 7,43% of fibrosis from the transplanted patients, and a percentage of 1,99% of fibrosis in the control patients. The percentage of fibrosis was considered significant in the transplanted patients (p= 0,037 in Kolmogorov-Sminov test, and p= 0,000 in Shapiro-Wilk test), and considered significant in the control group by Shapiro-Wilk test (p= 0,001). The correlation of fibrosis area and data of diastolic cardiac function (E/E’) and physical capacity (mean VO2 after six minutes, max VO2) for each transplanted patient resulted in significance values all above 0,05. Conclusion: The presence of fibrosis in the myocardial tissue in heart transplant patients was considered significant in comparison with the control group. However, it was not possible to establish a correlation of the area of fibrosis and the diastolic heart dysfunction and physical capacity in transplanted patients.

Inflammation, immunity, and hypertensive end-organ damage.

For >50 years, it has been recognized that immunity contributes to hypertension. Recent data have defined an important role of T cells and various T cell-derived cytokines in several models of experimental hypertension. These studies have shown that stimuli like angiotensin II, deoxycorticosterone acetate-salt, and excessive catecholamines lead to formation of effector like T cells that infiltrate the kidney and perivascular regions of both large arteries and arterioles. There is also accumulation of monocyte/macrophages in these regions. Cytokines released from these cells, including interleukin-17, interferon-γ, tumor necrosis factorα, and interleukin-6 promote both renal and vascular dysfunction and damage, leading to enhanced sodium retention and increased systemic vascular resistance. The renal effects of these cytokines remain to be fully defined, but include enhanced formation of angiotensinogen, increased sodium reabsorption, and increased renal fibrosis. Recent experiments have defined a link between oxidative stress and immune activation in hypertension. These have shown that hypertension is associated with formation of reactive oxygen species in dendritic cells that lead to formation of gamma ketoaldehydes, or isoketals. These rapidly adduct to protein lysines and are presented by dendritic cells as neoantigens that activate T cells and promote hypertension. Thus, cells of both the innate and adaptive immune system contribute to end-organ damage and dysfunction in hypertension. Therapeutic interventions to reduce activation of these cells may prove beneficial in reducing end-organ damage and preventing consequences of hypertension, including myocardial infarction, heart failure, renal failure, and stroke.

ANALYTIC MULTIPLICATIVE SEPARATION AND EXISTENCE INVESTIGATION OF NON-LINEAR OXYGEN TRANSPORT WITH POISEUILLE HEMODYNAMIC FLOW IN A SEMI-GENERALIZED COORDINATE SYSTEM

A well known governing nonlinear PDE used to model oxygen transport is formulated in a generalized co-ordinate system where the Laplacian is expressed in metric tensor form. A reduction of the pde to simpler problem, which has never been done before, subject to specific integrability conditions is shown. A specific form of the initial equation to be reduced has been used by Nair and coworkers [1-3] describing the intraluminal problem of oxygen transport in large capillaries or arterioles and more recent work by [4] describing release of ATP in microchannels. In each of these cases, a tube with a central core, rich in red blood cells, and with a thin plasma region near the boundary wall, free of RBCs is considered. A co-ordinate transformation to solve reduced pde in core region is adopted. An extension and modification of the work of Erbe and Wang [5] is derived and existence of positive solutions of an ode obtained in the general formulation is obtained for nonhomogeneous mixed boundary conditions and on general positive interval. Finally a solution method is given to solve a linear equation used by Nair [1-3] in the plasma layer.

Retinal Arterial Macroaneurysms (RAM)--pathology, differenzial diagnoses, and therapy

Retinal arterial macroaneurysms (RAM) are unilateral, solitary, acquired saccular or fusiform dilatations of the large arterioles of the retina, usually within the first three orders of bifurcation. They are associated with systemic vascular conditions such as hypertension and arteriosclerotic disease and occur most commonly in elderly women. Cases of simple RAM are predominated by the vascular ectasia. These macroaneurysms regress without treatment and without causing decreased visual acuity and will usually remain undetected. Complex RAM often go along with vision loss due to haemorrhage or oedema affecting the macula. Poor visual outcome may occur secondary to foveal exudates and subfoveal haemorrhage, the latter appear as pre-retinal, intra-, and subretinal haemorrhage. This overview discusses conservative and surgical therapeutic options for complex cases.

Direct effects of Rho-kinase inhibitor on pial microvessels in rabbits.

Rho-kinase inhibitor is widely used for prevention of cerebral vascular spasm. However, the cerebral pial vascular action of Rho-kinase inhibitor has not been investigated. We therefore evaluated the direct effects of Y-27632, a Rho-kinase inhibitor, on pial microvessels. Experiments were performed on anesthetized rabbits. A closed cranial window was used to visualize the pial microcirculation. After baseline hemodynamic and pial vascular measurements, the cranial window was superfused with four increasing concentrations of Y-27632 (10(-9), 10(-7), 10(-6), 10(-5) moll(-1); n=7) dissolved in artificial cerebrospinal fluid for 7min each. We measured the diameters of pial vessels, mean arterial pressure (MAP), heart rate (HR), and rectal temperature at 7min after application of each Y-27632 concentration. MAP, HR, rectal temperature, arterial pH, PaCO2, PaO2, and plasma Na(+), K(+) and glucose concentrations did not change significantly during the experimental period. Y-27632 at 10(-9) to 10(-7) moll(-1) did not produce any significant change in pial arterioles. Topical application of Y-27632 at 10(-6) and 10(-5) moll(-1) produced pial large (8.4±5.7 and 19.8±12.7%) and small (10.1±8.5 and 18.1±12.3%) arterioles dilation. However, Y-27632 did not produce any change in pial large and small venules. We evaluated the direct effects of Y-27632 on pial microvessels. Y-27632 dilates only pial arterioles in a concentration-dependent manner, and most at a concentration of 10(-5) moll(-1). Y-27632 is a potent cerebral pial arteriolar dilator but is not a venular dilator.

LEUKOCYTE PLUGGING OF CAPILLARIES REDUCES BRAIN BLOOD FLOW IN MOUSE MODELS OF ALZHEIMER'S DISEASE

Cerebral blood flow reductions of ∼30% are observed in patients and animal models of Alzheimer's disease (AD). Although it likely contributes to cognitive impairment and disease progression, no physiological explanation for this brain hypoperfusion has emerged. Using in vivo two-photon excited fluorescence imaging, we examined cortical blood flow in transgenic AD mice. While we found no obstructions in larger arterioles or venules, we found an elevation in the number of brain capillaries with stalled blood flow in transgenic AD mice (median ∼1.8%) as compared to age-matched controls (0.25%). Because one stalled capillary causes decreased flow in many downstream vessels, the impact of this capillary stalling on global brain blood flow is significant. We further determined that these capillary stalls are caused by leukocytes that are firmly stuck in individual capillary segments, suggesting an inflammation–mediated mechanism. By depleting leukocytes, we found that capillary stalling in AD mice can be reduced to near zero, leading to ∼30% increases in cerebral blood flow. We also found that capillary stalling begins early in disease progression, before deposition of amyloid plaques. Hypoperfusion likely contributes to cognitive deficits in AD patients, and recent work has shown that flow reductions increase the rate of amyloid-beta deposition, suggesting a positive feedback mechanism between amyloid-beta aggregation and brain blood flow decreases, with each impacting neural function.

Functional sympatholysis and sympathetic escape in a theoretical model for blood flow regulation.

A mathematical simulation of flow regulation in vascular networks is used to investigate the interaction between arteriolar vasoconstriction due to sympathetic nerve activity (SNA) and vasodilation due to increased oxygen demand. A network with 13 vessel segments in series is used, each segment representing a different size range of arterioles or venules. The network includes five actively regulating arteriolar segments with time-dependent diameters influenced by shear stress, wall tension, metabolic regulation, and SNA. Metabolic signals are assumed to be propagated upstream along vessel walls via a conducted response. The model exhibits functional sympatholysis, in which sympathetic vasoconstriction is partially abrogated by increases in metabolic demand, and sympathetic escape, in which SNA elicits an initial vasoconstriction followed by vasodilation. In accordance with experimental observations, these phenomena are more prominent in small arterioles than in larger arterioles when SNA is assumed to act equally on arterioles of all sizes. The results imply that a mechanism based on the competing effects on arteriolar tone of SNA and conducted metabolic signals can account for several observed characteristics of functional sympatholysis, including the different responses of large and small arterioles.

Hemodynamic consequences of spatially‐dependent sympathetic regulation in skeletal muscle arteriolar trees (678.14)

The sympathetic nervous system (SNS) elicits vasoconstriction on skeletal muscle arterioles via release of neurotransmitters norepinephrine (NE; acting on α1‐ and α2R), neuropeptide Y (NPY; acting on Y1R), and adenosine‐triphosphate (ATP; acting on P2X1R). Previous studies have shown that the level of α‐adrenoreceptor modulation is dependent on vessel branch order. However, to date, no studies have investigated the integrated roles of α1R, α2R, Y1R, and P2X1R modulation on arteriolar network hemodynamics. Thus, we evaluated the effects of phenylephrine (PE; α1R agonist), UK 14,304 (UK; α2R agonist), NPY, and ATP on arteriolar diameters in continuously branching arteriolar trees (1st order to 5th order; 1A‐5A). In male rats, concentration‐response curves (PE and ATP: 10‐9‐10‐4M; UK: 10‐9‐10‐5M; NPY: 10‐13‐10‐8M) of arteriolar diameter changes were evaluated in the gluteus maximus muscle (n蠅5 rats/group). Like others, we observed that α1R and α2R control is greatest at large (1A‐2A) arterioles, with declining sensitivity in subsequent branch orders approaching capillaries. Beyond this, we have observed that NPY and ATP elicit the greatest constrictor effects in arterioles closest to capillaries, with declining effects in descending branch orders approaching feed arterioles. Using our theoretical flow model, simulations assessed total flow and red blood cell (RBC) flow heterogeneity within the network using our experimental pharmacological data. Using our experimental inputs, we are the first to illustrate that spatial differences in ligand sensitivity enable the SNS to modify bulk tissue blood flow and RBC distribution differentially in branching networks.Grant Funding Source: NSERC

What's in an eponym?

The vasculitides are a diverse group of disorders, many of which have peripheral nerve involvement.1Gwathmey KG Burns TM Collins MP Dyck PJB Vasculitic neuropathies.Lancet Neurol. 2014; 13: 67-82Summary Full Text Full Text PDF PubMed Scopus (98) Google Scholar In common with many diseases, several of these are named in honour of the person who first described them in any detail; however, as two researchers discovered when they submitted an article to The Lancet, these namegivers can turn out to be divisive figures. Isolated cases of nerve large arteriole vasculitis have been documented since 1866, but it was the presentation of the full pathological picture by the German pathologist Friedrich Wegener in 1936 and 1939, with resurgences in interest in 1954 and 1986, that led to the coining of the eponym Wegener's granulomatosis.2Woywodt A Haubitz M Matteson EL Wegener's granulomatosis.Lancet. 2006; 367: 1362-1366Summary Full Text Full Text PDF PubMed Scopus (90) Google Scholar In 2000, 10 years after his death, Woywodt and Matteson submitted a biographical article on Wegener for publication in the newly commissioned eponyms section in The Lancet. They were devastated to receive a rejection on the grounds of a reviewer comment that Wegener had been imprisoned for his activities during the Nazi regime, which had also precluded him from subsequently practising as a pathologist.2Woywodt A Haubitz M Matteson EL Wegener's granulomatosis.Lancet. 2006; 367: 1362-1366Summary Full Text Full Text PDF PubMed Scopus (90) Google Scholar Although rumours of such involvement had been rife since his death, key biographical works on Wegener lacked detail about the years 1939–45. With their interest thus piqued, Woywodt and Matteson spent the next 5 years exhaustively combing the war archives in Germany, USA, UK, and Poland, looking for substantiation or refutation of his complicity in Nazi atrocities.3Woywodt A Matteson EL Wegener's granulomatosis—probing the untold past of the man behind the eponym.Rheumatology. 2006; 45: 1303-1306Crossref PubMed Scopus (49) Google Scholar While their findings confirmed that he had indeed been a member of the National Socialist movement at some juncture, they could find no direct testament that he was guilty or ever convicted of war crimes, only a wealth of circumstantial associations. Their investigations did, however, provide lots of original biographical material for their article.4DeRemee RA Wegener's granulomatosis.Lancet. 2006; 368: 346Summary Full Text Full Text PDF PubMed Scopus (3) Google Scholar When this was finally published in 2006, it prompted a fierce rebuttal in the letters pages,4DeRemee RA Wegener's granulomatosis.Lancet. 2006; 368: 346Summary Full Text Full Text PDF PubMed Scopus (3) Google Scholar admittedly from a close friend of Wegener's, that levelled accusations of McCarthyism at Woywodt and Matteson for their tangential accusations and their suggestion that the eponym, which Wegener reportedly disliked, should be revoked, a sentiment that has been reiterated by many since publication of the article.

Dieulafoy Lesion: An Uncommon Cause of Esophageal Bleeding

Introduction: A Dieulafoy lesion refers to an abnormally large arteriole that retains the large caliber of its feeding vessel as it approaches the mucosa. It is an uncommon cause of gastrointestinal (GI) bleeding and when identified, is rarely found in the esophagus. Case Report: A 74-year-old African-American male with hypertension, diabetes, hyperlipidemia, chronic kidney disease, and coronary artery disease presented with nausea and dark brown emesis for 1 day. Emergency room assessment included a nasogastric lavage which was positive for 600 mL of dark red bloody aspirate. Urgent esophagogastroduodenoscopy was planned. Visualization of the esophagus revealed a pigmented spot with a protuberance, appearing like a volcano, with ulceration at its tip (Figure 1). This was thought to be arterial bleeding consistent with a Dieulafoy lesion. The lesion was injected with 4 mL of 1:10,000 epinephrine and placement of clips was performed to achieve hemostasis (Figure 2).Figure 1: Esophageal protuberance with ulceration and arterial bleed due to Dieulafoy lesion.Figure 2: Post-endoscopic injection of epinephrine and clip placement.Discussion: Dieulafoy lesions, also termed exulceratio simplex, are twice as common in males as in females and seem to have a predilection for the elderly population. Comorbidities are present in 90% of patients, most frequently cardiopulmonary disease and chronic renal failure. Although they are typically found in the lesser curvature of the stomach (80-95%), esophageal Dieulafoy lesions are rarely reported in the literature. While it accounts for only 1-2% of GI bleeds, the potential for grave outcomes demands heightened surveillance during endoscopic assessment for acute GI bleed.

Retinal arterial macroaneurysms

Retinal arterial macroaneurysms are acquired saccular or fusiform dilatations of the large arterioles of the retina, usually within the first three orders of bifurcation. They are associated with systemic vascular conditions such as hypertension and arteriosclerotic disease occurring most commonly in elderly women. The primary reported symptom is a sudden loss of vision due to haemorrhage or oedema affecting the macula. Most of macroaneurysms regress without treatment and without causing decreased visual acuity. Poor visual outcome may occur secondary to foveal exudates and subfoveal haemorrhage.

Stability of shunt flow pathways following thermal injury confirmed by multi‐wavelength laser speckle contrast imaging of oxy‐hemoglobin.

Our goal was to determine the stability of flow shunt pathways causing increased heterogeneity of flow with inflammation. Thermal injury (50C thermocouple controlled 300um spot burn) was used as a non‐pharmacological means to create a zone of inflammation with control regions in the same tissue. Intravital microscopy of the cheek pouch in male hamsters (N=10, isoflurane) was viewed. Rhodamine labeled RBC confirmed shunt pathways through all terminal arteriolar networks (NETS) within 500um of a spot burn (burn zone, paired locations before v 15m‐2hr after). Flow was redirected along arcades away from the burn zone. Oxy‐and deoxy‐hemoglobin (HbO 630nm v HbR 570nm) was measured (multi‐wavelength laser speckle contrast imaging) across a 2×2cm area containing the burn. Total Hb was consistent with tube hematocrit of 5–40%. Locations within 500um of the burn rim (near) v further away (far) show HbO was 30% less in perfused large arterioles (&gt;;50um) near v far from the burn, and 24% less in perfused large venules near vs far. Within NETS far from the burn, HbO was 7% higher along the shunt vs the nonshunt pathway. Near the burn, HbO is 71% greater along the shunt vs the non‐shunt pathway. Comparing HbO along shunt pathways, HbO was decreased 52% near vs far from the burn rim. Data with HbO or RBC flux agreed. Thus, a diminished oxygen shunt pathway is initiated by thermal injury and maintained for several hours. AHA 0655908T

Magnetic resonance imaging of microvessels using iron-oxide nanoparticles

The visualization of microstructures including blood vessels with an inner overall cross-sectional area below approximately 200 μm remains beyond the capabilities of current clinical imaging modalities. But with magnetic resonance (MR) imaging, magnetic entities cause susceptibility artifacts in the images by disrupting the homogeneous magnetic field in a much larger scale than their actual size. As validated in this paper through simulation and in-vitro experiments, these artifacts can serve as a source of contrast, enabling microvessels with an inner diameter below the spatial resolution of any medical imaging modalities to be visualized using a clinical MR scanner. For such experiments, micron-sized agglomerations of iron-oxide (Fe3O4) nanoparticles were injected in microchannels with internal diameters of 200 and 50 μm equivalent to a narrower artery or a larger arteriole, and down to a smaller arteriole, respectively. The results show the feasibility of the proposed method for micro-particle detection and the visualization of microvessels using a 1.5 T clinical MR scanner. It was confirmed that the method is reproducible and accurate at the sub-pixel level.

New Data on the Process of Circulation and Blood Oxygenation in the Lungs under Physiological Conditions

Blood flow through the human lungs weighing 600 g is about 5 to 6 liters per minute. Blood capacity of human lung is about 500 ml. Therefore, 500 ml blood is oxygenated for 5 sec. Questions arise how such a large volume of blood passes through such a small mass of the lungs and what causes very rapid blood oxygenation. Since the structure of the lungs in mammals is almost the same, the work was carried out on rats (in rats 20-22 ml of blood per minute passes through the lungs weighing 1.5-2.0 g). Intensive blood circulation was proved to be linked with a large diameter pulmonary arterioles and high blood flow velocity in them. The oxygenation rate is explained by special structure of the alveoli and special blood flow conditions, which creates ideal conditions for oxygen diffusion.

Microcirculation and left-ventricular hypertrophy

Microcirculation and left-ventricular hypertrophy