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Modern functional imaging techniques of the brain measure local hemodynamic responses evoked by neuronal activity. Capillary pericytes recently were suggested to mediate neurovascular coupling in brain slices, but their role in vivo remains unexplored. We used two-photon microscopy to study in real time pericytes and the dynamic changes of capillary diameter and blood flow in the cortex of anesthetized mice, as well as in brain slices. The thromboxane A₂ analog, 9,11-dideoxy-9α, 11α-methanoepoxy Prostaglandin F2α (U46619), induced constrictions in the vicinity of pericytes in a fraction of capillaries, whereas others dilated. The changes in vessel diameter resulted in changes in capillary red blood cell (RBC) flow. In contrast, during brief epochs of seizure activity elicited by local administration of the GABA A receptor antagonist, bicuculline, capillary RBC flow increased without pericyte-induced capillary diameter changes. Precapillary arterioles were the smallest vessels to dilate, together with penetrating and pial arterioles. Our results provide in vivo evidence that pericytes can modulate capillary blood flow in the brain, which may be important under pathological conditions. However, our data suggest that precapillary and penetrating arterioles, rather than pericytes in capillaries, are responsible for the blood flow increase induced by neural activity.

The pathogenesis of coma in severe Plasmodium falciparum malaria remains poorly understood. Obstruction of the brain microvasculature because of sequestration of parasitized red blood cells (pRBCs) represents one mechanism that could contribute to coma in cerebral malaria. Quantitative postmortem microscopy of brain sections from Vietnamese adults dying of malaria confirmed that sequestration in the cerebral microvasculature was significantly higher in patients with cerebral malaria (CM; n = 21) than in patients with non-CM (n = 23). Sequestration of pRBCs and CM was also significantly associated with increased microvascular congestion by infected and uninfected erythrocytes. Clinicopathological correlation showed that sequestration and congestion were significantly associated with deeper levels of premortem coma and shorter time to death. Microvascular congestion and sequestration were highly correlated as microscopic findings but were independent predictors of a clinical diagnosis of CM. Increased microvascular congestion accompanies coma in CM, associated with parasite sequestration in the cerebral microvasculature.

Bias has been described as one important obstacle in scientific research. The aim of this study was to explore \"awareness of treatment\" as a possible source of bias in subjective grading of ocular complications. Thirty subjects with similar, basic experience with grading scales participated in the study. The Efron grading scales were used to grade 24 images of three different ocular conditions (eight images each of bulbar hyperaemia, limbal vascularization and corneal staining). Three consecutive, two weeks apart, grading sessions were scheduled, in which the same images were graded, although in the third session images were deceptively labelled as either \"treated\" or \"untreated\". Grading results from the first and second sessions were compared to determine grading reliability and discrepancies with the third session informed of grading bias originating from \"awareness of treatment\". Moderate to good test-retest reliability was found for all conditions, with median intraclass correlation values of 0.80 (0.62-0.84) for bulbar hyperaemia, 0.68 (0.65-0.77) for limbal vascularization and 0.68 (0.66-0.74) for corneal staining. Grading values from the first and third sessions evidenced negative and positive systematic errors (bias) for \"treated\" and \"untreated\" conditions, respectively. Statistically significant differences were found between the average grading discrepancies of session 1 and session 2 and those of session 1 and session 3 (all p<0.001). \"Awareness of treatment\" may be considered a source of bias of subjective grading of ocular complications, although the actual effect of bias is unlikely to be of clinical significance.

Impaired nitric oxide (NO)-dependent endothelial function is associated with the development of cardiovascular diseases. We hypothesized that erythrocyte levels of nitrosylated hemoglobin (HbNO-heme) may reflect vascular endothelial function in vivo. We developed a modified subtraction method using Electron Paramagnetic Resonance (EPR) spectroscopy to identify the 5-coordinate α-HbNO (HbNO) concentration in human erythrocytes and examined its correlation with endothelial function assessed by peripheral arterial tonometry (PAT). Changes in digital pulse amplitude were measured by PAT during reactive hyperemia following brachial arterial occlusion in a group of healthy volunteers (50 subjects). Erythrocyte HbNO levels were measured at baseline and at the peak of hyperemia. We digitally subtracted an individual model EPR signal of erythrocyte free radicals from the whole EPR spectrum to unmask and quantitate the HbNO EPR signals. Mean erythrocyte HbNO concentration at baseline was 219+/-12 nmol/L (n = 50). HbNO levels and reactive hyperemia (RH) indexes were higher in female (free of contraceptive pills) than male subjects. We observed a dynamic increase of HbNO levels in erythrocytes isolated at 1-2 min of post-occlusion hyperemia (120+/-8% of basal levels); post-occlusion HbNO levels were correlated with basal levels. Both basal and post-occlusion HbNO levels were significantly correlated with reactive hyperemia (RH) indexes (r = 0.58; P<0.0001 for basal HbNO). The study demonstrates quantitative measurements of 5-coordinate α-HbNO in human venous erythrocytes, its dynamic physiologic regulation and correlation with endothelial function measured by tonometry during hyperemia. This opens the way to further understanding of in vivo determinants of NO bioavailability in human circulation.

Current clinical and anatomical studies show that the venous problem associated with the deep inferior epigastric perforator flap results from poor midline-crossing. We examined the venous anatomy of the infraumbilical midline area and the dynamic venous flow of the deep inferior epigastric perforator flap in nine fresh cadavers. All nine abdominal specimens were harvested between the subcostal margin and the groin crease. Two specimens were used to analyze the abdominal venous anatomy, one of which was divided into two hemi-abdominal specimens. The remaining seven specimens were harvested as deep inferior epigastric perforator flaps with one major paraumbilical perforator. Venous cannulation and serial angiographic agent injection were performed in several conditions. Each specimen was radiographed using a soft X-ray system. For additional information, computed tomography (CT) angiography-visualized superficial inferior epigastric veins (SIEVs) and the supraumbilical branch were analyzed. We noted that the venous drainage between the bilateral SIEVs was easier to configure in the supraumbilical area than in the infraumbilical area. Only one to two short polygonal venous networks connect the bilateral superficial inferior epigastric veins in the supraumbilical area; however, long and multiple polygonal venous networks connect the bilateral superficial inferior epigastric veins in the infraumbilical area, which could be a predisposing factor for venous congestion. The mean distance from the umbilicus upper border to evident supraumbilical midline crossover was 18.39±4.03 mm (range: 10.10–28.49) in CT angiograms. In cadaver specimens, the mean distance was 10.87±4.85 mm (range: 4.6–18.9). Supraumbilical midline crossover was more favorable than infraumbilical midline crossover in venous flow.

The purpose of this study is to investigate the effect of various degrees of percentage stenosis on hemodynamic parameters during the hyperemic flow condition. 3D patient-specific coronary artery models were generated based on the CT scan data using MIMICS-18. Numerical simulation was performed for normal and stenosed coronary artery models of 70, 80 and 90% AS (area stenosis). Pressure, velocity, wall shear stress and fractional flow reserve (FFR) were measured and compared with the normal coronary artery model during the cardiac cycle. The results show that, as the percentage AS increase, the pressure drop increases as compared with the normal coronary artery model. Considerable elevation of velocity was observed as the percentage AS increases. The results also demonstrate a recirculation zone immediate after the stenosis which could lead to further progression of stenosis in the flow-disturbed area. Highest wall shear stress was observed for 90% AS as compared to other models that could result in the rupture of coronary artery. The FFR of 90% AS is found to be considerably low.

Background Fontan associated liver disease (FALD) is an increasingly recognized complication of the single ventricle circulation characterized by hepatic venous congestion leading to hepatic fibrosis. Within the Fontan myocardium, fibrotic myocardial remodeling may occur and lead to ventricular dysfunction. Magnetic resonance imaging (MRI) T1 mapping can characterize both myocardial and liver properties. Objective The aim of this study was to compare myocardial and liver T1 between single ventricle patients with and without a Fontan and biventricular controls. Materials and methods A retrospective study of 3 groups of patients: 16 single ventricle patients before Fontan (SV pre 2 newborns, 9 pre-Glenn, 5 pre-Fontan, 31% single right ventricle [SRV]), 16 Fontans (56% SRV) and 10 repaired d-transposition of the great arteries (TGA). Native modified Look-Locker inversion T1 times were measured in the myocardium and liver. Cardiac MRI parameters, myocardial and liver T1 values were compared in the three groups. Correlations were assessed between liver T1 and cardiac parameters. Results Myocardial T1 was higher in SV pre (1,056 ± 48 ms) and Fontans (1,047 ± 41 ms) compared to TGA (1,012 ± 48 ms, P  < 0.05). Increased liver T1 was found in both SV pre (683 ± 82 ms) and Fontan (727 ± 49 ms) patients compared to TGA patients (587 ± 58 ms, P  < 0.001). There was no difference between single left ventricle (SLV) versus SRV myocardial or liver T1. Liver T1 showed moderate correlations with myocardial T1 (r = 0.48, confidence interval [CI] 0.26–0.72) and ejection fraction (r = -0.36, CI -0.66–0.95) but not with other volumetric parameters. Conclusion Increased liver T1 at both pre- and post-Fontan stages suggests there are intrinsic liver abnormalities early in the course of single ventricle palliation. Increased myocardial T1 and its relationship to liver T1 suggest a combination of edema from passive venous congestion and/or myocardial fibrosis occurring in this population. Liver T1 may provide an earlier marker of liver disease warranting further study.

The systolic forward travelling compression wave (sFCW) and diastolic backward travelling decompression waves (dBEW) predominantly accelerate coronary blood flow. The effect of a coronary stenosis on the intensity of these waves in the distal vessel is unknown. We investigated the relationship between established physiological indices of hyperemic coronary flow and the intensity of the two major accelerative coronary waves identified by Coronary Wave Intensity analysis (CWIA). Simultaneous intracoronary pressure and velocity measurement was performed during adenosine induced hyperemia in 17 patients with pressure / Doppler flow wires positioned distal to the target lesion. CWI profiles were generated from this data. Fractional Flow Reserve (FFR) and Coronary Flow Velocity Reserve (CFVR) were calculated concurrently. The intensity of the dBEW was significantly correlated with FFR (R = -0.70, P = 0.003) and CFVR (R = -0.73, P = 0.001). The intensity of the sFCW was also significantly correlated with baseline FFR (R = 0.71, p = 0.002) and CFVR (R = 0.59, P = 0.01). Stenting of the target lesion resulted in a median 178% (interquartile range 55-280%) (P<0.0001) increase in sFCW intensity and a median 117% (interquartile range 27-509%) (P = 0.001) increase in dBEW intensity. The increase in accelerative wave intensity following PCI was proportionate to the baseline FFR and CFVR, such that stenting of lesions associated with the greatest flow limitation (lowest FFR and CFVR) resulted in the largest increases in wave intensity. Increasing ischemia severity is associated with proportionate reductions in cumulative intensity of both major accelerative coronary waves. Impaired diastolic microvascular decompression may represent a novel, important pathophysiologic mechanism driving the reduction in coronary blood flow in the setting of an epicardial stenosis.

Abstract Hemoptysis is a frequently encountered symptom in many clinical settings, and etiologic diagnosis can sometimes prove challenging. Bronchoscopy may not promptly reveal the source or the cause of bleeding and few reports have focused so far on the abnormalities of bronchial mucosa vasculature that may unveil the underlying pathophysiology. In this special feature article, we present a series of cases presenting with hemoptysis after angiographic interventions in the thoracic vessels. Localized hyperemia and vascular dilatations in the bronchial mucosa observed during bronchoscopy as unique findings became clues enabling the correct diagnosis and management. We suggest the relevant pathophysiological mechanisms and discuss the available published experience on similar clinical entities.

The purpose of the study was to investigate the influence of lifetime physical activity (PA) on selected indices of atherosclerosis in longitudinal observation of middle-aged men. The subject of the study was a cohort of 101 men (mean age 59,7 ± 9,0 years), free of cardiovascular symptoms and treatment, participating in follow-up examinations in the years 1985/90-2011/12. Self-report PA was assessed by interviewer-administered Seven-Day PA Recall and Historical PA questionnaire. Subclinical atherosclerosis was measured by assessing the coronary artery calcification (CAC) according to Agatston's method using multi-slice computed tomography; the carotid intima-media thickness (IMT) using high-resolution B-mode ultrasound; and the reactive hyperemia index (RHI) using peripheral arterial tonometry (EndoPAT2000). The participants were initially divided into three groups according to tertiles of exercise-related energy expenditure (EE) in kcal/week at baseline, i.e. <2050 (low-to-moderate; n = 33), 2050-3840 (high; n = 34), >3840 (very high; n = 34). The low-to-moderate, high and very high PA groups were comparable in terms of age and atherosclerosis risk factors at baseline. No linear relationship was found between PA and CAC, IMT and RHI. Men who maintained low-to-moderate (n = 26), high (n = 21) and very high (n = 15) PA level had the mean CAC of 286.1 ± 361.9, 10.7 ± 28.9, and 106.1 ± 278.3 (p<0.001 for low-to moderate vs high; p<0.05 for low-to-moderate vs very high); the mean IMT of 0.751 ± 0.19 mm, 0,641 ± 0.26 mm, and 0.750 ± 0.60 mm (p>0.05); and the mean RHI of 1.69 ± 0.4, 2.00 ± 0.4, and 2.13 ± 0.5 (p for trend = 0.050), respectively. No cases of CAC>400, IMT ≥ 0.9 and RHI<1.67 were noted only among men with maintained high PA level. At final examination men with high and very high PA had more favorable cardiometabolic profile than men with lower PA. Maintaining regular high PA level through young and middle adulthood may protect against atherosclerosis as measured by CAC, IMT and RHI.