Edge Detection System Research Articles

Edge-Detection Method for Image Processing Based on Generalized Type-2 Fuzzy Logic

This paper presents an edge-detection method that is based on the morphological gradient technique and generalized type-2 fuzzy logic. The theory of alpha planes is used to implement generalized type-2 fuzzy logic for edge detection. For the defuzzification process, the heights and approximation methods are used. Simulation results with a type-1 fuzzy inference system, an interval type-2 fuzzy inference system, and with a generalized type-2 fuzzy inference system for edge detection are presented. The proposed generalized type-2 fuzzy edge-detection method was tested with benchmark images and synthetic images. We used the merit of Pratt measure to illustrate the advantages of using generalized type-2 fuzzy logic.

Salvia miltiorrhiza (Danshen) inhibits L-type calcium current and attenuates calcium transient and contractility in rat ventricular myocytes

Ethnopharmacological relevanceSalvia miltiorrhiza (SM, Danshen), a traditional Chinese herbal drug, has been widely used for hundreds of years to treat coronary artery disease. Materials and methodsWe studied the effects of SM on the L-type Ca2+ current (ICa-L) with whole-cell patch-clamp technique in rat ventricular myocytes, and its influence on Ca2+ transient and contractility using video-based edge detection and dual excitation fluorescence photomultiplier systems as well. ResultsExposure to SM solution caused a concentration- and voltage-dependent blockade of ICa-L, and the dose of SM solution (10g/l) decreased the maximal inhibitory effect of 35.2±1.2%. However, SM solution did not significantly change the current–voltage relationship or reversal potential of ICa-L, nor did it altered the activation and inactivation gating properties of cardiac Ca2+ channels. Meanwhile, SM decreased the amplitude of myocyte shortening and the peak value of Ca2+ transient with a significant decrease in the time to 90% of the baseline (Tr), but the time to 10% of the peak (Tp) was not dramatically prolonged. ConclusionsThe results indicated that SM significantly inhibited L-type Ca2+ channels, decreased [Ca2+]i and contractility in adult rat cardiac myocytes. These findings may be relevant to the cardioprotective efficacy of SM.

Boundary displacement measurements using multi-energy soft x-rays.

The Multi-Energy Soft X-ray (ME-SXR) system on NSTX provides radial profiles of soft X-ray emission, measured through a set of filters with varying thickness, which have been used to reconstruct the electron temperature on fast time scales (∼10 kHz). In addition to this functionality, here we show that the ME-SXR system can be used to measure the boundary displacement of the NSTX plasma with a few mm spatial resolution during magnetohydrodyamic (MHD) activity. Boundary displacement measurements can serve to inform theoretical predictions of neoclassical toroidal viscosity, and will be used to investigate other edge phenomena on NSTX-U. For example, boundary measurements using filtered SXR measurements can provide information on pedestal steepness and dynamic evolution leading up to and during edge localized modes (ELMs). Future applications include an assessment of a simplified, filtered SXR edge detection system as well as its suitability for real-time non-magnetic boundary feedback for ELMs, MHD, and equilibrium position control.

Effects of superoxide donor menadione in adult Rat myocardium are associated with increased diastolic intracellular calcium

Superoxide anions have been associated with many aspects of cardiovascular disease. Menadione is a superoxide anion donor that alters the heart’s electrical and mechanical functions. The aim of this study was to demonstrate simultaneous changes in intracellular Ca 2+ ([Ca 2+ ]i) and mechanical activity in intact adult cardiac myocytes, and mechanical activity and electrical activity in isolated whole hearts in order to provide greater insight into the mechanisms associated with the detrimental effects of menadione on the myocardium. Isolated hearts from adult male Wistar rats (n = 11, 200–250 g) were Langendorff perfused at 38°C with a Krebs–Henseleit solution. A saline-filled balloon was placed in the left ventricle (LV) in order to measure diastolic and developed pressure. Monophasic action potentials were simultaneously recorded from the epicardial surface. External stimulation at 5 Hz and intrinsic pacing were used throughout a 10 min control period and 30 min exposure to 50 µM menadione. Single LV myocytes (n = 7 from n = 4 animals) were loaded with the Ca2+-indicator Fura4-AM, stimulated at 1 Hz and exposed to 50 µM menadione. Myocyte length was simultaneously measured with [Ca 2+ ]i using a video edge detection system. In isolated hearts, exposure to menadione significantly decreased contractility and action potential duration (with a simi lar time course); intrinsic heart rate and rhythmicity. Diastolic pressure was significantly increased. In single adult myocytes, menadione caused a significant increase in diastolic [Ca 2+ ]i and a decrease in resting cell length and led to spontaneous release of [Ca 2+ ]i. We conclude that the effects of menadione upon electrical and mechanical activity of the heart are at least in part a consequence of dysregulation of [Ca 2+ ]i handling and the subsequent increase in diastolic [Ca 2+ ] alterations in [Ca 2+ ]i are consistent with the generation of delayed after depolarization arrhythmias.

Association of multiple biomarkers and classical risk factors with early carotid atherosclerosis: results from the Gutenberg Health Study

In the Gutenberg Health Study, a random sample of the population was scanned with vascular ultrasound for early atherosclerosis. A continuous classical risk marker model (waist circumference, HbA1c, LDL/HDL ratio, pack years and pulse pressure) was compared to a model of modern biomarkers (C-reactive protein, troponin I, N-terminal pro B-type natriuretic peptide, copeptin, mid-regional pro-adrenomedullin, and asymmetric dimethylarginine) with regard to the ability of ruling out abnormal intima-media thickness (IMT), respectively, carotid plaques. Data of the first consecutive 5,000 participants (aged 35-74 years; 2,540 men, 2,460 women) were analyzed. IMT was measured at both common carotid arteries using an edge detection system. Plaques were defined as protrusion of ≥1.5 mm in common, internal and external carotid artery. For classical risk factors, in comparison to a model of six modern biomarkers, regarding the variable (a) IMT>0.85 mm negative and positive predictive value (NPV and PPV) were 0.98 and 0.16 for both the classical risk factor model and the biomarker model. The second variable (b) presence of plaque could be ruled out with an NPV of 0.84 and identified with a PPV of 0.61 for classical risk factors, and 0.84 and 0.58 for biomarkers, respectively. Values were calculated using logistic regression analysis. Classical risk factors allow ruling out pathologic IMT and presence of carotid plaques in a population of primary prevention in a reliable way. Modern biomarkers performed almost equally well but did not provide further information.

Autophagy Inhibition Rescues Against Leptin-Induced Cardiac Contractile Dysfunction

Leptin hormone plays a vital role in the pathophysiological changes in heart geometry and function. Nonetheless, the precise mechanism(s) triggering leptin-induced cardiomyocyte contractile dysfunction is not well understood. The present study was designed to examine if autophagy plays a role in leptin-induced cardiac contractile anomalies. Cardiomyocyte contractile function was evaluated using an IonOptix edge detection system in cardiomyocytes following treatment with leptin in the presence or absence of the autophagy inhibiting chemical 3-methyladenine (3-MA). Immunoblotting was employed to evaluate expression of AMPK, Beclin1, Atg 5, p62 and LC3-II. GFP-LC3 puncta was used to assess autophagosome formation. Leptin suppressed cardiac contractile function as evidenced by decreased peak shortening, maximal velocity of shortening and relengthening, increased time-to-90% relengthening, all the observed effects were reduced or obliterated by autophagy inhibition. Leptin promoted superoxide generation, AMPK activation and overt autophagy induction. Leptin promoted autophagy as evidenced by enhanced LC3-II, Beclin, Atg 5 and decreased p62 levels. Pharmacological inhibition of reactive oxygen species (ROS) using tempol significantly attenuated leptin-induced autophagosome formation and cardiac contractile anomalies. In addition, genetic deletion of AMPKα2 or pharmacological inhibition of AMPK using compound C abrogated leptin or superoxide induced cardiac contractile dysfunction and autophagosome formation. In summary, our data revealed that leptin impairs cardiac contractile function through a superoxide generation-AMPK activation-and autophagy dependent mechanism.

History of depression but not current depression is associated with signs of atherosclerosis: data from the Gutenberg Health Study

To test the vascular depression hypothesis in the general population, we analyzed the association between current depression, medical history of depression, cognitive and somatic depressive symptom dimensions and measures of atherosclerosis [intima-media thickness (IMT) and carotid plaques]. We included a representative sample of 5000 participants from the Gutenberg Health Study (GHS). Depression was assessed by the nine-item Patient Health Questionnaire (PHQ-9), and IMT and carotid plaques were measured at both common carotid arteries using an edge detection system. Regression analyses were performed separately for participants with and without cardiovascular disease, adjusting for medical history, cardiovascular risk factors and psychotropic medication. Contrary to hypotheses, we found no increased IMT for somatic symptoms of depression; the same was true for depression and cognitive symptoms in the fully adjusted model. Only a moderate relationship between medical history of depression and the presence of atherosclerotic plaques was maintained after correction. The relationship between depression and atherosclerosis may be more complex than previously assumed. Although the vascular depression hypothesis was not supported, our results support the hypothesis that lasting depression leads to arteriosclerosis.

Inhibition of protein kinase C βII isoform rescues glucose toxicity-induced cardiomyocyte contractile dysfunction: Role of mitochondria

AimsHyperglycemia leads to cytotoxicity in the heart. Although theories were postulated for glucose toxicity-induced cardiomyocyte dysfunction including oxidative stress, the mechanism involved still remains unclear. Recent evidence has depicted a role of protein kinase C (PKC) in diabetic complications while high concentrations of glucose stimulate PKC. This study examined the role of PKCβII in glucose toxicity-induced cardiomyocyte contractile and intracellular Ca2+ aberrations. Main methodsAdult rat cardiomyocytes were maintained in normal (NG, 5.5mM) or high glucose (HG, 25.5mM) medium for 12h. Contractile and intracellular Ca2+ properties were measured using a video edge-detection system including peak shortening (PS), maximal velocity of shortening/relengthening (±dL/dt), time-to-PS (TPS), time-to-90% relengthening (TR90), rise in intracellular Ca2+ Fura-2 fluorescence intensity and intracellular Ca2+ decay. Production of ROS/O2− and mitochondrial integrity were examined using fluorescence imaging, aconitase activity and Western blotting. Key findingsHigh glucose triggered abnormal contractile and intracellular Ca2+ properties including reduced PS, ±dL/dt, prolonged TR90, decreased electrically-stimulated rise in intracellular Ca2+ and delayed intracellular Ca2+ clearance, the effects of which were ablated by the PKCβII inhibitor LY333531. Inhibition of PKCβII rescued glucose toxicity-induced generation of ROS and O2−, apoptosis, cell death and mitochondrial injury (reduced aconitase activity, UCP-2 and PGC-1α). In vitro studies revealed that PKCβII inhibition-induced beneficial effects were mimicked by the NADPH oxidase inhibitor apocynin and were canceled off by mitochondrial uncoupling using FCCP. SignificanceThese findings suggest the therapeutic potential of specific inhibition of PKCβII isoform in the management of hyperglycemia-induced cardiac complications.

A sub-pixel edge detection algorithm based on Zernike moments

A novel hybrid technique of combining an improved morphological gradient operator and Zernike moments, named MGZ edge detection algorithm, is developed to meet the stringent requirements for measuring accuracies of charge coupled device metrology system. The mathematical morphological gradient and Zernike moment algorithm are discussed based on the pixels grey-scale and spatial structure information of the images. To improve the algorithm process, the image edge is oriented and extracted by using improved morphological gradient operator firstly; then, the calculation errors of the typical ideal step edge model are analysed and corrected by the proposed error compensation formula. The edge point is relocated with sub-pixel accuracy by means of Zernike moment operator based on the edge point vectors and the threshold value. Finally, the sub-pixel edge detecting of the image is attained. The extensive experimental results show that the measuring error of the edge point is compensated reliably and accurately, and the new algorithm has short operation time, more precise and stronger robustness to noise than the prior similar algorithms. Meanwhile, the proposed method can well meet the need of charge coupled device metrology system for sub-pixel edge detection.

Cardiovascular and eletrocardiographic parameters after tonin administration in Wistar rats

In order to understand the mechanisms of interaction between tonin–angiotensin and renin–angiotensin systems (RAS) we evaluated, “in vivo” and “in vitro”, in Wistar rats, cardiovascular and electrocardiographic parameters after tonin administration. Arterial pressure (AP) and electrocardiogram (ECG) were recorded in awake animals before and after tonin administration. Langendorff technique was used to analyze cardiac function in isolated heart in the presence of tonin and video motion edge detection system was used to evaluate the effect of tonin upon contractile function of isolated rat ventricular cardiomyocytes. After tonin infusion rats presented significantly higher diastolic and mean arterial pressure (MAP) and heart rate (HR) as compared with control. The ECG analysis revealed shorter RR interval, increase in the low-frequency (LF) range of the heart rate variability (HRV) power (%) and decrease in the high-frequency (HF) of HRV power (%). Isolated hearts perfused with tonin presented an increase in the arterial coronary pressure (ACP) and decline in the ventricular systolic tension (ST), maximal (dT/dt+) and minimal (dT/dt) contractility. The rates of contraction and relaxation of isolated ventricular cardiomyocytes were significantly increased due to the presence of tonin. The angiotensin II (Ang II) levels in the coronary sinus effluent increased in the presence of tonin in a dose-dependent manner and the effect of tonin upon ACP was completely blocked by candesartan. Tonin is able to generate the vasoconstrictor peptide Ang II in the isolated heart of the rat and the cardiovascular response induced by tonin was completely blocked by candesartan, an indication that the action of Ang II on Ang II type 1 (AT1) receptors is the major mechanism of the heart effects. Tonin affects cardiomyocyte contractile function which may be due to interference with Ca2+ handling.

Cardiac-specific catalase overexpression rescues anthrax lethal toxin-induced cardiac contractile dysfunction: role of oxidative stress and autophagy

BackgroundLethal and edema toxins secreted by Bacillus anthracis during anthrax infection were found to incite serious cardiovascular complications. However, the underlying mechanisms in anthrax lethal toxin-induced cardiac anomalies remain unknown. This study was designed to evaluate the impact of antioxidant enzyme catalase in anthrax lethal toxin-induced cardiomyocyte contractile dysfunction.MethodsWild type (WT) and cardiac-specific catalase overexpression mice were challenged with lethal toxin (2 μg/g, intraperotineally (i.p.)). Cardiomyocyte contractile and intracellular Ca2+ properties were assessed 18 h later using an IonOptix edge-detection system. Proteasome function was assessed using chymotrypsin-like and caspase-like activities. GFP-LC3 puncta and Western blot analysis were used to evaluate autophagy and protein ubiquitination.ResultsLethal toxin exposure suppressed cardiomyocyte contractile function (suppressed peak shortening, maximal velocity of shortening/re-lengthening, prolonged duration of shortening/re-lengthening, and impaired intracellular Ca2+ handling), the effects of which were alleviated by catalase. In addition, lethal toxin triggered autophagy, mitochondrial and ubiquitin-proteasome defects, the effects of which were mitigated by catalase. Pretreatment of cardiomyocytes from catalase mice with the autophagy inducer rapamycin significantly attenuated or ablated catalase-offered protection against lethal toxin-induced cardiomyocyte dysfunction. On the other hand, the autophagy inhibitor 3-MA ablated or significantly attenuated lethal toxin-induced cardiomyocyte contractile anomalies.ConclusionsOur results suggest that catalase is protective against anthrax lethal toxin-induced cardiomyocyte contractile and intracellular Ca2+ anomalies, possibly through regulation of autophagy and mitochondrial function.

The effect of ligustrazine on L-type calcium current, calcium transient and contractility in rabbit ventricular myocytes

Ethnopharmacological relevanceLigustrazine, the biologically active ingredient isolated from a popular Chinese medicinal plant, Ligusticum chuanxiong Hort. (Umbelliferae), has been used effectively to treat ischemic heart diseases, cerebrovascular and thrombotic vascular diseases since the 1970s. Materials and methodsAt present, the effect of ligustrazine on L-type calcium current (ICa-L) of ventricular myocytes remains controversial. In this study, we use the whole-cell patch-clamp techniques and video-based edge detection and dual excitation fluorescence photomultiplier systems to study the effects of ligustrazine on ICa-L, and calcium transient and contractility in rabbit ventricular myocytes in the absence and presence of isoprenaline (ISO). ResultsLigustrazine (5μM) in low concentration did not affect ICa-L (P>0.05), higher concentrations of this drug (10, 20, 40, 80μM) inhibited ICa-L in a concentration-dependent manner and reduced ICa-L by 9.6±2.9%, 21.0±4.3%, 33.9±4.3%, and 51.6±7.3%, respectively. Under normal conditions, ligustrazine (40μΜ) reduced baseline of fura-2 fluorescence intensities (FFI, 340/380 ratio), namely diastolic calcium concentration, changes in FFI (ΔFFI, 340/380 ratio) and maximal velocity of Ca2+ rise and decay (340/380ratio/ms) by 6.3%, 26.1%, 25.2%, and 26.5%, and decreased sarcomere peak shorting (PS) and maximal velocity of shorting and relengthening by 36.4%, 31.9%, and 25.0%, respectively. Similarly, ligustrazine (40μM) reduced baseline FFI, ΔFFI, and maximal velocity of Ca2+ rise and decay by 14.1%, 51.1%, 35.2%, and 41.1%, and reduced sarcomere PS and maximal velocity of shorting and relengthening by 38.6%, 50.0% and 39.1%, respectively, in the presence of ISO. ConclusionsLigustrazine not only significantly inhibits ICa-L in a concentration-dependent manner but also suppressed calcium transient and contraction in the absence and presence of ISO.

Sophocarpine Attenuates the Na+-dependent Ca2+ Overload Induced by Anemonia Sulcata Toxin—Increased Late Sodium Current in Rabbit Ventricular Myocytes

Many studies indicate that an increase in late sodium current (I(Na.L)) of cardiomyocytes causes intracellular Na overload and subsequently raises the reverse Na/Ca exchanger current (INCX), ultimately resulting in intracellular Ca overload. Therefore, using drugs to inhibit the increased INa.L under various pathological conditions can lower intracellular Ca overload. This study was intended to explore the effect of sophocarpine (SOP) on the increase in INa.L, INCX, calcium transient and contraction in rabbit ventricular myocytes induced by Anemonia sulcata toxin II (ATX II), an opener of sodium channel, with the application of whole-cell patch-clamp techniques, the video-based motion edge detection system, and the intracellular calcium concentration determination system. The results indicate that tetrodotoxin (TTX, 4 μM ) obviously decreased INa.L and INCX enlarged by ATX II (30 nM), and SOP (20, 40, and 80 μM) also inhibited both the parameters concentration dependently in rabbit ventricular myocytes. However, transient sodium current remained unaffected by the above-mentioned concentrations of ATX II, TTX, and SOP. In addition, SOP also reversed diastolic calcium concentration, calcium transient amplitude, and ventricular muscle contractility augmented by ATX II. Its effects were similar to those of TTX, a specific inhibitor of the sodium channel. In conclusion, SOP inhibits INa.L, INCX, diastolic Ca concentration, and contractility in rabbit ventricular myocytes, which suggests that relief of intracellular Ca overload through inhibiting INa.L is likely to become a new therapeutic mechanism of SOP against arrhythmia and myocyte damage associated with intracellular Ca overload.

Abstract 142: Vascular Function in Himalayan Healthy High-Altitude Dwellers

Purpose: Endothelial function and carotid intima-media thickness (IMT), are established markers of vascular aging. Aim of the study was to investigate the presence of early markers of atherosclerosis in rural Sherpa population of Kumbu Valley (Nepal), in comparison with lowlanders Caucasian subjects. Methods: 99 Sherpa subjects, living at 2500-3800 m s.l. (34±12 years, BMI 24±3 kg/mq, mean BP 88±9 mmHg), free of cardiovascular disease and risk factors, were recruited, and compared to 60 Caucasian sea-level healthy volunteers (36±12 years, BMI 23±2 kg/mq, mean BP 86±8 mmHg). Endothelial function in the brachial artery (flow-mediated dilation, FMD, and response to glyceryl trinitrate, GTN), and carotid IMT were measured by automated edge-detection system. Left and right ventricular (LV and RV) systolic and diastolic function and pulmonary systolic pressure (PASP), and pulmonary vascular resistance (PVR) were evaluated by echocardiogram. In 11 subjects with reduced FMD, the protocol was repeated, after 100% O 2 administration for 1 hour, titrated to maintain O 2 saturation around 100%. Results: High-altitude group presented higher heart rate and lower pulse pressure than sea-level group. FMD was also reduced (5.2±3.1 vs 6.8±3.0%, p=0.01), despite similar brachial artery diameter (3.7±0.6 vs 3.6±0.7 mm, p=0.64), and response to GTN (8.3±3.1 vs 7.6±2.2%, p=0.13). Conversely, IMT was lower in high altitude group than in the sea-level group (0.51 vs 0.61 mm, p<0.001). Sherpa people showed normal LV and RV systolic and diastolic function, PASP(28±6 mmHg) and PVR (0.16±0.4). In the overall population FMD (5.2±3.1%) was not correlated to O 2 saturation (r=-0.03, p=0.74) and was similar in people with O 2 saturation >90% and in those <90% (5.3 vs 5.0%, p=0.74). In the subgroup receiving O 2 administration, FMD (from 3.1±2.5 to 3.8±2.6, p=0.46), response to GTN (from 8.9±2.7 to 8.7±1.9%), and echocardiographic parameters remained unchanged. Conclusions: Endothelial function is reduced in healthy Sherpa high-altitude dwellers, in the presence of normal RV and LV function and pulmonary pressures, independently of cardiovascular risk factors and hypoxia. This finding is accompanied with a lower IMT and might represent a physiological adaptation to high altitude.

Novel Adaptive Neuro-Fuzzy based Edge Detection Technique

Digital image processing is a subset of the electronic domain where the image is converted to an array of small integers, called pixels, symbolizing a physical quantity such as scene radiance, stored in a digital memory, and processed by computer or other digital hardware. Interest in digital image processing methods stems from two principals applications areas: improvement of pictorial information for human interpretation; and processing of image data for storage, transmission, and representation for autonomous machine perception. Edges characterize boundaries and edge detection is one of the most difficult tasks in image processing hence it is a problem of fundamental importance in image processing. Edges in images are areas with strong intensity contrasts and a jump in intensity from one pixel to the next can create major variation in the picture quality. Edge detection of an image significantly reduces the amount of data and filters out useless information, while preserving the important structural properties in an image. This research problem deals with a novel adaptive neuro-fuzzy inference system (ANFIS) for edge detection in digital images. The internal parameters of the proposed ANFIS edge detector are optimized by training using by proposed training pattern. The edges are directly determined by ANFIS network

Assessment of flow-mediated dilation reproducibility

Impaired flow-mediated dilation (FMD) is associated with cardiovascular risk factors and provides prognostic information. Despite the noninvasive nature of this technique, a major limitation to its widespread use is low reproducibility. The aim of this study was to evaluate impact of methodological standardization among different investigation sites on brachial artery FMD reproducibility. Seven Italian centers recruited 135 healthy volunteers, aged 20-60 years. FMD was assessed by high-resolution ultrasound equipped with a stereotactic probe-holding device. Certified sonographers recorded brachial artery scans at baseline (day 1a), 1 h after (day 1b), and 1 month later (day 30). Endothelium-independent vasodilation (EIVD) to sublingual glyceril-trinitrate was recorded at day 1 and day 30. FMD and EIVD were blindly evaluated at the coordinating center by an automated edge detection system. The intra-session (day 1a versus 1b) and inter-session (day 1a versus 30) coefficients of variation were calculated. FMD was not significantly (P = 0.91) different at day 1a, day 1b and day 30 (6.52 ± 2.9, 6.42 ± 3.1, 6.57 ± 2.8%, respectively). The FMD intra-session coefficient of variation was 9.9 ± 8.4% (from 7.6 to 11.9% across centers). The FMD inter-session coefficient of variation was 12.9 ± 11.6% (from 11.6 to 16.1% across centers). Inter-session coefficient of variation for EIDV was 19.7 ± 16.8%. This study shows a homogeneous coefficient of variation for FMD among different centers. The inter-session coefficient of variation was similar to the intra-session coefficient of variation, representing the intrinsic FMD variability. We demonstrate for the first time that rigorous and standardized procedure may provide reproducible FMD assessment to study endothelial function in multicenter clinical trials.

Edge detection based on morphological amoebas

Detecting the edges of objects within images is critical for quality image processing. We present an edge-detection technique that uses morphological amoebas that adjust their shape based on variation in image contours. We evaluate the method both quantitatively and qualitatively for edge detection of images, and compare it to classic morphological methods. Our amoeba-based edge-detection system performed better than the classic edge detectors.

Morfologia e contratilidade em cardiomiócitos de ratos com baixo desempenho para o exercício físico

Aerobic capacity is essential to physical performance, and low aerobic capacity is related to the triggering of various cardiovascular diseases. To compare the morphology and contractility of isolated rat cardiomyocytes with low performance and standard performance for exercise. Wistar rats with 10 weeks of age underwent a protocol of treadmill running to fatigue, and were divided into two groups: Low Performance (LP) and Standard Performance (SP). Then, the animals were sacrificed, the heart was quickly removed and, by means of enzymatic dissociation, left ventricular cardiomyocytes were isolated. The cell and sarcomeres length and width of cardiomyocytes were measured using an edge detection system. The isolated cardiomyocytes were electrically stimulated at 1 and 3 Hz and cell contraction was measured by registering the change of their length. The cell length was shorter in the LP group (157.2 ± 1.3 µm; p < 0.05) compared to SP (161.4 ± 1.3 µm), and the same result was observed for the volume of cardiomyocytes (LP, 25.5 ± 0.4 vs. SP, 26.8 ± 0.4 pL; p < 0.05). The time to peak contraction (LP, 116 ± 1 vs. SP 111 ± 2 ms) and total relaxation (LP, 143 ± 3 vs. SP 232 ± 3 ms) were higher in the LP group. We conclude that left ventricular myocytes of animals with low performance for exercise are smaller than animals with standard performance. In addition to that, they present losses in contractile capacity.

Effect of mild hyperisulinemia on conduit vessel endothelial function

The evidence that an exogenously induced modest hyperinsulinemia deteriorates conductance artery endothelial function - flow-mediated dilatation (FMD) - in healthy individuals is in contrast with in-vitro and in-vivo studies that consistently found that insulin facilitates both nitric oxide release and the endothelium-dependent dilatation. The aim of this study was to verify whether this effect is caused by the enhancement of insulin-induced adrenergic tone. In 10 healthy male volunteers, endothelium-dependent (FMD) and endothelium-independent (glyceryl trinitrate, GTN) dilatation were evaluated by high-resolution ultrasound of the brachial artery, combined with a computerized edge detection system, at baseline (-60 and 0 min) and after 120 and 240 min during insulin infusion (INS study). In five participants, randomly selected from the initial group, the study was repeated during an isotonic saline (0.9% sodium chloride) intravenous infusion (SAL study). In an additional five participants, insulin infusion was preceded by an intravenous infusion of clonidine started 40 min before insulin and continued throughout the study (INS + CLN study). Plasma norepinephrine concentration increased in the INS study from 260 ± 40 to 333 ± 62 pg/ml (P < 0.05), whereas it remained stable throughout the INS + CLN study. In the INS study, no change in FMD was observed, whereas the response to GTN tended to decrease (P = 0.09). In the INS + CLN study, no significant changes in FMD response were observed, whereas GTN response was completely restored. Physiological hyperinsulinemia has no effect on endothelium-dependent vasodilatation in conduit vessels of healthy individuals, but it induces a slight decline in endothelium-independent vasodilatation, which is entirely explained by the insulin-induced noradrenergic activation.

Type 2 diabetes mellitus worsens arterial stiffness in hypertensive patients through endothelial dysfunction

Endothelium-derived factors are thought to be physiological modulators of large artery stiffness. The aim of the study was to investigate whether endothelial function could be a determinant of arterial stiffness in essential hypertensive patients, in relation with the concomitant presence of type 2 diabetes mellitus. The study included 341 participants (84 hypertensive patients with and 175 without type 2 diabetes mellitus, 82 matched controls). Brachial artery endothelium-dependent flow-mediated dilation (FMD) was determined by high-resolution ultrasound and computerised edge detection system. Applanation tonometry was used to measure carotid-femoral pulse wave velocity (PWV). Hypertensive patients with diabetes had higher PWV (10.1 ± 2.3 m/s vs 8.6 ± 1.4 m/s, p < 0.001) and lower FMD (3.51 ± 2.07 vs 5.16 ± 2.96%, p < 0.001) than non-diabetic hypertensive patients, who showed impaired vascular function when compared with healthy participants (7.9 ± 1.6 m/s and 6.68 ± 3.67%). FMD was significantly and negatively correlated to PWV only in hypertensive diabetic patients (r = -0.456, p < 0.001), but not in hypertensive normoglycaemic patients (r = -0.088, p = 0.248) or in healthy participants (r = 0.008, p = 0.946). Multivariate analysis demonstrated that, in the diabetic group, FMD remained an independent predictor of PWV after adjustment for confounders (r(2) = 0.083, p = 0.003). Subgroup analysis performed in non-diabetic hypertensive patients revealed that neither obesity nor the metabolic syndrome affected the relationship between FMD and PWV. Endothelial dysfunction is a determinant of aortic stiffness in hypertensive diabetic patients but not in hypertensive patients without diabetes. These results suggest that type 2 diabetes mellitus on top of hypertension might worsen arterial compliance by endothelium-related mechanisms.