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Статті в журналах з теми "Flux coronaire"

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Автор: Grafiati

Опубліковано: 12 червня 2021

Оновлено: 14 лютого 2022

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1

Meimoun, P., S. Sayah, B. Maitre, A. L. Bore, T. Benali, M. Beausoleil, and J. Bailly. "Mesure du flux et de la réserve coronaire par échographie transthoracique : un vieux concept, un outil moderne, des intérêts multiples." Annales de Cardiologie et d'Angéiologie 53, no. 6 (November 2004): 325–34. http://dx.doi.org/10.1016/j.ancard.2004.09.009.

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2

Pinaquy, J. B., P. Ferenczi, F. Debordeaux, L. Bordenave, H. Douard, T. Couffinhal, and Y. Pucheu. "Corrélation entre les flux myocardiques, la réserve coronaire et les scores de risque cardiovasculaire Framingham et ESC-SCORE(+ Running poster)." Médecine Nucléaire 45, no. 4 (July 2021): 203. http://dx.doi.org/10.1016/j.mednuc.2021.06.056.

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3

Bailly, M., F. Thibault, M. Courtehoux, G. Metrard, and M. J. Santiago Ribeiro. "Effet de la correction d’atténuation sur le calcul des flux et de la réserve coronaire en scintigraphie myocardique sur caméra CZT." Médecine Nucléaire 44, no. 2 (March 2020): 101–2. http://dx.doi.org/10.1016/j.mednuc.2020.01.118.

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4

Huang, Qiaobing, Mac Wu, Cynthia Meininger, Katherine Kelly, and Yuan Yuan. "Neutrophil-dependent augmentation of PAF-induced vasoconstriction and albumin flux in coronary arterioles." American Journal of Physiology-Heart and Circulatory Physiology 275, no. 4 (October 1, 1998): H1138—H1147. http://dx.doi.org/10.1152/ajpheart.1998.275.4.h1138.

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Platelet-activating factor (PAF) has been implicated in the pathogenesis of ischemic heart disease, reperfusion injury, and inflammatory reactions. Although neutrophils have been shown to primarily mediate PAF-induced microvascular dysfunction, the vasoactive effect of PAF and its neutrophil-dependent mechanism have not been directly and systematically studied in coronary resistance vessels. Therefore, the aim of this study was to examine the effects of PAF on coronary arteriolar function and neutrophil dynamics using an isolated and perfused microvessel preparation. Topical application of PAF to the vessels induced a dose-dependent decrease in the diameter but an increase in the apparent permeability coefficient of albumin. Disruption of the endothelium abolished the vasomotor response to PAF, and perfusion of neutrophils significantly augmented PAF-induced changes in vasomotor tone and permeability. Furthermore, the interaction between neutrophils and the endothelium was studied in the intact perfused coronary arterioles. Under control conditions, there were no adherent neutrophils observed in the vessels at varied intraluminal flow velocities. However, administration of PAF caused neutrophil adhesion to the endothelium of coronary arterioles at low flow velocities. Western blot analysis indicated that PAF upregulated the expression of intercellular adhesion molecule-1 in cultured coronary microvascular endothelial cells. Taken together, the results suggest that 1) PAF induces vasoconstriction and hyperpermeability in coronary arterioles via an endothelium-dependent and neutrophil-mediated mechanism, and 2) PAF is able to stimulate neutrophil adhesion in coronary arterioles under a condition of low flow rate.

5

ROGERS, S., A. KHALATBARI, B. DATTA, S. ELLERY, V. PAUL, M. FRENNEAUX, and P. JAMES. "NO metabolite flux across the human coronary circulation." Cardiovascular Research 75, no. 2 (July 15, 2007): 434–41. http://dx.doi.org/10.1016/j.cardiores.2007.04.019.

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6

SYRRIS, Petros, Nicholas D. CARTER, James C. METCALFE, Paul R. KEMP, David J. GRAINGER, Juan C. KASKI, David C. CROSSMAN та ін. "Transforming growth factor-β1 gene polymorphisms and coronary artery disease". Clinical Science 95, № 6 (1 грудня 1998): 659–67. http://dx.doi.org/10.1042/cs0950659.

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1. A meta-analysis of 17 years of literature on erythrocyte Na+/Li+ countertransport (NLCT) and Na+/K+ co-transport (COT) measurements in relation to essential hypertension is presented. The analysis aimed to answer two questions: (i) Which clinical or laboratory variables influence NLCT and COT flux values? (ii) How useful are NLCT and COT measurements as a diagnostic aid in essential hypertension? 2. Regression analysis was performed on the mean flux values and relevant clinical and laboratory values. Studies in both normotensive and hypertensive subjects were stratified for variables which showed a significant association with the measured flux. For hypertensive subjects the studies were also stratified for medication. Means of strata were calculated after weighing the mean of a study by the inverse of its own variance and were compared in normotensive as well as hypertensive subjects using a t-test. 3. The analysis did not demonstrate systematic effects of laboratory variables for either NLCT or COT. It was found that essential hypertension, family history of hypertension, gender and antihypertensive medication are main determinants for the flux values of both transport systems. After stratification for these determinants, significant differences in weighed mean flux values between normotensive and hypertensive subjects were demonstrated. However, these differences are much smaller than the variance in the weighed mean flux values, suggesting the existence of other unknown variables that strongly affect the flux rates. 4. In conclusion, NLCT and COT measurements cannot be of diagnostic use in essential hypertension.

7

Jardine, Moira M. "Topology of stellar coronae." Proceedings of the International Astronomical Union 2, no. 14 (August 2006): 289–90. http://dx.doi.org/10.1017/s1743921307010642.

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AbstractWhile the existence of cycles in stellar chromospheric flux has been known for some time, the nature of the corresponding coronal response has been more elusive. We describe recent results on the relationship between cyclic variations in surface magnetic flux and coronal structure and re-assess the role of prominence observations in understanding the topology of stellar coronas. We present a new paradigm for prominence support which allows for extended prominences to co-exist with a compact corona. We discuss briefly the recent results on coronal structure in high- and low-mass stars and their implications for dynamo theory.

8

Schrijver, Carolus J., and Alan M. Title. "The Heating of Cool‐Star Coronae: From Individual Loops to Global Flux‐Flux Scalings." Astrophysical Journal 619, no. 2 (February 2005): 1077–83. http://dx.doi.org/10.1086/426709.

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9

Noll, T., A. Hempel, and H. M. Piper. "Neuropeptide Y reduces macromolecule permeability of coronary endothelial monolayers." American Journal of Physiology-Heart and Circulatory Physiology 271, no. 5 (November 1, 1996): H1878—H1883. http://dx.doi.org/10.1152/ajpheart.1996.271.5.h1878.

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The effect of neuropeptide Y (NPY) on cellular adenosine 3',5'-cyclic monophosphate (cAMP) contents and macromolecule permeability was studied in cultured monolayers of microvascular coronary endothelial cells from rat. Macromolecule permeability was continuously determined as passage of albumin across the monolayers. NPY (10(-10)-10(-7) M) decreased albumin flux and cellular cAMP content in a dose-dependent manner, with a half-maximal effect on albumin flux at 1.4 x 10(-9) M and on cAMP contents at 0.7 x 10(-9) M. A maximum effect of NPY was observed at 10(-7) M, decreasing albumin flux by 71 +/- 8% and cellular cAMP contents by 80 +/- 9% (mean +/- SD, n = 6, P < 0.05) compared with control. The effect of NPY on albumin flux was not altered in the presence of 10(-5) M indomethacin (an inhibitor of cyclooxygenase) and 10(-5) M NG-nitro-L-arginine (an inhibitor of nitric oxide synthase). NPY (10(-7) M) also antagonized the increase of albumin flux and cAMP content induced by 10(-6) M isoproterenol. Pretreatment of endothelial monolayers with pertussis toxin (1 microgram/ml for 2 h) abolished the effect of NPY on albumin flux and cAMP contents. This study shows that NPY can modulate macromolecule permeability of endothelial monolayers by reducing the cellular cAMP contents. Together with the effect of pertussis toxin, the data suggest that NPY exerts its antiadrenergic effect on cAMP metabolism and endothelial barrier function by receptors linked to adenylyl cyclase via an inhibitory guanosine-binding protein in coronary endothelial cells.

10

Honig, C. R., J. L. Frierson, and T. E. Gayeski. "Anatomical determinants of O2 flux density at coronary capillaries." American Journal of Physiology-Heart and Circulatory Physiology 256, no. 2 (February 1, 1989): H375—H382. http://dx.doi.org/10.1152/ajpheart.1989.256.2.h375.

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Calculations indicate that the PO2 in plasma falls to zero approximately 3 microns from an erythrocyte at O2 consumption (VO2) characteristic of myocardium (Federspiel, W.A., and A. Popel, Microvasc. Res. 32: 164-189, 1986). We measured distances between individual red cells along capillaries in rat hearts rapidly frozen in situ. Cell spacing varied widely even in branches of the same capillary. Plasma gaps between red cells were divided into two populations, those less than 5 microns and those greater than 5 microns. Mean gap lengths were 2.1 and 16.5 microns, respectively. Although the number of long plasma gaps was underestimated, gaps greater than 5 microns accounted for one-third of observed capillary length. Frozen muscles were also viewed in cross section. Because the depth of penetration of light was approximately equal to 3 microns, counts of red cell-containing capillary profiles in cross section depend on cell spacing as well as on number of cell-containing flow paths. Counts varied markedly with arterial O2 partial pressure, indicating that the capillary surface area functional for O2 transport changes in response to stress. The adaptive role of change in O2 flux density (flux per area) is discussed in light of new knowledge of tissue O2 gradients.

11

Brana, Q., F. Thibault, M. Courtehoux, G. Metrard, M. J. Santiago Ribeiro, D. Angoulvant, and M. Bailly. "Regadenoson versus dipyridamole : évaluation des flux coronaires avec une caméra CZT." Médecine Nucléaire 45, no. 4 (July 2021): 186. http://dx.doi.org/10.1016/j.mednuc.2021.06.030.

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12

Oliver, R., and J. L. Ballester. "A Fibril Structure Model for Stellar Prominences." International Astronomical Union Colloquium 167 (1998): 247–50. http://dx.doi.org/10.1017/s0252921100047680.

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AbstractExtensive observational background exists about the presence of cool material clouds embedded in the stellar coronae of rapidly rotating, late-type stars. Observations of such clouds in HKAqr (Gliese 890) and HD 197890 suggest that the clouds are at heights smaller than the star’s corotation radius and could be looked at as a phenomenon similar to that of solar prominences. Recent observations of solar prominences have reinforced the evidence about their fibril structure made of many long, thin magnetic flux tubes making angles about 25 degrees with the direction of the filament channel, with only the central 10–20% of the magnetic flux tubes filled with cool matter, which can produce a depression at the summits of the flux tubes. Then, assuming a similar structure for the stellar cool clouds, we have looked for the physical characteristics of such stellar prominences, i.e. the size of the flux tube depression, the density, temperature, half-width and supported mass of the cool region, taking into account gravity variation with height and centrifugal acceleration, since such clouds have been detected at great heights within stellar coronae belonging to rapid rotators.

13

Bartelds, Beatrijs, Jan-Willem C. Gratama, Hennie Knoester, Janny Takens, Gioia B. Smid, Jan G. Aarnoudse, Hugo S. A. Heymans, and Jaap R. G. Kuipers. "Perinatal changes in myocardial supply and flux of fatty acids, carbohydrates, and ketone bodies in lambs." American Journal of Physiology-Heart and Circulatory Physiology 274, no. 6 (June 1, 1998): H1962—H1969. http://dx.doi.org/10.1152/ajpheart.1998.274.6.h1962.

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No information is available on perinatal changes in myocardial metabolism in vivo. We measured myocardial supply and flux of fatty acids, carbohydrates, and ketone bodies in chronically instrumented fetal, newborn (1–4 days), and juvenile (7 wk) lambs, by measuring aorta-coronary sinus concentration differences and blood flow. In the fetal lambs, myocardial supply and flux of fatty acids were zero. In the newborn lambs, the supply of fatty acids increased tenfold, but there was no flux of fatty acids. Carbohydrates were the major energy source in fetal and newborn lambs, accounting for 89 and 69% of myocardial oxygen consumption, respectively. In the juvenile lambs, the flux of fatty acids was increased threefold. The supply and flux of carbohydrates were decreased (by 31 and 82%, respectively). The supply and flux of ketone bodies gradually increased with age. We show that the myocardium of the lamb in vivo does not switch immediately after birth from carbohydrates to fatty acids. The mechanisms involved in the development of myocardial fatty acid oxidation remain to be elucidated.

14

Wyatt, D. A., M. C. Edmunds, R. Rubio, R. M. Berne, R. D. Lasley, and R. M. Mentzer. "Adenosine stimulates glycolytic flux in isolated perfused rat hearts by A1-adenosine receptors." American Journal of Physiology-Heart and Circulatory Physiology 257, no. 6 (December 1, 1989): H1952—H1957. http://dx.doi.org/10.1152/ajpheart.1989.257.6.h1952.

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This study was designed to assess the role of adenosine in the regulation of exogenous glucose utilization by myocardium. Perfusion of isolated rat hearts with buffer containing D-[3-3H]glucose and analysis of the coronary effluent for 3H2O production was used as an indicator of glycolytic flux. Initially, glycolytic flux was determined during five different conditions: 1) normoxia; 2) normoxia plus 100 microM adenosine; 3) normoxia plus 100 microM adenosine and 10 microM 8-(sulfophenyl)-theophylline (SPT), an adenosine receptor antagonist; 4) hypoxia; and 5) hypoxia plus 10 microM SPT. Both adenosine and hypoxia produced an approximate threefold increase in glycolytic flux that was attenuated by adenosine receptor blockade with SPT. Next, hearts were perfused during normoxic conditions with various concentrations of either R-phenylisopropyladenosine (PIA), an A1-adenosine receptor agonist, or 5'-N-ethylcarboxamidoadenosine (NECA), an A2-adenosine receptor agonist. Significant increases in glycolytic flux occurred with PIA, whereas NECA treatment resulted in only a marginal stimulation of glycolytic flux. These data provide evidence that: 1) exogenous adenosine stimulated glycolytic flux in the normoxic myocardium; 2) endogenous adenosine stimulated glycolytic flux during hypoxia; and 3) the effect of adenosine on glycolytic flux was mediated by interaction with A1-adenosine receptors.

15

Huxley, V. H., and D. A. Williams. "Basal and adenosine-mediated protein flux from isolated coronary arterioles." American Journal of Physiology-Heart and Circulatory Physiology 271, no. 3 (September 1, 1996): H1099—H1108. http://dx.doi.org/10.1152/ajpheart.1996.271.3.h1099.

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We have developed a new method to quantify solute flux per unit surface area and concentration gradient (JS/S delta C) from arterioles isolated from pig hearts. The apparent permeability (Ps) was assessed from measurements of JS/S delta C for two proteins, alpha-lactalbumin (alpha-lactalb) and porcine serum albumin (PSA), labeled with the fluorescent dye tetramethylrhodamine isothiocyanate at a mean hydrostatic pressure of 16 +/- 1 cmH2O. Ps for alpha-lactalb (Ps alpha-lactalb) was 16.5 +/- 4.6 x 10(-7) cm/s (mean +/- SE, N = 8 pigs), a value significantly higher than Ps for PSA (PsPSA) (7.1 +/- 1.4 x 10(-7) cm/s, N = 11 pigs, P < 0.05). Suffusion of the arterioles (44 +/- 10 microns diam; n = 48 arterioles) with 10(-5) M adenosine resulted in a 35% decrease in Ps alpha-lactalb and 29% decrease in PsPSA. Data from the present study are consistent with adenosine altering arteriole Js independently from its ability to change arteriolar caliber. One implication of these results is that changes in coronary exchange capacity reflect not only changes in flow through, but also solute permeation from, the microvasculature.

16

Motreff, P., L. Sarry, E. Geoffroy, R. Rodriguez, J. M. Garcier, J. R. Lusson, J. Cassagnes, and L. Boyer. "Evaluation fonctionnelle des stenoses coronaires par mesure videodensitometrique des vitesses de flux." Journal de Radiologie 85, no. 9 (September 2004): 1585. http://dx.doi.org/10.1016/s0221-0363(04)77958-5.

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17

Hempel, A., T. Noll, A. Muhs, and H. M. Piper. "Functional antagonism between cAMP and cGMP on permeability of coronary endothelial monolayers." American Journal of Physiology-Heart and Circulatory Physiology 270, no. 4 (April 1, 1996): H1264—H1271. http://dx.doi.org/10.1152/ajpheart.1996.270.4.h1264.

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The role of the intracellular second messengers guanosine 3', 5'-cyclic monophosphate (cGMP) and adenosine 3', 5'-cyclic monophosphate (cAMP) in the control of macromolecule permeability was studied in cultured monolayers of microvascular coronary endothelial cells from rat. Macromolecule permeability was determined as passage of fluorescein isothiocyanate (FITC)-labeled albumin across the monolayers. Activation of adenylyl cyclase by the beta-adrenoceptor agonist isoproterenol (Iso; 10(-5) M) and the A2-adenosine receptor agonist 5'-(N-ethylcarboxamido)-adenosine (NECA; 10(-7) M) induced an increase in cellular cAMP contents that was accompanied by an increase in albumin flux. Effects of Iso and NECA on cellular cAMP level and albumin flux could be antagonized by a stimulator of the particular guanylyl cyclase, atrial natriuretic peptide (ANP; 10(-7) M), and stimulators of the soluble guanylyl cyclase, 3-morpholinosydnonimine (SIN-1; 10(-7) M) and sodium nitroprusside (SNP; 10(-6) M). ANP, SIN-1, and SNP also reduced cAMP content and basal macromolecule flux in unstimulated monolayers. 8-Bromoguanosine 3', 5'-cyclic monophosphate (8-BrcGMP; 5 x 10(-6) M), a stimulator of protein kinase G, reduced the increase in albumin flux under Iso (10(-5) M), NECA (10(-7) M), or 8-bromoadenosine 3', 5'-cyclic monophosphate (8-BrcAMP; 5 x 10(-6) M). The present study shows that cGMP and cAMP are functional antagonists in the control of macro molecule permeability.

18

Noll, T., A. Muhs, M. Besselmann, H. Watanabe, and H. M. Piper. "Initiation of hyperpermeability in energy-depleted coronary endothelial monolayers." American Journal of Physiology-Heart and Circulatory Physiology 268, no. 4 (April 1, 1995): H1462—H1470. http://dx.doi.org/10.1152/ajpheart.1995.268.4.h1462.

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How the initiation of energy depletion affects macromolecule permeability of a barrier of coronary endothelial cells was investigated. Cultured monolayers of adult rat coronary endothelial cells were exposed to 5 mM KCN and 5 mM 2-deoxy-D-glucose (2-DG). Transendothelial flux of albumin, cellular ATP content, and cytosolic Ca2+ concentration were monitored. Within the first minute, a merely partial loss (28%) of ATP reserves provoked a distinct increase (41%) in albumin flux. Rise of permeability was dependent on Ca2+ release from a thapsigargin- and ATP-sensitive endogenous store, and hyperpermeability was greatly attenuated when energy depletion was extremely rapid, as under sequential addition of 20 mM 2-DG and 5 mM KCN. Attenuation of hyperpermeability could also be achieved by use of 5-20 mM 2,3-butanedione monoxime, an inhibitor of actin-myosin interaction. This finding, together with dependence on Ca2+ and availability of residual energy, indicates that the rapid initiation of hyperpermeability is caused by a contractile mechanism.

19

Huxley, Virginia H., and Donna A. Williams. "Role of a glycocalyx on coronary arteriole permeability to proteins: evidence from enzyme treatments." American Journal of Physiology-Heart and Circulatory Physiology 278, no. 4 (April 1, 2000): H1177—H1185. http://dx.doi.org/10.1152/ajpheart.2000.278.4.h1177.

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Whereas the glycocalyx of endothelial cells has been shown to influence solute flux from capillary microvessels, little is known about its contribution to the movement of macromolecules across the walls of other microvessels. We evaluated the hypothesis that a glycocalyx contributes resistance to protein flux measured in coronary arterioles. Apparent solute permeability ( P s) to two proteins of different size and similar charge, α-lactalbumin (α-lactalb) and porcine serum albumin (PSA), was determined in arterioles isolated from the hearts of 43 female Yucatan miniature swine. P s was assessed in arterioles with an “intact” glycocalyx under control conditions and again after suffusion with adenosine (Ado, 10− 5 M, n = 42 arterioles, N = 29 pigs). In a second set of experiments ( n = 21 arterioles, N = 21 pigs) arteriolar P s was determined before and after perfusion with enzyme (pronase or heparinase), which was used to digest the glycocalyx. P s was assessed a third time on those microvessels after exposure to Ado. Consistent with the hypothesis, P s for PSA ([Formula: see text]) and P sfor α-lactalb ([Formula: see text]) increased from basal levels following enzyme treatment. Subsequent suffusion with Ado, a significant metabolite known to alter coronary vascular smooth muscle tone and permeability, resulted in a significant reduction of basal [Formula: see text] in both untreated and enzyme-treated arterioles. Furthermore, in untreated arterioles, [Formula: see text] was unchanged by Ado suffusion, whereas Ado induced a pronounced reduction in[Formula: see text] of enzyme-treated vessels. These data demonstrate that in intact coronary arterioles an enzyme-sensitive layer, most likely at the endothelial cell surface, contributes significantly to net barrier resistance to solute flux.

20

Schrijver, Carolus J. "The magnetic field of the nearest cool star A Paradigm for Stellar Activity." Symposium - International Astronomical Union 176 (1996): 1–16. http://dx.doi.org/10.1017/s0074180900083054.

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Looking at the Sun forges the framework within which we try to interpret stellar observations. The stellar counterparts of spots, plages, flux tubes, chromospheres, coronae, etc., are readily invoked when attempting to interpret stellar data. This review discusses a selection of solar phenomena that are crucial to understand stellar atmospheric activity. Topics include the interaction of magnetic fields and flows, the relationships between fluxes from different temperature regimes in stellar atmospheres, the photospheric flux budget and its impact on the measurement of the dynamo strength, and the measurement of stellar differential rotation.

21

Decking, Ulrich K. M., Stefan Skwirba, Marc F. Zimmerman, B. Preckel, R. Loncar, V. Thamer, A. Deussen, and J. Schrader. "Does local coronary flow control metabolic flux rates? A13C-NMR study." Magma: Magnetic Resonance Materials in Physics, Biology, and Medicine 6, no. 2-3 (September 1998): 133–34. http://dx.doi.org/10.1007/bf02660934.

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22

Motreff, P., L. Sarry, E. Geoffroy, R. Rodriguez, J. M. Garcier, J. R. Lusson, J. Cassagnes, and L. Boyer. "CV5 Evaluation fonctionnelle des stenoses coronaires par mesure videodensitometrique des vitesses de flux." Journal de Radiologie 85, no. 9 (September 2004): 1485. http://dx.doi.org/10.1016/s0221-0363(04)77578-2.

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23

Barua, Samuzal, V. Jithesh, Ranjeev Misra, Gulab C. Dewangan, Rathin Sarma, and Amit Pathak. "NuSTAR observation of Ark 564 reveals the variation of coronal temperature with flux." Monthly Notices of the Royal Astronomical Society 492, no. 2 (January 10, 2020): 3041–46. http://dx.doi.org/10.1093/mnras/staa067.

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ABSTRACT The hard X-ray spectral index of some active galactic nuclei (AGN) has been observed to steepen with the source flux. This has been interpreted in a Comptonization scenario, where an increase in the soft flux decreases the temperature of the corona, leading to steepening of the photon index. However, the variation of the coronal temperature with flux has been difficult to measure due to the presence of complex reflection component in the hard X-rays and the lack of high-quality data at that energy band. Recently, a 200 ks Nuclear Spectroscopic Telescope Array(NuSTAR) observation of Ark 564 in 3–50 keV band revealed the presence of one of the coolest coronae with temperature kTe ∼ 15 keV in the time-averaged spectrum. Here, we reanalyse the data and examined the spectra in four flux levels. Our analysis shows that the coronal temperature decreased from ∼17 to ∼14 keV as the flux increased. The high energy photon index Γ ∼ 2.3 varied by less than 0.1, implying that the optical depth of the corona increased by about 10 per cent as the flux increased. This first reporting of coronal temperature variation with flux shows that further long observation by NuSTAR of this and other sources would shed light on the geometry and dynamics of the inner regions of the accretion flow.

24

Jern, Christina, Helene Seeman-Lodding, Göran Johansson, Sören Häggmark, Michael Broomé, Björn Biber та Barbro Österlund. "Intracoronary β2 receptor activation induces dynamic local t-PA release in the pig". Thrombosis and Haemostasis 90, № 11 (2003): 796–802. http://dx.doi.org/10.1160/th02-09-0013.

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SummaryTo investigate β2-adrenergic agonist-mediated effects on coronary fluxes of local fibrinolytic factors, healthy anaesthetised and instrumented pigs (n=10) were studied during infusion of isoprenaline (IPR) into the left main coronary artery. Coronary net fluxes of total t-PA antigen, active t-PA and total PAI-1 antigen were determined at baseline and at 3, 5, 7 and 10 minutes of IPR infusion. During IPR, net release of total t-PA increased in a biphasic pattern with transiently high levels at 3 (+440 %) and 7 minutes (+620%) and returned towards baseline at 10 minutes. Net coronary release of active t-PA increased with maximum levels at 3 minutes (+50%). Baseline coronary net flux of total PAI –1 showed a decrease which was most pronounced at 10 minutes. To conclude, a fast β2agonist-mediated local release of t-PA into the coronary vasculature was demonstrated. For total t-PA, this response was characterised by a biphasic release profile.

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Lippi, Giuseppe, Nicola Tessitore, Martina Montagnana, Gian Luca Salvagno, Antonio Lupo, and Gian Cesare Guidi. "Influence of Sampling Time and Ultrafiltration Coefficient of the Dialysis Membrane on Cardiac Troponin I and T." Archives of Pathology & Laboratory Medicine 132, no. 1 (January 1, 2008): 72–76. http://dx.doi.org/10.5858/2008-132-72-iostau.

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Abstract Context.—The measurement of cardiac troponin I (TnI) and T (TnT) is essential to diagnose, guide therapy, and predict outcomes of the acute coronary syndrome. Increased levels of troponins, especially TnT, are frequently observed in patients on chronic hemodialysis (HD), reflecting ongoing and subclinical myocardial damage. Objective.—Because these markers are increasingly used for stratification of cardiac risk in these patients, their behavior during HD should be acknowledged to optimize their clinical usefulness. Design.—TnI and TnT were measured in 34 patients pre-HD and post-HD by either high- or low-flux membranes. The post-HD concentrations were corrected for hemoconcentration. Results.—Pre-HD levels above the 99th percentile reference limits of the general population of TnI (>0.06 ng/ mL) and TnT (>0.01 ng/mL) were observed in 9% (13% high-flux, 6% low-flux membranes) and 88% (94% high-flux; 83% low-flux membranes) of the patients, respectively. No significant difference was observed in mean pre-HD values between patients dialyzed by low- and high-flux membranes. The overall decrease post-HD of both troponins (−21% and −17% for TnI and TnT, respectively) only reached statistical significance in patients dialyzed by low-flux membranes (−27% and −37% for TnI and TnT, respectively). A significant correlation was observed between absolute variations of TnI and TnT pre-HD to post-HD. Conclusions.—Results of our investigation attest that high-flux membranes clear both troponins more efficiently from circulation than low-flux membranes. Therefore, sampling time and ultrafiltration coefficient of the HD membrane should be regarded as potential sources of variability in the clinical interpretation of troponin measurement in HD patients.

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Hammer, R. "On the existence of hot coronae around cool stars." Symposium - International Astronomical Union 122 (1987): 361–62. http://dx.doi.org/10.1017/s0074180900156712.

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A star cannot have a solar-like corona if the available mechanical energy flux in the chromosphere is either too large or decreases outward more rapidly than the pressure. This result might be relevant for hybrid stars and cool giants.

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Belcaro, G., A. N. Nicolaides, G. Laurora, M. R. Cesarone, M. T. De Sanctis, L. Incande, and A. Ricci. "Laser Doppler Flux in the Venous Wall." Phlebology: The Journal of Venous Disease 11, no. 2 (June 1996): 68–72. http://dx.doi.org/10.1177/026835559601100208.

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Objectives: To evaluate in vivo the perfusion of the venous wall in normal veins, varicose veins and in femoral veins of post-phlebitic limbs recording wall flux with laser Doppler flowmetry. As there is some evidence that both structure and microcirculatory dynamic responses are altered in the abnormal vein wall, we also aimed to study the response of vein wall perfusion to locally induced vasodilatation following papaverine infusion. Design: Open prospective study in patients with venous insufficiency and in patients undergoing coronary revascularization with a normal venous system. Setting: Cardiovascular Institute, Chieti University, Pierangeli Clinic, Italy and Irvine Laboratory, St Mary's Hospital, London, UK. Patients: Twenty-four normal long saphenous veins and 11 common femoral veins (35 normal veins, 35 subjects) and 42 varicose veins (42 patients). Measurements: Venous wall flux was measured on the external surface of normal long saphenous veins and common femoral veins. Measurements were also made on varicose veins before ligation of the sapheno-femoral junction. All measurements were made when at least three-quarters of the adventitia and periadventitia tissue were still intact for a length of 3 cm. Results: Flux in the normal vein wall was higher ( t = 5.88; p<0.05) than in varicose veins and in veins of post-phlebitic limbs. There was no difference in flux between varicose veins and post-phlebitic veins. After intravenous papaverine injection in a subgroup of eight normal and eight varicose veins, in the wall of normal veins there was a significant increase in flux (from 8.5 (SD 5.1) units to 13.2 (SD 3.8) units; p<0.05) which was not observed in varicose veins. Conclusions: A higher vein wall perfusion was observed in normal veins compared with varicose veins and post-phlebitic limb veins. Greater vascular reactivity to intraluminal papaverine injection was observed in normal veins.

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Decking, U. "Does local coronary flow control metabolic flux rates? A 13C-NMR study." Magnetic Resonance Materials in Biology, Physics, and Medicine 6, no. 2-3 (September 1998): 133–34. http://dx.doi.org/10.1016/s1352-8661(98)00041-6.

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Satur, Christopher M. R., John R. Andersen, Alison Jennings, Kenneth Newton, Paul G. Martin, Unikrishnan Nair, and Duncan R. Walker. "Magnesium flux caused by coronary artery bypass operation: Three patterns of deficiency." Annals of Thoracic Surgery 58, no. 6 (December 1994): 1674–78. http://dx.doi.org/10.1016/0003-4975(94)91657-8.

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30

Balkhy, Husam H., L. Samuel Wann, and Susan Arnsdorf. "Early Patency Evaluation of New Distal Anastomotic Device in Internal Mammary Artery Grafts Using Computed Tomography Angiography." Innovations: Technology and Techniques in Cardiothoracic and Vascular Surgery 5, no. 2 (March 2010): 109–13. http://dx.doi.org/10.1097/imi.0b013e3181d714ba.

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Introduction Traditional coronary artery bypass grafting is performed using a hand sewn technique. The C-Port xA and Flex A anastomotic stapling devices (Cardica Inc., Redwood City, CA) were cleared by the Food and Drug Administration for use in distal coronary anastomoses in November 2006 and April 2007, respectively. They provide the ability to create a compliant, consistently reproducible, and automated anastomosis. Multidetector computed tomography (CT) has been shown to be effective in evaluating coronary artery bypass graft patency. Methods The first 24 patients to undergo internal mammary artery (IMA) anastomosis using the automated device in our practice were included in the study. Twenty-five IMA grafts (24 left IMA and 1 right IMA) were created using the C-Port xA or Flex A anastomotic device as part of multivessel off-pump coronary revascularization by sternotomy. Graft patency was evaluated at 30 days in the first 10 grafts and at 90 days in the next 15 grafts using multidetector (64 slice) CT. Results There were no device failures. There were no perioperative strokes, myocardial infarctions, or deaths. All 10 IMA grafts evaluated at 30 days were patent using multidetector CT. One of the 15 IMA grafts studied at 90 days was occluded using multidetector computed tomography. Conclusions The C-Port xA and Flex A distal anastomotic devices provided a safe and effective means to create a left IMA-left anterior descending artery anastomoses in coronary bypass surgery with excellent short to midterm patency in this early experience. Long-term follow-up is warranted. These findings will have important implications for future sternal sparing coronary bypass surgery.

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Luna, G. J. M., K. Mukai, J. L. Sokoloski, T. Nelson, P. Kuin, A. Segreto, G. Cusumano, M. Jaque Arancibia, and N. E. Nuñez. "Dramatic change in the boundary layer in the symbiotic recurrent nova T Coronae Borealis." Astronomy & Astrophysics 619 (November 2018): A61. http://dx.doi.org/10.1051/0004-6361/201833747.

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A sudden increase in the rate at which material reaches the most internal part of an accretion disk, i.e., the boundary layer, can change its structure dramatically. We have witnessed such a change for the first time in the symbiotic recurrent nova T CrB. Our analysis of XMM-Newton, Swift Burst Alert Telescope (BAT)/X-Ray Telescope (XRT)/UltraViolet Optical Telescope (UVOT), and the American Association of Variable Stars Observers (AAVSO) V- and B-band data indicates that during an optical brightening event that started in early 2014 (ΔV ≈ 1.5) the following occurred: (i) the hard X-ray emission as seen with BAT almost vanished; (ii) the XRT X-ray flux decreased significantly, while the optical flux remained high; (iii) the UV flux increased by at least a factor of 40 over the quiescent value; and (iv) the X-ray spectrum became much softer and a bright, new blackbody-like component appeared. We suggest that the optical brightening event, which could be a similar event to that observed about 8 years before the most recent thermonuclear outburst in 1946, is due to a disk instability.

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Mattig, Sabine, and Andreas Deussen. "Significance of adenosine metabolism of coronary smooth muscle cells." American Journal of Physiology-Heart and Circulatory Physiology 280, no. 1 (January 1, 2001): H117—H124. http://dx.doi.org/10.1152/ajpheart.2001.280.1.h117.

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A detailed understanding of adenosine metabolism of vascular smooth muscle cells (VSMC) is highly desirable to critically evaluate possible autocrine effects of adenosine in this cell species. Therefore, this study quantified intra- and extracellular adenosine flux rates, the transmembrane concentration gradient, and the adenosine surface concentration in porcine VSMC and, for comparison, aortic endothelial cells (PAEC). Cell-covered microcarrier beads packed in a chromatography column were superfused with a HEPES buffer. With the use of specific inhibitors of adenosine kinase (iodotubericidine, 10 μM), adenosine deaminase [ erythro-9-(2-hydroxy-3-nonyl)-adenine, 5 μM], ecto-5′-nucleotidase (α,β-methylene-adenosine 5′-diphosphate, 50 μM), and adenosine membrane transport ( n-nitrobenzylthioinosine, 1 μM), total production rates of 12.3 ± 2.7 and 7.5 ± 1.3 pmol · min−1· μl cell volume−1were obtained for VSMC and PAEC, respectively. Despite prevailing intracellular adenosine production (76 and 70% of total production, respectively), transmembrane concentration gradients under control conditions were directed toward the cytosol as a result of rapid intracellular adenosine rephosphorylation and continuous extracellular hydrolysis from 5′-AMP. Surface concentrations were ∼18 nM in VSMC and PAEC under control conditions and increased to ∼60 nM during partial inhibition of adenosine metabolism. Simultaneously, the transmembrane adenosine concentration gradient was reversed. We conclude that adenosine flux rates in VSMC and PAEC are quantitatively similar and that VSMC may influence the interstitial adenosine concentration under basal steady-state conditions.

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Panchal, Ashish R., Blandine Comte, Hazel Huang, Todd Kerwin, Ahmed Darvish, Christine Des Rosiers, Henri Brunengraber, and William C. Stanley. "Partitioning of pyruvate between oxidation and anaplerosis in swine hearts." American Journal of Physiology-Heart and Circulatory Physiology 279, no. 5 (November 1, 2000): H2390—H2398. http://dx.doi.org/10.1152/ajpheart.2000.279.5.h2390.

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The goal of this study was to measure flux through pyruvate carboxylation and decarboxylation in the heart in vivo. These rates were measured in the anterior wall of normal anesthetized swine hearts by infusing [U-13C3]lactate and/or [U-13C3] pyruvate into the left anterior descending (LAD) coronary artery. After 1 h, the tissue was freeze-clamped and analyzed by gas chromatography-mass spectrometry for the mass isotopomer distribution of citrate and its oxaloacetate moiety. LAD blood pyruvate and lactate enrichments and concentrations were constant after 15 min of infusion. Under near-normal physiological concentrations of lactate and pyruvate, pyruvate carboxylation and decarboxylation accounted for 4.7 ± 0.3 and 41.5 ± 2.0% of citrate formation, respectively. Similar relative fluxes were found when arterial pyruvate was raised from 0.2 to 1.1 mM. Addition of 1 mM octanoate to 1 mM pyruvate inhibited pyruvate decarboxylation by 93% without affecting carboxylation. The absence of M1 and M2 pyruvate demonstrated net irreversible pyruvate carboxylation. Under our experimental conditions we found that pyruvate carboxylation in the in vivo heart accounts for at least 3–6% of the citric acid cycle flux despite considerable variation in the flux through pyruvate decarboxylation.

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Watanabe, S., C. W. Buffington, and G. Moresea. "Comparison of myocardial ischemia induced by endothelin vs. mechanical stenosis in pigs." American Journal of Physiology-Heart and Circulatory Physiology 268, no. 3 (March 1, 1995): H1276—H1283. http://dx.doi.org/10.1152/ajpheart.1995.268.3.h1276.

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We have determined the transmural distribution of myocardial flow and ischemia during endothelin (ET-1) infusion and compared these results with the effects of mechanical stenosis. In anesthetized pigs, coronary flow was reduced 15, 30, and 50% from baseline values with a mechanical stenosis (n = 7) or increasing doses of intracoronary ET-1 (n = 8). The inner-to-outer flow ratio decreased with decreasing total flow during mechanical stenosis, and S-T segment elevation occurred predominantly in the subendocardium. In contrast, the inner-to-outer flow ratio exceeded 1.0 and actually increased during ET-1 infusion. ET-1 limited the electrocardiographic evidence of subendocardial ischemia and attenuated contractile dysfunction compared with mechanical stenosis at the same coronary flows, even though lactate flux was similar. Reactive hyperemia was retained with ET-1, even when coronary flow was reduced enough to cause lactate production. These results demonstrate a more uniform transmural distribution of flow caused by microvascular constriction than by a large-vessel stenosis.

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Basri, G., and G. W. Marcy. "Limits on the Magnetic Flux of a Pre-Main Sequence Star." International Astronomical Union Colloquium 130 (1991): 401–6. http://dx.doi.org/10.1017/s0252921100080003.

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AbstractWe attempt to detect a magnetic field on the weak T Tauri star, TAP35, via the enhanced equivalent widths of Zeeman-broadened absorption lines. We synthesize 25 Fe I lines, having a range of Zeeman sensitivities, using an LTE Stokes line-transfer calculation. The oscillator strengths of all lines are empirically determined a priori using the same line-transfer code applied to the spectrum of the magnetically quiet star, τ Ceti. The Fe abundance of TAP35 was established by synthesizing lines that are insensitive to Zeeman splitting. We find that the equivalent widths, Weq, of Zeeman-sensitive lines in TAP35 are systematically enhanced relative to the Zeeman-insensitive lines, consistent with the presence of widespread, kilogauss fields. The excess Weq can be explained by a product of field strength and surface filling factor (Bf) of 1 kiloGauss. A strong upper limit can be placed on the product of those two quantities, Bf < 2 kG. This measurement bears on the physics of T Tauri coronae, chromospheres, dynamos, and accretion-disk boundary layers.

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Panchal, Ashish R., Blandine Comte, Hazel Huang, Basil Dudar, Bridgette Roth, Margaret Chandler, Christine Des Rosiers, Henri Brunengraber, and William C. Stanley. "Acute hibernation decreases myocardial pyruvate carboxylation and citrate release." American Journal of Physiology-Heart and Circulatory Physiology 281, no. 4 (October 1, 2001): H1613—H1620. http://dx.doi.org/10.1152/ajpheart.2001.281.4.h1613.

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In the well-perfused heart, pyruvate carboxylation accounts for 3–6% of the citric acid cycle (CAC) flux, and CAC carbon is lost via citrate release. We investigated the effects of an acute reduction in coronary flow on these processes and on the tissue content of CAC intermediates. Measurements were made in an open-chest anesthetized swine model. Left anterior descending coronary artery blood flow was controlled by a extracorporeal perfusion circuit, and flow was decreased by 40% for 80 min to induce myocardial hibernation ( n = 8). An intracoronary infusion of [U-13C3]lactate and [U-13C3]pyruvate was given to measure the entry of pyruvate into the CAC through pyruvate carboxylation from the13C-labeled isotopomers of CAC intermediates. Compared with normal coronary flow, myocardial hibernation resulted in parallel decreases of 65% and 79% in pyruvate carboxylation and net citrate release by the myocardium, respectively, and maintenance of the CAC intermediate content. Elevation of the arterial pyruvate concentration by 1 mM had no effect. Thus a 40% decrease in coronary blood flow resulted in a concomitant decrease in pyruvate carboxylation and citrate release as well as maintenance of the CAC intermediates.

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Richards, John R. "Mechanisms for the Risk of Acute Coronary Syndrome and Arrhythmia Associated With Phytogenic and Synthetic Cannabinoid Use." Journal of Cardiovascular Pharmacology and Therapeutics 25, no. 6 (June 26, 2020): 508–22. http://dx.doi.org/10.1177/1074248420935743.

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Phytogenic cannabinoids from Cannabis sativa and synthetic cannabinoids are commonly used substances for their recreational and medicinal properties. There are increasing reports of cardiotoxicity in close temporal association with cannabinoid use in patients with structurally normal hearts and absence of coronary arterial disease. Associated adverse events include myocardial ischemia, conduction abnormalities, arrhythmias, and sudden death. This review details the effects of phytogenic and synthetic cannabinoids on diverse receptors based on evidence from in vitro, human, and animal studies to establish a molecular basis for these deleterious clinical effects. The synergism between endocannabinoid dysregulation, cannabinoid receptor, and noncannabinoid receptor binding, and impact on cellular ion flux and coronary microvascular circulation is delineated. Pharmacogenetic factors placing certain patients at higher risk for cardiotoxicity are also correlated with the diverse effects of cannabinoids.

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Olgac, Ufuk, Vartan Kurtcuoglu, and Dimos Poulikakos. "Computational modeling of coupled blood-wall mass transport of LDL: effects of local wall shear stress." American Journal of Physiology-Heart and Circulatory Physiology 294, no. 2 (February 2008): H909—H919. http://dx.doi.org/10.1152/ajpheart.01082.2007.

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The work herein represents a novel approach for the modeling of low-density lipoprotein (LDL) transport from the artery lumen into the arterial wall, taking into account the effects of local wall shear stress (WSS) on the endothelial cell layer and its pathways of volume and solute flux. We have simulated LDL transport in an axisymmetric representation of a stenosed coronary artery, where the endothelium is represented by a three-pore model that takes into account the contributions of the vesicular pathway, normal junctions, and leaky junctions also employing the local WSS to yield the overall volume and solute flux. The fraction of leaky junctions is calculated as a function of the local WSS based on published experimental data and is used in conjunction with the pore theory to determine the transport properties of this pathway. We have found elevated levels of solute flux at low shear stress regions because of the presence of a larger number of leaky junctions compared with high shear stress regions. Accordingly, we were able to observe high LDL concentrations in the arterial wall in these low shear stress regions despite increased filtration velocity, indicating that the increase in filtration velocity is not sufficient for the convective removal of LDL.

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Xu, Ming, Xiao-xue Li, Jing Xiong, Min Xia, Erich Gulbins, Yang Zhang, and Pin-Lan Li. "Regulation of autophagic flux by dynein-mediated autophagosomes trafficking in mouse coronary arterial myocytes." Biochimica et Biophysica Acta (BBA) - Molecular Cell Research 1833, no. 12 (December 2013): 3228–36. http://dx.doi.org/10.1016/j.bbamcr.2013.09.015.

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40

Meiliana, Anna, Nurrani Mustika Dewi, and Andi Wijaya. "The High Density Lipoprotein Cholesterol Hypothesis Revisited." Indonesian Biomedical Journal 10, no. 2 (August 2, 2018): 84–103. http://dx.doi.org/10.18585/inabj.v10i2.465.

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BACKGROUND: The strong inverse association of plasma levels of high-density lipoprotein cholesterol (HDL-C) with coronary heart disease (CHD) found in human epidemiological studies led to the development of the ‘HDL-C hypothesis’, which posits that intervention to raise HDL-C will result in reduced risk of CHD. However, recent evidence has raised doubts about the hypotheses that elevating HDL-C is necessarily therapeutic. Genetic variations that associate with altered HDL-C do not strongly associate with altered cardiovascular disease risk.CONTENT: HDL-mediated cholesterol efflux from macrophage foam cells or measurements of the flux of cholesterol from macrophages to the liver and feces seem to correlate better with atherosclerotic burden than with HDL-C levels. Thus, it may be time to modify the HDL-C hypothesis to the ‘HDL flux hypothesis’, where intervention to promote cholesterol efflux and reverse cholesterol transport will reduce CHD risk, regardless of whether it affects plasma HDL-C levels. A deeper understanding of the complex biology of HDL metabolism and its relationship to reverse cholesterol transport and atherothromobotic events is urgently needed. This might lead to biomarkers of HDL flux and functionality that are more informative than simple measurements of HDL-C levels.SUMMARY: It is now clear from recent clinical trial and genetic studies that some approaches to raising HDL-C levels may have no effect on CHD. This suggests the need to evaluate HDL-C-raising therapies in different clinical populations, as well as therapies targeted toward HDL flux and function rather than simply HDL-C elevation. Perhaps moving from a focus on the HDL-C hypothesis to a focus on the HDL flux hypothesis will permit a biologically based reassessment of the optimal therapeutic approach to targeting HDL for reduction in cardiovascular risk.KEYWORDS: reverse cholesterol transport, cholesterol efflux capacity, HDL dysfunction, HDL particle size, HDL lipidomics, HDL proteomics

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Rubio, R., G. Ceballos, and J. Suarez. "Coronary flow stimulates auricular-ventricular transmission in the isolated perfused guinea pig heart." American Journal of Physiology-Heart and Circulatory Physiology 269, no. 4 (October 1, 1995): H1177—H1185. http://dx.doi.org/10.1152/ajpheart.1995.269.4.h1177.

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In the heart in situ coronary flow stimulates oxygen consumption, glycolytic flux, myocardial contractility, and the release of bioactive substances. Studies have indicated that the coronary flow-enhanced contraction is similar to a hormonelike effect because the enhanced contraction results from an elevation in intracellular free calcium. In fact, if extracellular calcium is raised sufficiently, the contraction amplitude rises and remains constant and independent of coronary flow. We hypothesized that coronary flow could also stimulate other calcium-dependent cardiac functions such as auricular-ventricular (A-V) transmission. This hypothesis was tested in isolated guinea pig hearts perfused at constant flow. Our results show that increases in coronary flow (6-25 ml/min range) decrease the A-V delay solely as a result of reduced propagation time in the A-V node and not in atrial or ventricular propagation. When coronary vascular resistance was altered by dilation (nitroglycerin, bradykinin, nitroprusside, and adenosine) or by constriction (angiotensin II), this dromotropic effect of flow remained the same despite wide changes in perfusing pressure. Also, this dromotropic effect of flow was not altered by energy-altering substrates in the perfusate or by perfusion of adenosine receptor blockers. Furthermore, the effectiveness of flow as a dromotropic stimulus varied inversely with changes in calcium entry caused either by elevation or reduction of extracellular calcium. In addition, enhanced viscosity of the perfusing medium amplifies the positive dromotropic effect of flow. These results suggest that coronary flow is a stimulus that exerts a positive dromotropic effect mediated by shear stress.

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Kim, Jong Yeob, Johanna Steingroever, Keum Hwa Lee, Jun Oh, Min Jae Choi, Jiwon Lee, Nicholas G. Larkins, et al. "Clinical Interventions and All-Cause Mortality of Patients with Chronic Kidney Disease: An Umbrella Systematic Review of Meta-Analyses." Journal of Clinical Medicine 9, no. 2 (February 1, 2020): 394. http://dx.doi.org/10.3390/jcm9020394.

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Patients with chronic kidney disease (CKD) have altered physiologic processes, which result in different treatment outcomes compared with the general population. We aimed to systematically evaluate the efficacy of clinical interventions in reducing mortality of patients with CKD. We searched PubMed, MEDLINE, Embase, and Cochrane Database of Systematic Reviews for meta-analyses of randomized controlled trials (RCT) or observational studies (OS) studying the effect of treatment on all-cause mortality of patients with CKD. The credibility assessment was based on the random-effects summary estimate, heterogeneity, 95% prediction intervals, small study effects, excess significance, and credibility ceilings. Ninety-two articles yielded 130 unique meta-analyses. Convincing evidence from OSs supported mortality reduction with three treatments: angiotensin-converting-enzyme inhibitors or angiotensin II receptor blockers for patients not undergoing dialysis, warfarin for patients with atrial fibrillation not undergoing dialysis, and (at short-term) percutaneous coronary intervention compared to coronary artery bypass grafting for dialysis patients. Two treatment comparisons were supported by highly credible evidence from RCTs in terms of all-cause mortality. These were high-flux hemodialysis (HD) versus low-flux HD as a maintenance HD method and statin versus less statin or placebo for patients not undergoing dialysis. Most significant associations identified in OSs failed to be replicated in RCTs. Associations of high credibility from RCTs were in line with current guidelines. Given the heterogeneity of CKD, it seems hard to assume mortality reductions based on findings from OSs.

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Cilla, Myriam, Estefanía Peña, and Miguel A. Martínez. "Mathematical modelling of atheroma plaque formation and development in coronary arteries." Journal of The Royal Society Interface 11, no. 90 (January 6, 2014): 20130866. http://dx.doi.org/10.1098/rsif.2013.0866.

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Atherosclerosis is a vascular disease caused by inflammation of the arterial wall, which results in the accumulation of low-density lipoprotein (LDL) cholesterol, monocytes, macrophages and fat-laden foam cells at the place of the inflammation. This process is commonly referred to as plaque formation. The evolution of the atherosclerosis disease, and in particular the influence of wall shear stress on the growth of atherosclerotic plaques, is still a poorly understood phenomenon. This work presents a mathematical model to reproduce atheroma plaque growth in coronary arteries. This model uses the Navier–Stokes equations and Darcy's law for fluid dynamics, convection–diffusion–reaction equations for modelling the mass balance in the lumen and intima, and the Kedem–Katchalsky equations for the interfacial coupling at membranes, i.e. endothelium. The volume flux and the solute flux across the interface between the fluid and the porous domains are governed by a three-pore model. The main species and substances which play a role in early atherosclerosis development have been considered in the model, i.e. LDL, oxidized LDL, monocytes, macrophages, foam cells, smooth muscle cells, cytokines and collagen. Furthermore, experimental data taken from the literature have been used in order to physiologically determine model parameters. The mathematical model has been implemented in a representative axisymmetric geometrical coronary artery model. The results show that the mathematical model is able to qualitatively capture the atheroma plaque development observed in the intima layer.

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Böhm-Vitense, E. "Emission measures and heating mechanisms for stellar transition regions and coronae." Symposium - International Astronomical Union 122 (1987): 359–60. http://dx.doi.org/10.1017/s0074180900156700.

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In order to determine the heating mechanisms for stellar transition regions and coronae we try to determine the damping lengths for the mechanical flux(es) responsible for the heating. For the lower part of the transition regions (30,000 < T≤100,000 K) the damping lengths are consistent with Shockwave damping. This appears to be also true for the upper part of the transition region in Procyon, while for the upper part of the solar transition region the damping length is much larger.

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Castor, J. I. "Heating and Momentum Deposition in Hot Stars." Highlights of Astronomy 9 (1992): 649–50. http://dx.doi.org/10.1017/s1539299600009928.

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The one great point of similarity between the coronae of hot and cool stars is that both are spatially extended regions of more-or-less tenuous gas that is flowing outward, and at least some of which is at a temperature in excess of 106 K. Coronae defined in this way are almost universal among stars—excepting cool supergiants—but this similarity may hide significant differences in the processes that produce coronae. There are two rather different paradigms for their origin: the cool-star paradigm and the hot star paradigm.The coronae of cool stars like the sun are of such a low density that radiative cooling is inefficient; the outward flow is weak enough that there is a fairly extended subsonic flow region. The outer corona is heated by a flux of wave energy, and some of this energy is then conducted inward to heat the inner corona. The outflow is driven by the pressure of the heated gas, assisted perhaps by wave pressure. The structure of the corona is greatly affected by the topology of the magnetic field, which channels the outflow and governs the transport of energy and momentum by waves.

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Chen, J., L. Wang, W. H. Liu, J. Shi, Y. Zhong, S. J. Liu, and S. M. Liu. "Aspirin protects human coronary artery endothelial cells by inducing autophagy." Physiology International 107, no. 2 (June 2020): 294–305. http://dx.doi.org/10.1556/2060.2020.00029.

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AbstractAlthough the use of aspirin has substantially reduced the risks of cardiovascular events and death, its potential mechanisms have not been fully elucidated. In a previous study, we found that aspirin triggers cellular autophagy. In the present study, we aimed to determine the protective effects of aspirin on human coronary artery endothelial cells (HCAECs) and explore its underlying mechanisms. HCAECs were treated with oxidized low-density lipoprotein (ox-LDL), angiotensin II (Ang-II), or high glucose (HG) with or without aspirin stimulation. The expression levels of endothelial nitric oxide (NO) synthase (eNOS), p-eNOS, LC3, p62, phosphor-nuclear factor kappa B (p-NF-κB), p-p38 mitogen-activated protein kinase (p-p38 MAPK), and Beclin-1 were detected via immunoblotting analysis. Concentrations of soluble intercellular adhesion molecule-1 (sICAM-1) and soluble vascular cell adhesion molecule-1 (sVCAM-1) were measured via ELISA. NO levels were determined using the Griess reagent. Autophagic flux was tracked by tandem mRFP-GFP-tagged LC3. Results showed that aspirin increased eNOS level and reduced injury to the endothelial cells (ECs) caused by ox-LDL, Ang-II, and HG treatment in a dose-dependent manner. Aspirin also increased the LC3II/LC3I ratio, decreased p62 expression, and enhanced autophagic flux (autophagosome and autolysosome puncta) in the HCAECs. p-NF-κB and p-p38 mitogen-activated protein kinase inhibition, sVCAM-1 and sICAM-1 secretion, and eNOS activity promotion by aspirin treatment were found to be dependent on Beclin-1. These results suggested that aspirin can protect ECs from ox-LDL-, Ang-II-, and HG-induced injury by activating autophagy in a Beclin-1-dependent manner.

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Spratt, D. I., M. Frohnauer, H. Cyr-Alves, R. S. Kramer, F. L. Lucas, J. R. Morton, D. F. Cox, K. Becker, and J. T. Devlin. "Physiological effects of nonthyroidal illness syndrome in patients after cardiac surgery." American Journal of Physiology-Endocrinology and Metabolism 293, no. 1 (July 2007): E310—E315. http://dx.doi.org/10.1152/ajpendo.00687.2006.

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In a prospective randomized placebo-controlled study, we assessed potential physiological effects of nonthyroidal illness syndrome (NTIS) in acute illness. Coronary artery bypass graft surgery was employed as a prospective model of acute illness and NTIS. Triiodothyronine (T3) or placebo was infused for 24 h after surgery, with a T3dose selected to maintain postoperative serum T3concentrations at preoperative levels. Patients were evaluated before coronary artery bypass graft and during the postoperative period. Cardiovascular function was monitored with Swan-Ganz catheter measurements and ECG. Urinary nitrogen excretion and l-[1-13C]leucine flux were used to evaluate protein metabolism. Serum measurements of relevant hormones, iron, and total iron-binding capacity were used to assess effects on sex steroid, growth hormone axis, and iron responses to illness. Cardiovascular function was not affected by T3infusion, except for a transient higher cardiac index in the T3group 6 h after surgery (3.04 ± 0.12 for T3and 2.53 ± 0.08 for placebo, P = 0.0016). Protein metabolism was not affected; changes in urinary nitrogen excretion and l-[1-13C]leucine flux were equivalent in the two groups ( P = 0.35 and P = 0.95, respectively). No differences were observed in changes in testosterone, estrogens, growth hormone, insulin-like growth hormone I, iron, or total iron-binding capacity between T3and placebo groups. We conclude that, in the early stages of major illness, the decrease in circulating T3concentrations in NTIS has only a minimal transient physiological impact on cardiac function and plays no significant role in protecting against protein catabolism or modulating other endocrine responses or iron responses to illness.

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Zhang, Yang, Ming Xu, Min Xia, Xiang Li, Krishna M. Boini, Mi Wang, Erich Gulbins, Paul H. Ratz, and Pin-Lan Li. "Defective autophagosome trafficking contributes to impaired autophagic flux in coronary arterial myocytes lacking CD38 gene." Cardiovascular Research 102, no. 1 (January 20, 2014): 68–78. http://dx.doi.org/10.1093/cvr/cvu011.

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HUXLEY, V. H., D. A. WILLIAMS, D. J. MEYER JR., and M. H. LAUGHLIN. "Altered basal and adenosine‐mediated protein flux from coronary arterioles isolated from exercise‐trained pigs." Acta Physiologica Scandinavica 160, no. 4 (July 1997): 315–25. http://dx.doi.org/10.1046/j.1365-201x.1997.661369000.x.

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DOAK, GREG J., and RICHARD I. HALL. "Does Hemoglobin Concentration Affect Perioperative Myocardial Lactate Flux in Patients Undergoing Coronary Artery Bypass Surgery?" Survey of Anesthesiology 40, no. 1 (February 1996): 6. http://dx.doi.org/10.1097/00132586-199602000-00007.

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