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  • About
  • The Global ETD Search service is a free service for researchers to find electronic theses and dissertations. This service is provided by the Networked Digital Library of Theses and Dissertations.
    Our metadata is collected from universities around the world. If you manage a university/consortium/country archive and want to be added, details can be found on the NDLTD website.
1

Oldtidens lacre om hjerte, kar og puls en medicinak-historia studie mit einer deutschen Zusammenfassung.

Gotfredzen, Edvard, January 1900 (has links)
Thesis--Københavns universitet. / Includes bibliographical references.
2

Alpha-Adrenergic Modulation of Coronary Blood Flow and Cardiac Function During Exercise in Dogs

Overn, Steven P. (Steven Paul) 12 1900 (has links)
In the present study alpha-receptor modulation of coronary flow and cardiac function was examined in exercising dogs, chronically instrumented to measure: circumflex blood flow velocity (CFV), heart rate (HR), global left ventricular function (LVP and dP/dt Max) and regional left ventricular function (%SL and dL/dt (s)max). During exercise, local adrenergic blockade was produced by intracoronary injection of 1.0 mg phentolamine ( anon-specific alpha-antagonist) or .5 mp prazosin. Exercise significantly increased HR, LVP, dP/dt max, CFV, %SL and dL/dt (s)max. Neither alpha-antagonist produced changes in HR, LVP or %SL; however, both phentolamine and prazosin produced significant increses in dP/dtmax, CFV and dL/dt(s)max of the alpha-blocked region, when compared to their exercise level before alpha-blockade. It is suggested that an alpha1-adrenergic vasoconstriction limits coronary vasodilation and, thereby, cardiac function during exercise.
3

Coronary perivascular adipose tissue and vascular smooth muscle function: influence of obesity

Noblet, Jillian Nicole 22 March 2016 (has links)
Indiana University-Purdue University Indianapolis (IUPUI) / Factors released from coronary perivascular adipose tissue (PVAT), which surrounds large coronary arteries, have been implicated in the development of coronary disease. However, the precise contribution of coronary PVAT-derived factors to the initiation and progression of coronary vascular dysfunction remains ill defined. Accordingly, this investigation was designed to delineate the mechanisms by which PVAT-derived factors influence obesity-induced coronary smooth muscle dysfunction. Isometric tension studies of coronary arteries from lean and obese swine demonstrated that both lean and obese coronary PVAT attenuate vasodilation via inhibitory effects on smooth muscle K+ channels. Specifically, lean coronary PVAT attenuated KCa and KV7 channel-mediated dilation, whereas obese coronary PVAT impaired KATP channel-mediated dilation. Importantly, these effects were independent of alterations in underlying smooth muscle function in obese arteries. The PVAT-derived factor calpastatin impaired adenosine dilation in lean but not obese arteries, suggesting that alterations in specific factors may contribute to the development of smooth muscle dysfunction. Further studies tested the hypothesis that leptin, which is expressed in coronary PVAT and is upregulated in obesity, acts as an upstream mediator of coronary smooth muscle dysfunction. Long-term administration (3 day culture) of obese concentrations of leptin markedly altered the coronary artery proteome, favoring pathways associated with calcium signaling and cellular proliferation. Isometric tension studies demonstrated that short-term (30 min) exposure to leptin potentiated depolarization-induced contraction of coronary arteries and that this effect was augmented following longer-term leptin administration (3 days). Inhibition of Rho kinase reduced leptin-mediated increases in coronary artery contractions. Acute treatment was associated with increased Rho kinase activity, whereas longer-term exposure was associated with increases in Rho kinase protein abundance. Alterations in Rho kinase signaling were also associated with leptin-mediated increases in coronary vascular smooth muscle proliferation. These findings provide novel mechanistic evidence linking coronary PVAT with vascular dysfunction and further support a role for coronary PVAT in the pathogenesis of coronary disease.
4

Effect of coronary perivascular adipose tissue on vascular smooth muscle function in metabolic syndrome

Owen, Meredith Kohr 19 December 2013 (has links)
Indiana University-Purdue University Indianapolis (IUPUI) / Obesity increases cardiovascular disease risk and is associated with factors of the “metabolic syndrome” (MetS), a disorder including hypertension, hypercholesterolemia and/or impaired glucose tolerance. Expanding adipose and subsequent inflammation is implicated in vascular dysfunction in MetS. Perivascular adipose tissue (PVAT) surrounds virtually every artery and is capable of releasing factors that influence vascular reactivity, but the effects of PVAT in the coronary circulation are unknown. Accordingly, the goal of this investigation was to delineate mechanisms by which lean vs. MetS coronary PVAT influences vasomotor tone and the coronary PVAT proteome. We tested the hypothesis that MetS alters the functional expression and vascular contractile effects of coronary PVAT in an Ossabaw swine model of the MetS. Utilizing isometric tension measurements of coronary arteries in the absence and presence of PVAT, we revealed the vascular effects of PVAT vary according to anatomical location as coronary and mesenteric, but not subcutaneous adipose tissue augmented coronary artery contractions to KCl. Factors released from coronary PVAT increase baseline tension and potentiate constriction of isolated coronary arteries relative to the amount of adipose tissue present. The effects of coronary PVAT are elevated in the setting of MetS and occur independent of endothelial function. MetS is also associated with substantial alterations in the coronary PVAT proteome and underlying increases in vascular smooth muscle Ca2+ handling via CaV1.2 channels, H2O2-sensitive K+ channels and/or upstream mediators of these ion channels. Rho-kinase signaling participates in the increase in coronary artery contractions to PVAT in lean, but not MetS swine. These data provide novel evidence that the vascular effects of PVAT vary according to anatomic location and are influenced by the MetS phenotype.

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