7 research outputs found
An experimental study
Deckblatt-Impressum
persönlicher Dank
Inhaltsverzeichnis
Abbildungsverzeichnis
Tabellenverzeichnis
Einleitung
Literatur
Eigene Untersuchungen
Ergebnisse
Diskussion
Zusammenfassung
Summary
Literaturverzeichnis
Danksagung
SelbständigkeitserklärungDie vorliegende Arbeit befasst sich mit der Punktion der Bursa podotrochlearis
am Gliedmaßenpräparat von Pferden im Hinblick auf das Podotrochlose-Syndrom.
Diese Untersuchungen werden durchgeführt, um zusätzliche Informationen zu
gewinnen zur Sicherstellung der Punktion der Bursa podotrochlearis. Aufgrund
von Rasse, Alter und Gewicht des Pferdes unterscheiden sich Hufform und
Hufgröße zumteil erheblich. Die Injektionsmethode, die in dieser Studie
beschrieben wird, ist sehr genau und kann bei allen Hufformen (spitz,
regelmäßig, stumpf) und allen Hufgrößen (klein, mittelgroß, groß) angewendet
werden. Die notwendige Eindringtiefe der Kanüle bei der Injektion in die Bursa
podotrochlearis wurde im Versuch an Gliedmaßenpräparaten mit verschiedensten
Hufgrößen und Hufformen jeweils aufgezeichnet (zwischen 4,6 bis 5,5 cm). Die
Ergebnisse können als Grundlage für die zukünftige Forschung am lebenden Pferd
dienen. Diese Injektionstechnik ermöglicht durch die Kenntnis der notwendigen
Kanülengröße und richtige Einschätzung der Eindringtiefe der Kanüle eine hohe
Sicherheit in der zuverlässigen Punktion der Bursa podotrochlearis. Eine
Aspiration von Synovia aus der Bursa podotrochlearis ist in der Regel nicht
möglich. Die Menge an Flüssigkeit, die in die Bursa injiziert werden kann,
variiert von Gliedmaße zu Gliedmaße (zwischen 1 bis 10 ml). Das Druckmessgerät
kann als Hilfsmittel für die Kontrolle der Lage der Kanüle eingesetzt werden.
Die beschriebene Technik ist zur sicheren Punktion der Bursa podotrochlearis
unter Praxisbedingungen geeignet. Die Resultate der vorliegenden Studie
zeigen, dass der Druck in der Bursa podotrochlearis der präparaten mit der
Zeit auf Null, abfällt. In dieser Studie konnte beobachtet werden, dass die
Stärke der Belastung keine deutlichen Auswirkungen auf die Druckverhältnisse
in der Bursa podotrochlearis hat. Der Druck in der Bursa podotrochlearis
steigt unter Flüssigkeitszugabe an. Bei Strahlbeinen mit deformierten Canales
sesamoidales ist der Bursadruckwert nicht höher als bei Strahlbeinen mit nicht
deformierten Canales sesamoidales.This study is about the puncture of the navicular bursa at the limbs of
slaughtered horses in the view of the podotrochlear syndrome. These
investigations are carried, to gain extra Imformations about the safe
positioning of the puncture of the navicular bursa. Depending on breed, age
and weight of the horses, the sizes and shapes of the hooves differ
significantly. The injection-method described in this study has prooved to be
very reliable and applicable to all hoof shapes (pointed, regular, edgeless)
and sizes (small, medium, large). On different hoof sizes of legs from
slaughtered horses, the necessary penetration depth for injections into the
navicular bursa has been determined (between 4.6 to 5.5 cm). This injection-
technique, with its determination of the appropriate cannula size and depth of
penetration, allows a high reliability in the punctuation of the navicular
bursa. The results of this study can be used as basis for further research
conducted with living horses. Another finding of this study is the fact that
aspiration of synovia from the navicular bursa is not possible. The mess of
fluence that can be injected in to the navicular bursa varies from limb to
limb (between 1 to 10 ml). The pressure measuring instrument used for the
aforementioned experiments can be used to help positioning the cannule. The
technique for a reliable punctuation of the navicular bursa as described above
is well applicable in practice. The results of this study show that the
pressure in the navicular bursa falls with the time at zero. In this study it
can be observed that the strength of the load has no meaningsful consequence
on the pressure ratio in the navicular bursa. The pressure in the navicular
bursa reises when fluids are reised. Limbs with a deformed Canales
sesamoidales do not have a higher bursapressure than limbs without a deformed
Canales sesamoidales
Chronic kidney disease induces a systemic microangiopathy, tissue hypoxia and dysfunctional angiogenesis
Chronic kidney disease (CKD) is associated with excessive mortality from cardiovascular disease (CVD). Endothelial dysfunction, an early manifestation of CVD, is consistently observed in CKD patients and might be linked to structural defects of the microcirculation including microvascular rarefaction. However, patterns of microvascular rarefaction in CKD and their relation to functional deficits in perfusion and oxygen delivery are currently unknown. In this in-vivo microscopy study of the cremaster muscle microcirculation in BALB/c mice with moderate to severe uremia, we show in two experimental models (adenine feeding or subtotal nephrectomy), that serum urea levels associate incrementally with a distinct microangiopathy. Structural changes were characterized by a heterogeneous pattern of focal microvascular rarefaction with loss of coherent microvascular networks resulting in large avascular areas. Corresponding microvascular dysfunction was evident by significantly diminished blood flow velocity, vascular tone, and oxygen uptake. Microvascular rarefaction in the cremaster muscle paralleled rarefaction in the myocardium, which was accompanied by a decrease in transcription levels not only of the transcriptional regulator HIF-1 alpha, but also of its target genes Angpt-2, TIE-1 and TIE-2, Flkt-1 and MMP-9, indicating an impaired hypoxia-driven angiogenesis. Thus, experimental uremia in mice associates with systemic microvascular disease with rarefaction, tissue hypoxia and dysfunctional angiogenesis
Vascular barrier regulation by PAF, ceramide, caveolae, and NO - an intricate signaling network with discrepant effects in the pulmonary and systemic vasculature
SCARA with Path trajectory
The following Matlab project contains the source code and Matlab examples used for SCARA with Path trajectory. By defining the initial position and final position the robot will follow the path between these two point
Platelet-activating factor reduces endothelial NO production : role of acid sphingomyelinase
Thoracic epidural anesthesia decreases endotoxin-induced endothelial injury
Background: The sympathetic nervous system is considered to modulate the endotoxin-induced activation of immune cells. Here we investigate whether thoracic epidural anesthesia with its regional symapathetic blocking effect alters endotoxin-induced leukocyte-endothelium activation and interaction with subsequent endothelial injury. Methods: Sprague Dawley rats were anesthetized, cannulated and hemodynamically monitored. E. coli lipopolysaccharide (Serotype 0127: B8, 1.5 mg x kg(-1) x h(-1)) or isotonic saline (controls) was infused for 300 minutes. An epidural catheter was inserted for continuous application of lidocaine or normal saline in endotoxemic animals and saline in controls. After 300 minutes we measured catecholamine and cytokine plasma concentrations, adhesion molecule expression, leukocyte adhesion, and intestinal tissue edema. Results: In endotoxemic animals with epidural saline, LPS significantly increased the interleukin-1 beta plasma concentration (48%), the expression of endothelial adhesion molecules E-selectin (34%) and ICAM-1 (42%), and the number of adherent leukocytes (40%) with an increase in intestinal myeloperoxidase activity (26%) and tissue edema (75%) when compared to healthy controls. In endotoxemic animals with epidural infusion of lidocaine the values were similar to those in control animals, while epinephrine plasma concentration was 32% lower compared to endotoxemic animals with epidural saline. Conclusions: Thoracic epidural anesthesia attenuated the endotoxin-induced increase of IL-1 beta concentration, adhesion molecule expression and leukocyte-adhesion with subsequent endothelial injury. A potential mechanism is the reduction in the plasma concentration of epinephrine