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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

Venoconstrição induzida por angiotensina  II em ratos normotensos e hipertensos: estudo de mecanismos de ação, localização e expressão de receptores AT1 e AT2. / Angiotensin II induced venoconstriction in normotensive and hypertensive rats: study of action mechanisms, localization and expression of AT1 and AT2 receptors.

Loiola, Rodrigo Azevedo 08 November 2007 (has links)
Neste estudo, avaliamos e caracterizamos o efeito de Ang II em leito venular mesentérico (LVM) e anéis de veia porta (AVP) de wistar e SHR. A reatividade vascular para Ang II foi estudada na presença e ausência de diferentes antagonistas para elucidar os mecanismos envolvidos na venoconstrição induzida por Ang II. Nossos resultados sugerem que a Ang II induz venoconstrição através da ativação de receptores AT1 e AT2 em Wistar e receptor AT1 em SHR. Essa venoconstrição parece ser contrabalanceada pelo receptor B2 em ambas as espécies. NO contribue para este efeito em wistar e metabólitos da COX em SHR. Há redução da venoconstrição induzida por Ang II em AVP de SHR que pode estar relacionado a redução da expressão protéica de receptores AT2. Esses resultados indicam diferentes mecanismos de regulação do tônus venoso de ratos wistar e SHR em resposta a Ang II que podem ter relevância no controle do retorno venoso e débito cardíaco. / In this study we have evaluated and characterized the effect of Ang II in the isolated perfused mesenteric venular bed (MVB) and portal vein rings (PVR) of SHR and wistar rats. Vascular reactivity to Ang II was studied in the absence and presence of different antagonists to elucidate the mechanisms involved in Ang II-induced venoconstriction. Our results suggest that Ang II induces venoconstriction by activation of AT1 and AT2 receptors in wistar and AT1 receptor in SHR. These venoconstriction seems to be counterbalanced by B2 receptor in both species. NO might contribute to this effect in wistar and COX metabolites in SHR. There is a decrease in Ang II induced venoconstriction in PVR of SHR that might be related to the decrease of protein expression of AT2 receptor. These results indicate different mechanisms of regulation of venous tonus of the SHR and wistar rats induced by Ang II that can be relevant in the control of the venous return and cardiac output.
2

Venoconstrição induzida por angiotensina  II em ratos normotensos e hipertensos: estudo de mecanismos de ação, localização e expressão de receptores AT1 e AT2. / Angiotensin II induced venoconstriction in normotensive and hypertensive rats: study of action mechanisms, localization and expression of AT1 and AT2 receptors.

Rodrigo Azevedo Loiola 08 November 2007 (has links)
Neste estudo, avaliamos e caracterizamos o efeito de Ang II em leito venular mesentérico (LVM) e anéis de veia porta (AVP) de wistar e SHR. A reatividade vascular para Ang II foi estudada na presença e ausência de diferentes antagonistas para elucidar os mecanismos envolvidos na venoconstrição induzida por Ang II. Nossos resultados sugerem que a Ang II induz venoconstrição através da ativação de receptores AT1 e AT2 em Wistar e receptor AT1 em SHR. Essa venoconstrição parece ser contrabalanceada pelo receptor B2 em ambas as espécies. NO contribue para este efeito em wistar e metabólitos da COX em SHR. Há redução da venoconstrição induzida por Ang II em AVP de SHR que pode estar relacionado a redução da expressão protéica de receptores AT2. Esses resultados indicam diferentes mecanismos de regulação do tônus venoso de ratos wistar e SHR em resposta a Ang II que podem ter relevância no controle do retorno venoso e débito cardíaco. / In this study we have evaluated and characterized the effect of Ang II in the isolated perfused mesenteric venular bed (MVB) and portal vein rings (PVR) of SHR and wistar rats. Vascular reactivity to Ang II was studied in the absence and presence of different antagonists to elucidate the mechanisms involved in Ang II-induced venoconstriction. Our results suggest that Ang II induces venoconstriction by activation of AT1 and AT2 receptors in wistar and AT1 receptor in SHR. These venoconstriction seems to be counterbalanced by B2 receptor in both species. NO might contribute to this effect in wistar and COX metabolites in SHR. There is a decrease in Ang II induced venoconstriction in PVR of SHR that might be related to the decrease of protein expression of AT2 receptor. These results indicate different mechanisms of regulation of venous tonus of the SHR and wistar rats induced by Ang II that can be relevant in the control of the venous return and cardiac output.
3

Der Einfluss der Körperposition auf die zerebrale venöse Drainage

Münster, Thomas von 11 December 2002 (has links)
Einleitung: Die Vena jugularis interna (VJI) gilt als das wichtigste Gefäß der zerebralen Drainage. Es gibt jedoch Hinweise darauf, dass das vertebrale Venensystem in Abhängigkeit von der Körperposition, an der zerebralen venösen Drainage beteiligt ist. Im Rahmen dieser Arbeit soll die Bedeutung der VJI und des vertebralen Venensystems für die zerebralvenöse Drainage in unterschiedlichen Körperpositionen untersucht werden. Methode: Bei 23 gesunden Probanden wurde der Blutfluss in den VJI und den Vv. vertebrales (VV) duplexsonographisch bestimmt. Dazu wurde die Person auf einem Kipptisch gelagert. Die Messungen wurden in den Positionen -15° (Kopftieflage), 0° (horizontal), 15°, 30°, 45°, und 90° (Stehen) durchgeführt. Der arterielle zerebrale Blutfluss (CBFA) wurde in den Positionen 0° und 45° bestimmt. Ergebnisse: Der Blutfluss der VJI ging von 810 ? 360 ml/min in Kopftieflage (-15°) auf 70 ? 100 ml/min im Stehen zurück. Gleichzeitig stieg der Blutfluss VV von 20 ? 15 ml/min in Kopftieflage auf 210 ? 120 ml/min im Stehen an. Der CBFA betrug 800 ? 153 ml/min in der 0°-Position und 720 ? 105 ml/min in der 45°-Position. Diskussion: Es konnte eine deutliche Lageabhängigkeit der zerebralvenösen Drainage nachgewiesen werden. Es zeigte sich, dass die zentrale Bedeutung der VJI für die zerebrale venöse Drainage auf die liegende Position beschränkt ist. Im Stehen verläuft die zerebrale venöse Drainage weitgehend über das vertebrale Venensystem. / Background: The internal jugular veins (IJV) are considered to be the main outflow of cerebral venous blood. However, there is evidence that the vertebral venous system also forms part of the cerebral venous outflow, depending on the position of the body. This paper asseses the hemodynamic consequences of postural changes in cerebral venous drainage by color-coded duplex sonography. Methods: Volume-blood-flow-measurements were conducted in 23 healthy volunteers in supine position on a tilt table. Both IJV and VV were studied in -15° (head-down tilt), 0°, 15°, 30°, 45°, and 90° (upright position) tilt. Arterial cerebral blood flow (CBFA) was measured in 0° and 45°-position. Results: Bloodflow in the IJV dropped from 810 ? 360 ml/min in the head-down-position (-15°) to 70 ? 100 ml/min at 90°. Simultaneously blood flow in the VV increased from 20 ? 15 ml/min in -15°-position to 210 ? 120 ml/min in the 90°-position. Discussion: The results show, that the cerebral blood drainage pathways depend heavily on the inclination of the body. The role of the IJV as the main drainage pathway of the cerebral blood appears to be confined to the supine position. In the erect position, the vertebral venous system was found to be the major outflow pathway in humans.

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