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The role of blood flow and nitric ox...

Lucitti, Jennifer Lynne.

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The role of blood flow and nitric oxide in chick (Gallus gallus) cardiovascular development.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	The role of blood flow and nitric oxide in chick (Gallus gallus) cardiovascular development./
作者:	Lucitti, Jennifer Lynne.
面頁冊數:	90 p.
附註:	Source: Dissertation Abstracts International, Volume: 64-12, Section: B, page: 5875.
Contained By:	Dissertation Abstracts International64-12B.
標題:	Biology, Animal Physiology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3116350
ISBN:	0496637851

The role of blood flow and nitric oxide in chick (Gallus gallus) cardiovascular development.
Lucitti, Jennifer Lynne.

The role of blood flow and nitric oxide in chick (Gallus gallus) cardiovascular development. - 90 p.

Source: Dissertation Abstracts International, Volume: 64-12, Section: B, page: 5875.

Thesis (Ph.D.)--New Mexico State University, 2003.

This dissertation examines the relationship between factors that alter intravascular nitric oxide (NO) concentrations and hemodynamic development in the embryonic chick (Gallus gallus). A considerable body of evidence suggests that the frictional forces of blood flow on vascular endothelium (shear stress) stimulate NO production, and that nitric oxide modulates cellular structure and function. Because the reshaping, or remodeling, of cardiac and vascular tissue is an essential part of normal cardiogenesis, and because cardiovascular form has a direct impact on function, it is hypothesized that alterations in both shear stress and NO during critical periods of development will affect the normal trajectory of hemodynamic parameters during embryogenesis. This hypothesis was tested in two ways. First, blood flow was altered via right lateral vitelline vein (RLVV) or posterior vitelline vein (PVV) obstruction at day 3 of a 21 day incubation period, corresponding to Hamburger and Hamilton (1951) stage 17. RLVV-clipping caused a more dramatic alteration of returning blood patterns than PVV-clipping and thus, was expected to show a more dramatic change in hemodynamic parameters. Briefly, RLVV-clipped embryos showed an elevated HR at stage 25, elevated blood pressure values at stage 32 and a higher dP/dt at stage 35 than PVV-clipped embryos or controls. The impact of PVV-clip was not apparent until stage 35, when embryos in this group presented with an elevated arterial pressure. These data suggest that early obstruction of the RLVV has its greatest hemodynamic impact at stage 32 (when cardiac septation is completing) while anomalies associated with PVV-ligation may take longer to manifest. Second, NO levels were elevated via exogenous suffusion of the NO donor NOC-18 or decreased with NO synthase (NOS) blockade (L-NNA) between stages 17 and 25. Stage 25 embryos exposed to a 10 mM NOC-18 solution presented with a lower pulse pressure and a dose dependent increase in HR was observed. Further, NOC-treated embryos had lower mean dorsal aortic blood flow and blood velocity. These data imply that NO may be an important regulator of cardiac pacemaker development in early stages. Pressure values in L-NNA treated embryos were similar at stage 25, although HR was significantly higher in the experimental group. By stage 32, this group had significantly elevated systolic and pulse pressures, as well as elevated dP/dt maximum values as compared to controls. (Abstract shortened by UMI.)

ISBN: 0496637851Subjects--Topical Terms:

1017835
Biology, Animal Physiology.

The role of blood flow and nitric oxide in chick (Gallus gallus) cardiovascular development.
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520 $a This dissertation examines the relationship between factors that alter intravascular nitric oxide (NO) concentrations and hemodynamic development in the embryonic chick (Gallus gallus). A considerable body of evidence suggests that the frictional forces of blood flow on vascular endothelium (shear stress) stimulate NO production, and that nitric oxide modulates cellular structure and function. Because the reshaping, or remodeling, of cardiac and vascular tissue is an essential part of normal cardiogenesis, and because cardiovascular form has a direct impact on function, it is hypothesized that alterations in both shear stress and NO during critical periods of development will affect the normal trajectory of hemodynamic parameters during embryogenesis. This hypothesis was tested in two ways. First, blood flow was altered via right lateral vitelline vein (RLVV) or posterior vitelline vein (PVV) obstruction at day 3 of a 21 day incubation period, corresponding to Hamburger and Hamilton (1951) stage 17. RLVV-clipping caused a more dramatic alteration of returning blood patterns than PVV-clipping and thus, was expected to show a more dramatic change in hemodynamic parameters. Briefly, RLVV-clipped embryos showed an elevated HR at stage 25, elevated blood pressure values at stage 32 and a higher dP/dt at stage 35 than PVV-clipped embryos or controls. The impact of PVV-clip was not apparent until stage 35, when embryos in this group presented with an elevated arterial pressure. These data suggest that early obstruction of the RLVV has its greatest hemodynamic impact at stage 32 (when cardiac septation is completing) while anomalies associated with PVV-ligation may take longer to manifest. Second, NO levels were elevated via exogenous suffusion of the NO donor NOC-18 or decreased with NO synthase (NOS) blockade (L-NNA) between stages 17 and 25. Stage 25 embryos exposed to a 10 mM NOC-18 solution presented with a lower pulse pressure and a dose dependent increase in HR was observed. Further, NOC-treated embryos had lower mean dorsal aortic blood flow and blood velocity. These data imply that NO may be an important regulator of cardiac pacemaker development in early stages. Pressure values in L-NNA treated embryos were similar at stage 25, although HR was significantly higher in the experimental group. By stage 32, this group had significantly elevated systolic and pulse pressures, as well as elevated dP/dt maximum values as compared to controls. (Abstract shortened by UMI.)
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