The internal vertebral venous plexus (IVVP) is an extensive vascular network recently implicated in various human and canine spinal disorders. Nevertheless, little recent information is available regarding normal anatomy of canine IVVP and its role in acute spinal injuries. The objectives of the study were; (1) to describe the normal IVVP morphology in the canine cervical region using transverse anatomy sections and computed tomography (CT), (2) to develop a technique for CT examination of the IVVP in vivo, (3) to analyze the quantitative characteristics of the IVVP, and (4) to assess the effect of acute experimental spinal cord compression on IVVP morphology. In the first experiment, CT of the cervical vertebral canal was performed in 6, normal, adult mixed-breed dogs. After dogs were euthanized, a gelatin and iothalamate mixture was injected into the right external jugular vein. Cadavers were then frozen to â 8°C, sliced into transverse sections, and compared with CT images. Vascular components such as the IVVP, interarcuate veins, intervertebral veins, and vertebral veins were accurately depicted on CT images. In the second experiment, CT venography was performed using a biphasic IV injection of iodinated contrast medium. Dimensions of the IVVP and other vertebral canal components were calculated for the C3-C7 vertebral region. Sagittal diameters of the IVVP ranged from 0.6 mm to 3.2 mm. The IVVP area occupied 30.61% of the cervical vertebral epidural space area. When C3-C7 segments were considered as a group, IVVP area dimensions were significantly correlated (r > 0.7, p < 0.0001) with vertebral canal area and dural sac area. In the last experiment, acute spinal cord compression (ASCC) was induced and maintained for 10 minutes using an angioplasty balloon catheter device over the C3/4 vertebral region in 6 dogs. Dogs were evaluated prior to, during, and after compression using digital subtraction venography (DSV) and CT venography. Results showed that ASCC produced a significant change in diameter of the IVVP at the site of compression. This effect persisted during the post-compression period. In conclusion, findings indicate that CT venography and DSV accurately depict the IVVP in dogs, and that significant changes of the IVVP morphology occur under ASCC conditions. / Ph. D.

Veins are ubiquitous features in deformed rocks. Despite observations on syntectonic veins spanning two centuries, fundamental questions remain unanswered. Their origin as fractures is largely established but it is still not known why these fractures initiate where they do and how the vein evolves once started. We studied veins from the Lower Ordovician Mazarn Formation in the Arkansas’ Ouachitas combining textural observations, stable isotopes, fluid inclusions, SEM-based cathodoluminescence and electron back-scattered diffraction to understand the initial stage of vein formation, its later evolution, the role of fluids and their environment of formation. The veins are located at boudin necks and are synchronous with cleavage formation. Texturally, veins are characterized by veinlets (thin veins between 5 and 25 μm thick) that parallel the vein-host interface and fibers (columns of quartz or calcite) perpendicular to the vein-host interface between 30 and 350 μm wide. Veinlets are localized fractures filled with quartz. The crystallographic orientation of the precipitated material in veinlets is inherited from host grains at the micron scale and replicated as fibers’ lengths grow to centimeters. The vein-forming fluid was cyclically supersaturated yet never very far from saturation. δ18O values of vein quartz and host are within 2‰ of each other suggesting that the fluid was rock-buffered. Nevertheless, δ18O and δ13C define a ‘J’ shaped trend. Although it is not possible to date any portion of this curve, the simplest explanation is that the fluid evolved from rock-buffered in a closed system to fluid-dominated in an open system. The range of pressure-temperature conditions of vein formation is between 275 and 385 °C and 1100 and 3400 bars, from fluid inclusions and quartz-calcite oxygen isotopes thermometry. By examining a vein from tip to middle, we have established a sequence of events from inception to maturity in vein growth. Vein formation starts with folding followed by flattening of resistant sandstone layers which in turn gives rise to boudinage. Boudinage formation allowed for fracture localization along boudin-necks. The vein grew by the repeated addition of veinlets in the neck region. Recrystallization later modified the fibers by obliterating some evidence of the veinlets and moving fiber walls.

Veins are ubiquitous features in deformed rocks. Despite observations on syntectonic veins spanning two centuries, fundamental questions remain unanswered. Their origin as fractures is largely established but it is still not known why these fractures initiate where they do and how the vein evolves once started. We studied veins from the Lower Ordovician Mazarn Formation in the Arkansas’ Ouachitas combining textural observations, stable isotopes, fluid inclusions, SEM-based cathodoluminescence and electron back-scattered diffraction to understand the initial stage of vein formation, its later evolution, the role of fluids and their environment of formation. The veins are located at boudin necks and are synchronous with cleavage formation. Texturally, veins are characterized by veinlets (thin veins between 5 and 25 μm thick) that parallel the vein-host interface and fibers (columns of quartz or calcite) perpendicular to the vein-host interface between 30 and 350 μm wide. Veinlets are localized fractures filled with quartz. The crystallographic orientation of the precipitated material in veinlets is inherited from host grains at the micron scale and replicated as fibers’ lengths grow to centimeters. The vein-forming fluid was cyclically supersaturated yet never very far from saturation. δ18O values of vein quartz and host are within 2‰ of each other suggesting that the fluid was rock-buffered. Nevertheless, δ18O and δ13C define a ‘J’ shaped trend. Although it is not possible to date any portion of this curve, the simplest explanation is that the fluid evolved from rock-buffered in a closed system to fluid-dominated in an open system. The range of pressure-temperature conditions of vein formation is between 275 and 385 °C and 1100 and 3400 bars, from fluid inclusions and quartz-calcite oxygen isotopes thermometry. By examining a vein from tip to middle, we have established a sequence of events from inception to maturity in vein growth. Vein formation starts with folding followed by flattening of resistant sandstone layers which in turn gives rise to boudinage. Boudinage formation allowed for fracture localization along boudin-necks. The vein grew by the repeated addition of veinlets in the neck region. Recrystallization later modified the fibers by obliterating some evidence of the veinlets and moving fiber walls.

No description available.

It has been deduced from indirect evidence that significant adjustments of vascular resistance take place in the venous network when blood flow changes in a organ. In the following experiments, we attempted to test the hypotheses that changes in postcapillary resistance in skeletal muscle may be due to changes in venous diameter, changes in the number of venules with blood flow, and/or changes in the apparent viscosity of blood in venules. The hypotheses were tested by observing the response of cat sartorius muscle venules (7-200 μm diameter) during arterial pressure reduction and muscle contraction. There was no observable change in venular diameter during any of the above perturbations. There was a significant decrease in the already low normalized velocity of blood in venules from a mean of 13 sec⁻¹ under control conditions to 5 sec⁻¹ during arterial pressure reduction to 20 mm Hg. At very low pressures, the number of venules with blood flow decreased. Combining our findings with Lipowsky's (1975) in vivo viscometry data, it was predicted that resistance in venules would increase 100% as a result of increases in blood viscosity when blood flow was reduced 60%. During post-contraction hyperemia the normalized velocity of blood in venules increased from 16 sec⁻¹ to 38 sec⁻¹ and the number of venules with blood flow increased a modest amount. Combining our observations with Lipowsky's data, we predict that venular resistance would fall 54% when blood flow increased 250% If shear rate changes cause substantial changes in blood viscosity in venules as suggested by the findings cited above, hydrostatic pressure in the small venules should tend to remain relatively constant as flow is altered. To determine whether this is the case, pressures of venules were measured using the servo-null technique during arterial pressure reduction. Pressures in the larger venules were a linear function of blood pressure and blood flow with an intercept not significantly different from the systemic venous pressure. Pressures in the smallest venules studied (24 μm), however, were somewhat insensitive to alterations in blood pressure (intercept of 10.4 mm Hg) and blood flow (intercept of 13.2 mm Hg). The stability of pressure in 40 venules supports the hypothesis that variable blood viscosity maintains the pressure drop in the venous network and the capillary hydrostatic pressure somewhat constant during changes in blood flow.

How patterns arise from an apparently uniform group of cells is one of the classical problems in developmental biology. The mechanism is complicated by the fact that patterning occurs on a growing medium. Therefore, changes in an organism’s size and shape affect the patterning processes. In turn, patterning itself may affect growth. This interaction between growth and patterning leads to the generation of complex shapes and structures from simpler ones. Studying such interactions requires the possibility to monitor both processes in vivo. To this end, we developed a new technique to monitor and quantify vein patterning in a growing leaf over time using the leaves of Arabidopsis thaliana as a model system. We used a transgenic line with fluorescent markers associated with the venation. Individual leaves are followed in many samples in vivo through time-lapse imaging. Custom-made software allowed us to extract the leaf surface and vein pattern from images of each leaf at each time point. Then average spatial maps from multiple samples that were generated revealed spatio-temporal gradients. Our quantitative description of wild type vein patterns during leaf development revealed that there is no constant size at which a part of tissue enclosed by vasculature will become irrigated by a new vein. Instead, it seemed that vein formation depends on the growth rate of the tissue. This is the first time that vein patterning in growing leaves was quantified. The techniques developed will later be used to explore the interaction between growth and patterning through a variety of approaches, including mutant analysis, pharmacological treatments and variation of environmental conditions.

How patterns arise from an apparently uniform group of cells is one of the classical problems in developmental biology. The mechanism is complicated by the fact that patterning occurs on a growing medium. Therefore, changes in an organism’s size and shape affect the patterning processes. In turn, patterning itself may affect growth. This interaction between growth and patterning leads to the generation of complex shapes and structures from simpler ones. Studying such interactions requires the possibility to monitor both processes in vivo. To this end, we developed a new technique to monitor and quantify vein patterning in a growing leaf over time using the leaves of Arabidopsis thaliana as a model system. We used a transgenic line with fluorescent markers associated with the venation. Individual leaves are followed in many samples in vivo through time-lapse imaging. Custom-made software allowed us to extract the leaf surface and vein pattern from images of each leaf at each time point. Then average spatial maps from multiple samples that were generated revealed spatio-temporal gradients. Our quantitative description of wild type vein patterns during leaf development revealed that there is no constant size at which a part of tissue enclosed by vasculature will become irrigated by a new vein. Instead, it seemed that vein formation depends on the growth rate of the tissue. This is the first time that vein patterning in growing leaves was quantified. The techniques developed will later be used to explore the interaction between growth and patterning through a variety of approaches, including mutant analysis, pharmacological treatments and variation of environmental conditions.

This study explored the possibility that upregulation of Hypoxia Inducible Factor-1 (Hif-1)-responsive genes in Human Umbilical Vein Endothelial Cells (HUVEC) would promote and stabilize HUVEC formation into inchoate vascular beds within artificial collagen gels. This experiment was designed to explore the above possibility by sub-cloning Hif-1[alpha], the related chimeric construct Hif-1[alpha]/VP16, and the marker gene dsRed into retroviral expression vectors, producing retroviral vectors containing these genes, and stably transducing HUVEC using these retroviruses. Transduced HUVEC were to be observed in cell culture as well as after implantation into artificial collagen gels that have previously supported vascular bed formation by HUVEC. Our results show, preliminarily, that HUVEC transduced with Hif-1[alpha]/VP16 go into cell-cycle arrest. Attempts to transduce HUVEC with Hif-1[alpha] failed to achieve high enough transduction efficiency to determine the cells angiogenic potential. This study concluded that more experiments need to be conducted to better characterize the effects of hypoxia-responsive gene upregulation in controlling HUVEC angiogenesis and cell-cycle signaling and that straightforward transduction of HUVEC by Hif-1[alpha]/VP16 is probably not sufficient, in itself, to induce in vitro vascular bed formation.

Thesis (Ph.D.)--Flinders University, Faculty of Medicine, Dept. of Human Physiology. / Typescript bound. Includes bibliographical references: (leaves 332-374) Also available online via the Web.

published_or_final_version / Nursing Studies / Master / Master of Nursing