No description available.

Thesis (M.S.)--University of Michigan, 1970.

Thesis (M.S.)--University of Michigan, 1970.

No description available.

No description available.

Thesis (Ph. D.)--University of Oregon, 2007. / Typescript. Includes vita and abstract. Includes bibliographical references (leaves 196-214). Also available for download via the World Wide Web; free to University of Oregon users.

No description available.

Control of blood flow to skeletal muscle is essential to maintain the overall homeostasis of an organism. The primary route that skeletal muscle uses to accommodate an increased metabolic demand associated with physical activity is to increase its blood flow through functional hyperemia. The importance of functional hyperemia in ensuring proper skeletal muscle function spurred 130 years of investigation into the mechanism(s) regulating its occurrence.Despite not identifying the essential factor(s) for controlling skeletal muscle blood flow, the last century of investigation has uncovered much about the process; including the observation that skeletal muscle functional hyperemia is impaired with ischemic disease. In patients, this can result in immobility, chronic ulcerations, gangrene, and at worst, amputation. To develop efficacious therapies, we as scientists must develop a better understanding of the molecular mechanisms underlying impaired vascular function during ischemia.The goal of this work was to lay the foundation for investigations examining the role of specific gene products involved in modulating blood flow control during ischemic revascularization by assessing vascular function in the mouse following an ischemic event. Unique among research animals, the mouse is routinely accessible for targeted genetic disruption, which allows investigators to assess the requirement of specific gene-products in a physiological process. Unfortunately, to date, no publication that I am aware of describes blood flow measurement to contracting mouse skeletal muscle following an ischemic/revascularization event. Therefore, the primary objective of this work was to assess vascular function in genetically unaltered animals.I found that unlike other species thus far examined, vascular dysfunction is not an obligatory response to hindlimb ischemic revascularization in the mouse. Ex vivo vasodilation responses to acetylcholine were statistically significantly impaired in the muscular branch artery 14 days following an ischemic event. However, using a newly developed fluorescent microsphere-based approach for determining skeletal muscle blood flow, I found that functional hyperemia was similar for the gracilis posterior muscle between non-ischemic and day-14 ischemic animals. In light of the primary literature, these findings suggest that vascular growth, and not ischemia per se is the primary regulator of vascular function during health and disease.

Thesis (M.S.)--University of Wisconsin--La Crosse, 2002. / Includes bibliographical references.

Skin blood flow (SKBF) demonstrates a biphasic response to innocuous, local heating. Much about the mechanism of the first phase is unknown. A type of ion channel (TRPV3) sensitive to and increasingly activated by temperatures from ~33 to ~45°C may be involved. TRPV3 channels are abundantly located in the keratinocytes and are believed to elicit the release of ATP, a putative cutaneous vasodilator, upon activation. This study investigated the possibility that TRPV3 channels and ATP have a role in the first phase of the SBKF response to local heat. Fifteen young, healthy subjects participated in the study. Two microdialysis probes were inserted into the dermis on the forearm. Using a peltier module, the skin above the probes (3cm x 3cm) was heated to 31, 35, 39, and 43°C to manipulate the level of activation of TRPV3 channels for eight minutes each. The probes were perfused with 0.9% saline at 2µl/min. Dialysate from each phase was analyzed for the concentration of ATP ([ATP]d). Cutaneous vascular conductance (CVC), measured by laser Doppler flowmetry, was monitored throughout. The [ATP]d decreased significantly when the skin was heated to temperatures known to strongly activate TRPV3 channels (i.e 39 and 43°C). [ATP]d demonstrated no relationship with CVC and only a very weak relationship with peltier temperature (r2 = 0.02, p<0.05). These data indicate that local heating and presumably heat-induced activation of the TRPV3 channels results in the decrease, not increase, of the release of ATP in human skin, and that the [ATP]d is not related to changes in skin blood flow. Significant dilation was observed at 35°C. This threshold, which is several degrees lower than the threshold previously reported, suggests that the TRPV3 channels may be involved in the dilator response in some way independent of interstitial ATP.