Changes in microvascular hematocrit during post-occlusive reactive hyperemia: descriptions and mechanisms
dc.contributor.author | Bopp, Christopher Michael | |
dc.date.accessioned | 2015-11-19T19:33:47Z | |
dc.date.available | 2015-11-19T19:33:47Z | |
dc.date.graduationmonth | December | en_US |
dc.date.issued | 2015-12-01 | en_US |
dc.date.published | 2015 | en_US |
dc.description.abstract | The primary aim of this dissertation was to describe the changes in microvascular hematocrit, as total[hemoglobin+myoglobin] (T[Hb+Mb] measured with near-infrared spectroscopy (NIRS), during post-occlusive reactive hyperemia (PORH). Mechanisms of reactive hyperemia within skeletal muscle were also explored. The investigation detailed in Chapter 2 of this dissertation found that the differing time courses of the kinetic responses of both oxy- and deoxy[Hb+Mb], are related to changes in T[Hb+Mb]. We also determined that adipose tissue thickness had no effect on a purely temporal analysis of NIRS data. In Chapter 3 we observed that brachial artery reactive hyperemia preceded changes in T[Hb+Mb] during reactive hyperemia. Assuming that myoglobin remained constant, we posited that changes in T[Hb+Mb] must reflect alterations in red blood cell concentration in the microvasculature, i.e., microvascular hematocrit. In Chapter 4 comparisons were made between brachial artery blood flow, cutaneous and skeletal muscle flux and T[Hb+Mb]. The conduit artery response was faster than the microvascular responses in all tissues. Within skeletal muscle, time to peak and the time constant for the on-kinetics were faster in T[Hb+Mb] compoared with intramuscular flux as measured with intramuscular laser-Doppler. We observed no differences in temporal responses between cutaneous and intramuscular measures and suggested that in a purely temporal analysis the cutaneous microvasculature could serve as an analog for the skeletal muscle microvasculature. Finally, in Chapter 5 we found that prostaglandin inhibition with ibuprofen altered the initial T[Hb+Mb] response during PORH without impacting cutaneous flux or brachial artery blood flow. Chapter 5 also discussed that the addition of a wrist cuff to our standard instrumentation prevented the accumulation of T[Hb+Mb] during the occlusion period. | en_US |
dc.description.advisor | Thomas J. Barstow | en_US |
dc.description.degree | Doctor of Philosophy | en_US |
dc.description.department | Department of Anatomy and Physiology | en_US |
dc.description.level | Doctoral | en_US |
dc.identifier.uri | http://hdl.handle.net/2097/20543 | |
dc.language.iso | en_US | en_US |
dc.publisher | Kansas State University | en |
dc.subject | Near-infrared spectroscopy | en_US |
dc.subject | Microvascular | en_US |
dc.subject | cutaneous | en_US |
dc.subject | skeletal muscle | en_US |
dc.subject | prostaglandins | en_US |
dc.subject.umi | Physiology (0719) | en_US |
dc.title | Changes in microvascular hematocrit during post-occlusive reactive hyperemia: descriptions and mechanisms | en_US |
dc.type | Dissertation | en_US |