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Thad Wilson, Ph.D.

Investigator Page

Contributions to Science

1.  Sweat glands: My contributions to the basic function and in the control and regulation of eccrine sweat glands include collaborative research identifying that: 1) baroreflexes do not contribute to the control and regulation of sweating during environmental-heat stress, 2) physical training improves sweating capacity and detraining reduces sweating capacity, but neither alters cholinergic dose-response sensitivity, and 3) calcium entry from interstitial fluid facilitates sweating during cholinergic induced sweating in humans. Additionally, I have initiated methods advancements in the quantification and regulation of skin sympathetic nerve activity as well as the translation of mechanisms developed in sweat gland cell lines and isolated sweat glands to in vivo human preparations. In the past few years I have been able to incorporate new techniques of nerve fiber densities and both coil and ductal epithelial transport into existing laboratories capabilities. This sweat gland work is clinically important for disorders such as hyperhidrosis and in modeling the factors affecting epithelial transport during sympathetic stimulation. Examples of projects for which I have directed or spearheaded writing and/or data collection are below:

a.  Review: Blackburn, S., Sammons, D. & Wilson, T. E.  Palmar-plantar and axillary hyperhidrosis: Physiology, pathophysiology and treatment options.  Journal of the American Osteopathic College of Dermatology, 22: 64-68, 2012.

b.  Wilson, T. E., Cui, J., & Crandall, C.G.  Absence of baroreflex modulation of skin sympathetic nerve activity and sweat rate during whole-body heating in humans.  Journal of Physiology (London), 536: 615-623, 2001.

c.  Wilson, T. E., Dyckman, D. J., & Ray, C. A.  Determinants of skin sympathetic nerve responses to isometric exercise.  Journal of Applied Physiology, 100: 1043-1048, 2006.

d.  Wilson, T. E., Monahan, K. D., Fogelman, A., Kearney, M. L., Sauder, C. L. & Ray, C. A.  Aerobic exercise training improves maximal in vivo cholinergic responsiveness but not sensitivity of eccrine sweat glands.  Journal of Investigative Dermatology, 130: 2328-2330, 2010.

e.  Metzler-Wilson, K., Sammons, D. L., Ossim, M. A., Metzger, N. R., Jurovcik, A. J., Krause, B. A. & Wilson, T. E. Extracellular calcium chelation and attenuation of calcium entry inhibit human in vivo cholinergic-induced eccrine sweating.  Experimental Physiology, 99:393-402, 2013.

2.  Physiology of Heat Stress: My contributions to the field of autonomic and cardiovascular responses to heat stress include collaborative research identifying that: 1) environmental heat stress modifies the operating point within a given Frank-Starling curve, but the inherent characteristics of that curve do not change, 2) heat stress increases cardiac contractility addition to heart rate, 3) aspects of the baroreflexes remain intact despite the sympathoexcitation associated with heat stress, 4) post-synaptic responsiveness of certain vasculature beds is blunted during heat stress, and 5) cerebral blood velocity decreases during heat stress and these decreases are related to heat syncope. Additionally, I have been involved with methods advancements indicating that central venous pressure tracks pulmonary capillary wedge pressure and with studies applying nuclear medicine studies to determine central and regional blood volume during heat stress. These data and interpretations have medical applications for hemorrhage, certain stages of shock, and the evaluation and prevention of heat-related illnesses. I have also been involved with testing colloid/crystalloid intravenous infusion and skin-surface cooling protocols as countermeasures for heat syncope. Examples of projects for which I have directed or and co-authored are below:

a.  Review: Crandall, C. G. & Wilson, T. E.   Human cardiovascular responses to passive heat stress.  Comprehensive Physiology, 5: 17-43, 2015.

b.  Wilson, T. E., Cui, J., & Crandall, C. G.  Effect of local and whole-body heating on human cutaneous alpha-adrenergic vasoconstrictor responsiveness.  Autonomic Neuroscience: Basic and Clinical, 97: 122-128, 2002.

c.  Wilson, T. E., Cui, J., Zhang, R., & Crandall, C. G.  Heat stress reduces cerebral blood velocity and markedly impairs orthostatic tolerance in humans.  American Journal of Physiology (Regulatory, Integrative, and Comparative Physiology), 291: R1443-R1448, 2006.

d.  Wilson, T. E., Brothers, R. M., Tollund, C., Dawson, E. A., Nissen, P., Yoshiga, C. C., Jons, C., Secher, N. H., Crandall, C. G.  Effect of thermal stress on Frank-Starling relations in humans.  Journal of Physiology (London), 587:3383-3392, 2009.

e.  Klabunde, R. E., LePorte, A. D., & Wilson, T. E.  Effect of temperature on isoproterenol-induced increases in left ventricular developed pressure.  Journal of Thermal Biology, 38: 369-373, 2013.

3.  Physiology of Cold Stress: My contributions to the autonomic and cardiovascular responses to cold stress include collaborative research identifying that: 1) myocardial supply and demand mismatches occur in older adults during non-shivering environmental cold stress, 2) cold stress increases pulmonary capillary wedge pressure without changing pulmonary vascular resistance, 3) renal, celiac, and superior mesenteric blood velocity decreases in addition to the standard decreases in peripheral blood flow during cold stress, and 4) precooling increases physical performance and thermal comfort and better maintains thermoregulation of individuals with multiple sclerosis. Additionally, I have been involved with unique applications of cardiac and vascular Doppler ultrasound, development of practical pre-cooling approaches, and new quantification approaches to cold-induced vasodilation. These data and interpretations have medical applications for older adults and those with temperature-sensitive neurological diseases and also have implications for myocardial infarctions and modeling of disease states. I have also been involved in testing cryotherapy and using focal and systemic cold stress in improving orthostatic intolerance and balance as well as improving worker performance and occupational health and safety. Examples of projects for which I have directed or spearheaded writing and/or data collection are below:

a.  Perspectives: Wilson, T. E., Klabunde, R. E. & Monahan, K. D.  Using thermal stress to model aspects of disease states. Journal of Thermal Biology, 43: 24-32, 2014.

b.  Wilson, T. E., Cui, J., Zhang, R., Witkowski, S., & Crandall, C. G.  Rapid skin-surface cooling maintains cerebral blood velocity and improves orthostatic tolerance during tilting in the heated human.  Journal of Applied Physiology, 93: 85-91, 2002.

c.  Wilson, T. E., Tollund, C., Yoshiga, C. C., Dawson, E. A., Nissen, P. , Secher, N. H. & Crandall, C. G.  Effects of heat and cold stress on central vascular pressures during orthostasis in humans.  Journal of Physiology (London), 585: 297-285, 2007.

d.  Wilson, T. E., Sauder, C. L., Kerney, M. L., Kuipers, N. T., Leuenberger, U. A., Monahan, K. D., & Ray, C. A.  Whole-body cold stress elicits peripheral and visceral vasoconstriction in humans.  Journal of Applied Physiology, 103: 1257-1262, 2007.

e.  Wilson, T. E., Gao, Z., Hess, K. L., & Monahan, K. D.  Effect of aging on cardiac function during cold stress in humans. American Journal of Physiology (Regulatory, Integrative, and Comparative Physiology), 298: R1627-R1633, 2010.

4.  Regional Differences in Cutaneous Biology: My contributions to regional differences in skin function include collaborative research identifying that: 1) cutaneous gravity reflexes can be regionally affected during head-down tilt bedrest but are not due to sympathetic mechanisms, 2) local heating and vasodilation can influence cutaneous gravity reflexes, 3) supraorbital skin sympathetic nerve activity is augmented in individuals with rosacea compared to controls during symptom trigger events, 4) facial skin blood flow is deferentially controlled compared to both glabrous and non-glabrous skin, and 5) glabrous skin, but not non-glabrous skin, can buffer alterations in arterial blood pressure. Additionally, I have been involved with methods advancements in direct recording of supraorbital sympathetic nerve activity, with novel applications to sensory afferent, adrenergic, and enzymatic blockade. These data and interpretations have medical applications for those with skin blood flow related-disorders or in conditions where local reflexes may be altered. Examples of projects I have directed and co-authored are below:

a.  Review: Gray, B. D., Metzler-Wilson, K., Dawes, K. W., & Wilson, T. E.  A neural link to understanding rosacea: Focusing on flushing triggers.  Journal of the American Osteopathic College of Dermatology, 33: 11-16, 2015.

b.  Davison, J. L., Short, D. S., & Wilson, T. E.  Effect of local heating and vasodilation on the cutaneous venoarteriolar response.  Clinical Autonomic Research, 14: 385-390, 2004.

c.  Wilson, T. E., Zhang, R., Levine, B. D., & Crandall, C. G.  Dynamic autoregulation of the cutaneous circulation: differential control in glabrous vs nonglabrous skin.  American Journal of Physiology (Heart & Circulatory Physiology), 289: H385–H391, 2005.

d.  Metzler-Wilson, K., Kellie, L. A., Tomc, C., Simpson, C., Sammons, D, & Wilson, T. E.  Differential vasodilatory responses to local heating in facial, glabrous and hairy skin.  Clinical Physiology and Functional Imaging, 32: 361-366, 2012.

e.  Metzler-Wilson, K., Toma, K., Sammons, D.L., Mann, S., Jurovcik, A. J., Demidova, O., & Wilson, T. E.  Augmented supraorbital skin sympathetic nerve activity responses to symptom trigger events in rosacea patients.  Journal of Neurophysiology, 114: 1530-1537, 2015.

For complete list of published research, please see
Scopus Author ID: https://www.scopus.com/authid/detail.uri?authorId=7403495604
ORCID: http://orcid.org/0000-0002-4345-1616

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