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Show 176 TEMPERATURE IN DUCED SYMPATHOLY SIS AND VASCULAR FUNCTION: THE ROLE OF ADVANCING AGE AND GENDER Cheyenne Schmid, (Russ Richardson) Department of Exercise and Sport Science University of Utah RESEARCH POSTERS ON THE HILL SPRING 2012 DISCUSSION Increased local temperature due to metabolism is likely a mechanism contributing to functional sympatholysis, which is a reduction in the vasoconstrictor responses to sympathetic nerve stimulation and subsequent increase in blood flow (1), so we sought to determine if temperature induced a sympatholytic response and if age affected this process. We saw that age had a greater impact on phenylephrine-induced vasoconstriction at 39°C than at 37°C. The effect of vasoconstriction can be opposed and even reversed by vasodilators (2). Temperature induces those vasodilators that oppose vasoconstrictors which could be less effective in the older, thus vasoconstriction declined in the young with increasing temperature and remained the same in the older. This decrease in phenylephrine-induced vasoconstriction in the young with heating was also observed in a study by Cui J. et al. (3). Age seemed to have less of an effect on the time required to reach the maximum phenylephrine-induced vasoconstriction with increased temperature. Temperature could possibly enhance cell permeability and/or diffusion and allow more vasoconstrictor function to occur, thus deceasing the time to the maximum peak. Perhaps vasoconstriction responsiveness remains intact, but the ability to produce and/or respond to vasodilators is reduced with age. This knowledge can be clinically applied to possibly show that older individuals are less sensitive to vasodilators (e.g. heat) and experience less hyperemia during exercise, thus resulting in poor exercise and mobility tolerance. References: 1. Dinenno, F.A. (2003). Advanced Experimental Medical Biology, 543, 237-248. 2. Rosenmeier, J.B., et al. (2008). Journal of Physiology, 586(20). 3. Cui, J., et al. (2002). Am J Physiol Regul Integr Comp Physiol, 283, R1221-R1226. Temperature-Induced Sympatholysis and Vascular Function: The Role of Advancing Age Cheyenne Schmid and Russell Richardson, Ph.D. Department of Exercise and Sports Science Cheyenne Schmid Russell Richardson Figure 3. Phenylephrine-induced vasoconstriction with regards to increasing age at different temperatures A) 37˚C. B) 39˚C. Figure 4. Time in seconds to the maximum phenylephrine-induced vasoconstriction with regards to increasing age at 37˚C (Blue) and 39˚C (Red). Figure 2. Vessel function characterized by vasoconstrictors and vasodilators. A) Potassium Chloride dose response (mg developed tension). B) Phenylephrine dose response (mg developed tension). C) Acetylcholine dose response (percent relaxation). D) Sodium Nitroprusside dose response (percent relaxation). Force Transducer Gas Inlet Vacuum ABSTRACT Aging has been documented to reduce skeletal muscle blood flow at rest and during exercise. Increased local temperature due to metabolism is likely a mechanism contributing to exercise hyperemia and functional sympatholysis. It is currently unknown whether aging impacts this response and if vascular function is a mediating factor. Therefore, we utilized an in vitro approach to determine if basal vascular function or the effect of temperature was different across age (<50, 50-65, >65yrs). METHODS: Human vessels (~500μM) supplying skeletal muscle were obtained during pre-scheduled surgeries (15 males, 11 females, 56 ± 15 yrs). Vessels were dissected into four 2 mm rings and mounted on a wire myograph. All vessels underwent a stepwise length tension procedure to determine LMAX (≤10% increase in vasoconstriction in response to 100mM KCl). Vessel function was characterized using potassium chloride (KCl), phenylephrine (PE), acetylcholine (Ach), and sodium nitroprusside (SNP) dose response curves to determine non-receptor and receptor mediated vasoconstriction and vasodilation. To determine if temperature exerts a sympatholytic effect, PE (1mM) was given at 37 and 39°C. Data are presented as mean±SE. RESULTS: Temperature reduced α1-mediated vasoconstriction (37°C 76±17 vs 39°C 46±8 %constriction, p< 0.05), however, this response was not influenced by age. Although the absolute maximal PE-induced tension varied largely by gender (p< 0.05), the %increase in PE-induced tension were similar. CONCLUSION: There seems to be no baseline differences in vascular function with regards to age. Increasing temperature could be a contributing factor to functional sympatholysis, but age appears not to influence this process. RESULTS METHODS Figure 1. A) Human arterial sample. B) Laboratory set up including dissecting microscope, wire myographs, and data acquisition computer. C) Wire myograph chamber used for functional studies of human arteries. Mounting Pins A B C Artery ACKNOWLEDGEMENTS: UROP, BioURP, and ACCESS programs Aging has been documented to reduce skeletal muscle blood flow. Increased local tempera ture due to metabolism is likely a mecha nism contributing to functional sympatholysis. It is currently unknown whether aging impacts this response and if vascular function is a mediating factor. Therefore, we utilized an in vitro approach to determine if basal vascular function or the effect of temperature was different across age (<50, 50-65, >65yrs) or gender. METHODS: Human vessels (~500 M) supplying skeletal muscle were obtained during pre-scheduled surgeries (15 males, 11 females; 56 ± 15 yrs). Vessels were dissected into four 2-mm rings and mounted on a wire myograph. All vessels underwent a stepwise length tension procedure to determine LMAX ( 10% increase in vasocontraction in response to 100mM KCl). Vessel function was characterized using potassium chloride (KCl), phenylephrine (PE), acetylcholine (Ach), and sodium nitroprusside (SNP) dose response curves to determine non-receptor and receptor mediated vasocontraction and vasorelaxation. To de-termine if temperature exerts a sympatholytic effect, PE (1mM) was given at 37°C and 39°C. Data are presented as mean±SE. RESULTS: Temperature reduced ¡1-mediated vasocontraction (37°C 76±17 vs 39°C 46±8 percent contraction; p< 0.05), however, this response was not influenced by age or gender. Although the absolute maximal PE-induced tension varied largely by gender (p< 0.05), the percent in-creases in PE-induced tension were similar. CONCLUSION: There seems to be no baseline differences in vascular function with regards to age or gender. Increasing temperature could be a contributing factor to functional sympatholysis, but gender and age appear not to influence this process. |
