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1 Institute for Exercise and Environmental Medicine, Presbyterian Hospital of Dallas, Dallas, Texas, USA
2 Institute for Exercise and Environmental Medicine, Presbyterian Hospital of Dallas, Dallas, Texas, USA; Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas, USA
* To whom correspondence should be addressed. E-mail: CraigCrandall{at}texashealth.org.
Orthostatic stress leads to a reduction in central venous pressure (CVP), which is an index of cardiac pre-load. Skin surface cooling has been shown to improve orthostatic tolerance, although the mechanism resulting in this outcome is unclear. One possible mechanism may be that skin surface cooling attenuates the drop in CVP during an orthostatic challenge, thereby preserving cardiac filling. To test this hypothesis, CVP, arterial blood pressure, heart rate, skin blood flow as well as skin and sublingual temperatures, were recorded in 9 healthy subjects during lower-body negative pressure (LBNP) in both normothermic and skin surface cooling conditions. Cardiac output was also measured via acetylene rebreathing. Progressive LBNP was applied at -10, -15, -20, and -40 mmHg at 5 min per stage. Prior to LBNP, skin surface cooling lowered mean skin temperature, increased CVP, increased mean arterial blood pressure (all p<0.001), but did not change mean heart rate (p=0.38). Compared with normothermic conditions, arterial blood pressure remained elevated throughout progressive LBNP. Although progressive LBNP decreased CVP under both thermal conditions, during cooling CVP at each stage of LBNP was significantly greater relative to normothermia. Moreover, at higher levels of LBNP with skin cooling, stroke volume was significantly greater relative to normothermic conditions. These data indicate that skin surface cooling induced an upward shift in CVP throughout LBNP, which may be a key factor for preserving pre-load, stroke volume, blood pressure, and improving orthostatic tolerance.
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