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Am J Physiol Heart Circ Physiol 289: H2429-H2433, 2005. First published July 15, 2005; doi:10.1152/ajpheart.00383.2005
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Effect of skin surface cooling on central venous pressure during orthostatic challenge

Jian Cui,1 Sylvain Durand,1 Benjamin D. Levine,1,2 and Craig G. Crandall1,2

1Institute for Exercise and Environmental Medicine, Presbyterian Hospital of Dallas and 2Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas

Submitted 19 April 2005 ; accepted in final form 13 July 2005

Orthostatic stress leads to a reduction in central venous pressure (CVP), which is an index of cardiac preload. 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, and skin blood flow, as well as skin and sublingual temperatures, were recorded in nine 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/stage. Before LBNP, skin surface cooling lowered mean skin temperature, increased CVP, and 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 preload, stroke volume, and blood pressure and improving orthostatic tolerance.

thermoregulation; cardiovascular regulation; orthostatic tolerance; lower body negative pressure



Address for reprint requests and other correspondence: C. G. Crandall, Inst. for Exercise and Environmental Medicine, Presbyterian Hospital of Dallas, 7232 Greenville Ave., Dallas, TX 75231 (e-mail: craig.crandall{at}utsouthwestern.edu)




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