Key result
Local heating-induced nitric oxide production did not attenuate cutaneous vasoconstrictor responsiveness during lower body negative pressure, whereas elevated local temperature itself did (P<0.05).
Why the study?
Does local heating-induced nitric oxide production attenuate cutaneous vasoconstrictor responsiveness to lower body negative pressure in human skin?
Does local heating-induced nitric oxide production attenuate cutaneous vasoconstrictor responsiveness to lower body negative pressure in human skin?
Absolute Event Rate: 7.9% vs 11.4%
p-value: p=>0.05
Local heating-induced nitric oxide production does not attenuate cutaneous vasoconstrictor responsiveness during high levels of lower body negative pressure, though elevated local temperature itself attenuates responsiveness via non-NO mechanisms.
Elevated local temperature attenuates cutaneous vasoconstriction independently of NO during LBNP; leaves open non-NO mechanisms in thermoregulatory-orthostatic interactions.
We tested the hypothesis that local heating-induced nitric oxide (NO) production attenuates cutaneous vasoconstrictor responsiveness. Eleven subjects (6 men, 5 women) had four microdialysis membranes placed in forearm skin. Two membranes were perfused with 10 mM of N(G)-nitro-L-arginine (L-NAME) and two with Ringer solution (control), and all sites were locally heated to 34 degrees C. Subjects then underwent 5 min of 60-mmHg lower body negative pressure (LBNP). Two sites (a control and an L-NAME site) were then heated to 39 degrees C, while the other two sites were heated to 42 degrees C. At the L-NAME sites, skin blood flow was elevated using 0.75-2 mg/ml of adenosine in the perfusate solution (Adn + L-NAME) to a similar level relative to control sites. Subjects then underwent another 5 min of 60-mmHg LBNP. At 34 degrees C, cutaneous vascular conductance (CVC) decreased (Delta) similarly at both control and L-NAME sites during LBNP (Delta7.9 +/- 3.0 and Delta3.4 +/- 0.8% maximum, respectively; P > 0.05). The reduction in CVC to LBNP was also similar between control and Adn + L-NAME sites at 39 degrees C (control Delta11.4 +/- 2.5 vs. Adn + L-NAME Delta7.9 +/- 2.0% maximum; P > 0.05) and 42 degrees C (control Delta1.9 +/- 2.7 vs. Adn + L-NAME Delta 4.2 +/- 2.7% maximum; P > 0.05). However, the decrease in CVC at 42 degrees C, regardless of site, was smaller than at 39 degrees C (P < 0.05). These results do not support the hypothesis that local heating-induced NO production attenuates cutaneous vasoconstrictor responsiveness during high levels of LBNP. However, elevated local temperature, per se, attenuates cutaneous vasoconstrictor responsiveness to LBNP, presumably through non-nitric oxide mechanisms.
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Low et al. (2007) studied this question. N(G)-nitro-L-arginine (L-NAME) and local heating vs. Ringer solution (control) was evaluated on Reduction in cutaneous vascular conductance (CVC) to lower body negative pressure at 39 degrees C (p=>0.05). Local heating-induced nitric oxide production did not attenuate cutaneous vasoconstrictor responsiveness during lower body negative pressure, whereas elevated local temperature itself did (P<0.05).
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