β-Adrenergic blockade enhances coronary vasoconstrictor response to forehead cooling

Forehead cooling activates the sympathetic nervous system and can trigger angina pectoris in susceptible individuals. However, the effect of forehead cooling on coronary blood flow velocity (CBV) is not well understood. In this human experiment, we tested the hypotheses that forehead cooling reduces...

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Published inAmerican journal of physiology. Heart and circulatory physiology Vol. 306; no. 6; pp. H910 - H917
Main Authors Muller, Matthew D., Gao, Zhaohui, Patel, Hardikkumar M., Heffernan, Matthew J., Leuenberger, Urs A., Sinoway, Lawrence I.
Format Journal Article
LanguageEnglish
Published United States American Physiological Society 01.03.2014
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ISSN0363-6135
1522-1539
1522-1539
DOI10.1152/ajpheart.00787.2013

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Summary:Forehead cooling activates the sympathetic nervous system and can trigger angina pectoris in susceptible individuals. However, the effect of forehead cooling on coronary blood flow velocity (CBV) is not well understood. In this human experiment, we tested the hypotheses that forehead cooling reduces CBV (i.e., coronary vasoconstriction) and that this vasoconstrictor effect would be enhanced under systemic β-adrenergic blockade. A total of 30 healthy subjects (age range, 23–79 years) underwent Doppler echocardiography evaluation of CBV in response to 60 s of forehead cooling (1°C ice bag on forehead). A subset of subjects (n = 10) also underwent the procedures after an intravenous infusion of propranolol. Rate pressure product (RPP) was used as an index of myocardial oxygen demand. Consistent with our first hypothesis, forehead cooling reduced CBV from 19.5 ± 0.7 to 17.5 ± 0.8 cm/s ( P < 0.001), whereas mean arterial pressure increased by 11 ± 2 mmHg (P < 0.001). Consistent with our second hypothesis, forehead cooling reduced CBV under propranolol despite a significant rise in RPP. The current studies indicate that forehead cooling elicits a sympathetically mediated pressor response and a reduction in CBV, and this effect is augmented under β-blockade. The results are consistent with sympathetic activation of β-receptor coronary vasodilation in humans, as has been demonstrated in animals.
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ISSN:0363-6135
1522-1539
1522-1539
DOI:10.1152/ajpheart.00787.2013