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Coronary blood flow during cold air breathing: mechanistic insights using pharmacological blockade

Recent work from our laboratory has demonstrated that cold air inhalation (CAI) impairs coronary blood flow velocity (CBV) in healthy humans. The first objective of this study was to determine if blockade of oropharyngeal afferents would improve coronary perfusion during CAI. The second objective was to determine if systemic beta‐adrenergic blockade would improve coronary perfusion during CAI. In study 1, ten subjects received upper airway anesthesia with lidocaine then underwent CAI (−15 to − 30°C) for 5 minutes. In study 2, eight subjects received intravenous propranolol prior to CAI. Control experiments were performed on separate days. HR, MAP, and CBV (from Doppler echocardiography) were obtained. Rate pressure product (RPP) was used as an index of myocardial O2 demand and CBV was an index of myocardial O2 supply; changes (Δ) from baseline were calculated. In study 1, lidocaine blocked the gag reflex but did not affect ΔRPP (428 ± 159 vs 496 ± 339) or ΔCBV (0.8 ± 1.2 vs 0.9 ± 0.9 cm/sec) to CAI compared to control. In study 2, intravenous propranolol lowered resting HR and completely blocked the HR increase to isoproterenol. Further, propranolol lowered O2 demand in response to CAI (ΔRPP=169 ± 285 vs 1106 ± 360) compared to control. These data indicate that the detrimental effects of CAI on the coronary circulation are due in part to activation of beta‐adrenergic receptors. Supported by NIH P01 HL096570 and UL1 TR000127.