Increased myocardial perfusion and sympathoadrenal activation during mild core hypothermia in awake humans

Potential mechanisms of cold-induced myocardial ischaemia are sympathetically mediated coronary vasoconstriction and/or catecholamine-induced increases in cardiac work. To examine these parameters, 11 human volunteers were each studied on one day with, and on another day without, beta-adrenoceptor blockade. On each day, warm (37degreesC) saline (control) and cold (4degreesC) saline (hypothermia) were given intravenously. Myocardial perfusion was assessed by positron emission tomography using (H2O)-O-15, and coronary vascular resistance was calculated. Plasma catecholamines were measured to assess sympathoadrenal activation. The core temperature decreased by 1.0+/-0.2degreesC with the cold saline, and was unchanged with warm saline. Myocardial perfusion increased by 20 % (P=0.01) and the rate-pressure product by 33 % (P=0.0004) with cold saline compared with warm saline. beta-Blockade eliminated these increases. Coronary vascular resistance was similar with warm and cold saline, and was unaffected by beta-blockade. Plasma adrenaline increased by 120 % and noradrenaline by 25 1 % during cold saline, but were unchanged during warm saline. In conclusion, core hypothermia triggers beta-adrenoceptor-mediated increased cardiac work, sympathoadrenal activation and increased myocardial perfusion. There is no evidence for hypothermia-induced coronary vasoconstriction.