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, β-adrenoceptor blockade. On each day, warm (37 °C) saline (control) and cold (4 °C) saline (hypothermia) were given intravenously. Myocardial perfusion was assessed by positron emission tomography using H215O, and coronary vascular resistance was calculated. Plasma catecholamines were measured to assess sympathoadrenal activation. The core temperature decreased by 1.0 ± 0.2 °C 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. β-Blockade eliminated these increases. Coronary vascular resistance was similar with warm and cold saline, and was unaffected by β-blockade. Plasma adrenaline increased by 120% and noradrenaline by 251% during cold saline, but were unchanged during warm saline. In conclusion, core hypothermia triggers β-adrenoceptor-mediated increased cardiac work, sympathoadrenal activation and increased myocardial perfusion. There is no evidence for hypothermia-induced coronary vasoconstriction.

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