The objectives of this study were to develop a reproducible behavioral model that simulates the anger state and to characterize its influence on myocardial blood flow in both the normal and compromised coronary circulations. Fourteen mongrel dogs of both sexes were studied. The animals were instrumented for the recording of electrocardiogram, arterial blood pressure, and left circumflex coronary arterial blood flow. A critical level of coronary stenosis was achieved with an adjustable occluder

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... laced just distal to the flow probe. Anger was induced in the instrumented animals by having another dog challenge their access to food. In the absence of coronary artery stenosis, provocation of anger increased heart rate from 107 + 6 to 215 + 15 beats/min, arterial blood pressure from 95 + 4 to 142 + 5 mm Hg, and coronary blood flow from 31 + 5 to 72 + 9 ml/min. These variables returned to the preanger levels within 2 to 4 min. Induction of anger was repeated after a critical stenosis was applied to the left circumflex coronary artery. Anger increased heart rate from 1 12 + 6 to 210 ± 16 beats/min, arterial blood pressure from 99 ± 3 to 142 ± 6 mm Hg, and coronary arterial flow from 23 ± 5 to 35 + 7 ml/min. Within 2 to 4 min after the bout of anger, all dogs exhibited significant reductions in coronary arterial flow (35% of baseline; p < .001), increases in coronary vascular resistance (557% of baseline; p < .002), and ischemic ST segment changes in leads II, III, and aVF. On the basis of these results and our preliminary findings that the delayed ischemia can be induced by stellate ganglion stimulation, we conclude that the poststress period is associated with a marked propensity for coronary vasoconstriction and that the sympathetic nervous system is implicated.