The hemodynamic, electrocardiographic, and coronary flow responses to a psychological test were studied in 13 pigs both in the absence (group 1, n = 8) and the presence (group 2, n = 5) of a transient occlusion of the left anterior descending coronary artery. The psychological test consisted of presenting food to a fasting but restrained animal for 3 minutes. In group 1, stress increased the heart rate from 128 +/- 5 to 176 +/- 8 beats/min (mean +/- SEM) and arterial pressure from 93 +/- 4 to 112 mm Hg. Comparing the individual increase in rate-pressure product with the increase in coronary conductance during the test, a parallel response was found in only two animals, whereas a relatively lower coronary conductance was observed in the remainder, suggesting vasoconstriction. Clinical signs of ischemia or life-threatening arrhythmias were never observed in this group of animals. Each group 2 animal underwent two occlusions of the left anterior descending coronary artery, randomly performed on separate days both in the presence and the absence of the food deprivation stress. When the latter was applied in the presence of occlusion, all animals developed ventricular fibrillation in less than 2 minutes (mean, 81.4 seconds). Conversely, only one animal had ventricular fibrillation when a 3-minute occlusion was performed without exposure to stress. This occurred despite the fact that more severe ischemia (as detected by an increase in left ventricular end-diastolic pressure and decreases in dP/dt and systolic pressure) was recorded at 3 minutes of occlusion. Therefore, 1) psychological stress did not provoke ischemia or arrhythmias in a normal heart, although a coronary vasoconstrictive effect could be detected; 2) transient coronary occlusion did not cause life-threatening ventricular arrhythmias, despite marked ischemia; and 3) in the presence of a transient occlusion, a psychological stress reduced the ventricular fibrillation latency.

Coronary flow and mental stress. Experimental findings.

1991

Abstract

The hemodynamic, electrocardiographic, and coronary flow responses to a psychological test were studied in 13 pigs both in the absence (group 1, n = 8) and the presence (group 2, n = 5) of a transient occlusion of the left anterior descending coronary artery. The psychological test consisted of presenting food to a fasting but restrained animal for 3 minutes. In group 1, stress increased the heart rate from 128 +/- 5 to 176 +/- 8 beats/min (mean +/- SEM) and arterial pressure from 93 +/- 4 to 112 mm Hg. Comparing the individual increase in rate-pressure product with the increase in coronary conductance during the test, a parallel response was found in only two animals, whereas a relatively lower coronary conductance was observed in the remainder, suggesting vasoconstriction. Clinical signs of ischemia or life-threatening arrhythmias were never observed in this group of animals. Each group 2 animal underwent two occlusions of the left anterior descending coronary artery, randomly performed on separate days both in the presence and the absence of the food deprivation stress. When the latter was applied in the presence of occlusion, all animals developed ventricular fibrillation in less than 2 minutes (mean, 81.4 seconds). Conversely, only one animal had ventricular fibrillation when a 3-minute occlusion was performed without exposure to stress. This occurred despite the fact that more severe ischemia (as detected by an increase in left ventricular end-diastolic pressure and decreases in dP/dt and systolic pressure) was recorded at 3 minutes of occlusion. Therefore, 1) psychological stress did not provoke ischemia or arrhythmias in a normal heart, although a coronary vasoconstrictive effect could be detected; 2) transient coronary occlusion did not cause life-threatening ventricular arrhythmias, despite marked ischemia; and 3) in the presence of a transient occlusion, a psychological stress reduced the ventricular fibrillation latency.
1991
Istituto di Fisiologia Clinica - IFC
STRESS TESTING
CORONARY OCCLUSION
ARRHYTHMIAS
NERVOUS SYSTEM. CENTRAL
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/20.500.14243/198378
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