Abstract
Changes in blood concentration of bradykinin (BK) and kininogen (KGN) during an anginal attack induced by means of supine bicycle ergometer or right atrial pacing were studied in 20 patients with angina pectoris of effort. BK levels were 6.6 0.6ng/ml in the coronary sinus (CS), 3.5 0.4 ng/ml in the left ventricle (LV) and 4.1 0.4 ng/ml in the cubital vein (CV) whenthe anginal pain appeared withischemic ST depression (stage 3). The levels were signifi. cantly higher than those before the induction of the anginal attack. On the other hand, there were no significant changes in blood BK levels when ischemic ST depression appeared without the chest pains (stage 2), nor at the time when there was neither ST change nor the pain (stage 1). KGN levels were 4.6 0.5μg/ml in CS, 5.6 0.6 μg/ml in LV and 5.0 0.6 μg/ml in CV at the stage 3. The levels were significantly lower than those before the induction of the anginal attack. No significant changes were observed in KGN at the stages 1 and 2. At the stage 3, concentration of BK was significantly higher and KGN was significantly lower in CS than in LV and CV. It was proved that there was significant negative correlation between the changes of BK and KGN in any of CS, LV and CV at all the stages. At the stage 3, kininase activity in CS and LV decreased whereas that in BK increased.
Myocardial lactate extraction ratio was negative in most of the patients at the stages 2 and 3. The difference between BK levels in LV and CS was measured. A significant positive correlation was observed between the difference and myocardial lactate extraction ratio at all the stages. The decrease in kininase activity was accompanied by an increase of lactate in CS. Prostaglandin E increased in CS only at the stage 3.
In 13 patients with acute myocardial infarction, the concentration of BK, when the chest pains were felt, was 40.6 ng/ml in the pulmonary artery (PA), 3.4 0.5ng/ml in the femoral artery (FA) and 3.4 0.7 ng/ml in CV, which were significantly higher than that when the chest pains disappeared. The level of BK was significantly higher in PA than in CV and FA.
These findings suggest that BK, activated from KGN in the ischemic area of myocardium, is responsible for the pain in angina pectoris of effort and acute myocardial infarction.
