Manabu Rokutanda

Effects of intracoronary injection of acetylcholine on coronary arterial diameter

The effects of intracoronary injection of acetylcholine on coronary arterial diameter was examined by coronary arteriography in 30 adult patients (13 men, 17 women), aged 23 to 67 years (mean 51), with normal or almost normal coronary arteriographic findings. Patients with angina pectoris, myocardial infarction and other severe cardiac diseases were excluded. Two minutes after injection of 30 to 100 micrograms of acetylcholine into the left coronary artery, significant diffuse narrowing (more than 25% reduction in diameter) of the left main trunk, the proximal, mid- and distal left anterior descending artery, and the proximal, mid- and distal left circumflex artery occurred in 1 (4%), 5 (20%), 3 (12%), 9 (36%), 6 (24%), 8 (32%) and 3 (12%) of 25 patients, respectively. After injection of 30 to 50 micrograms of acetylcholine into the right coronary artery, significant diffuse narrowing of the proximal, mid- and distal right coronary artery occurred in 5 (25%), 7 (35%) and 10 (50%) of 20 patients, respectively. However, significant diffuse dilatation (more than 25% increment in diameter) appeared in the left main trunk, left anterior descending, left circumflex and right coronary arteries in a few patients. These results indicate that acetylcholine induces coronary vasoconstriction in a significant number and coronary vasodilatation in a small number of adult humans, and that response of the coronary artery to acetylcholine varies along the course of the coronary artery.

Effects of magnesium on the tone of isolated human coronary arteries. Comparison with diltiazem and nitroglycerin.

To study the effects of magnesium (Mg2+) on human coronary arteries and to compare those effects with those of diltiazem and nitroglycerin, we measured the tension of ring segments from isolated human coronary arteries obtained at autopsy within 5 hours after death. Precontracted segments with 3 x 10(-6) M prostaglandin F2 alpha were studied after adding cumulative concentrations of these agents (1.0-8.0 mM, 10(-9)-10(-5) M, and 10(-10)-10(-6) M, respectively). Mg2+ significantly inhibited the tonic contraction compared with the time-matched controls at 1.0 and 2.0 mM (48.7 +/- 5.6% vs. 88.6 +/- 2.2%, p less than 0.01, 36.2 +/- 6.1% vs. 78.9 +/- 3.0%, p less than 0.01, respectively). 1.0 and 2.0 mM Mg2+ did not suppress, but actually increased, the amplitude of periodic contraction, but 8.0 mM Mg2+ reduced the amplitude compared with the controls (6.6 +/- 5.2% vs. 73.3 +/- 10.7%, p less than 0.01). Diltiazem at a concentration of 10(-5) M moderately inhibited the tonic contraction, and reduced the amplitude of periodic contraction almost completely. Nitroglycerin reduced the tonic contraction almost completely at a concentration of 10(-6) M but did not reduce the amplitude of periodic contraction at any concentration. We conclude that 1.0 and 2.0 mM Mg2+ inhibits the tonic contraction and that 8.0 mM Mg2+ inhibits the periodic as well as the tonic contraction of isolated human coronary arteries. Diltiazem inhibits the periodic contraction, whereas nitroglycerin suppresses tonic contraction without affecting the periodic contraction.

Blocking effect of verapamil on conduction over a catecholamine-sensitive bypass tract in exercise-induced Wolff-Parkinson-White syndrome

By intravenous administration of isoproterenol, 0.5 micrograms/min, a catecholamine-sensitive bypass tract was confirmed in two patients with exercise-induced Wolff-Parkinson-White syndrome. In a 24 year old woman, an intravenous bolus injection of 5 mg of verapamil suddenly blocked conduction over a catecholamine-sensitive bypass tract. In a 62 year old man, the exercise-induced Wolff-Parkinson-White syndrome disappeared after 3 days of oral administration of verapamil (120 mg/day). These observations suggest that a slow inward calcium current plays an important role in conduction over a catecholamine-sensitive bypass tract in exercise-induced Wolff-Parkinson-White syndrome.