Nice and I had argued that the higher contractions of fatigued muscle, that follow stimulation or injection of adrenin, could not be wholly due to improved blood flow through the muscle, for when by traction on the aorta or compression of the thorax arterial pressure in the hind legs was prevented from rising, splanchnic stimulation still caused a distinct improvement, the initial appearance of which coincided with the point in the blood-pressure curve at which evidence of adrenal secretion appeared. And, furthermore, the improvement was seen also when adrenin was given intravenously in such weak solution (1:100,000) as to produce a _fall_ instead of a rise of arterial pressure. Lyman and I had shown that this fall of pressure was due to a dilator effect of adrenin. Since the blood vessels of the fatigued muscle were dilated by severance of their nerves when the nerve trunk was cut, and, besides, as previously stated (see p. 86), were being stimulated through their nerves at a rate favorable to relaxation, it seemed hardly probable that adrenin could produce its beneficial effect by further dilation of the vessels and by consequent flushing of the muscle with an extra supply of blood.[87] The lowering of blood pressure had been proved to have no other effect than to impair the action of the muscle (see p. 103). Although the chances were thus against an interpretation of the beneficial influence of adrenin through action on the circulation, it was thought desirable to test the possibility by comparing its effect with that of another vasodilator--amyl nitrite. Figs. 21 and 22 are curves obtained from the left _tibialis anticus_ muscle. The rate of stimulation was 240 times a minute. The muscle in Fig. 21 contracted against a spring having an initial tension of 120 grams, and that in Fig. 22 against an initial tension of 100 grams. In Fig. 21, at the point indicated on the base line, 0.4 cubic centimeter of adrenin (1:100,000) was injected into the left external jugular vein. There resulted a fall of 25 millimeters of mercury in the arterial pressure and a concurrent betterment of 15 per cent in the height of contraction, requiring two minutes and fifteen seconds of fatigue (about 540 contractions) before it returned to the former level. In Fig. 22, at the point indicated by the arrow, a solution of amyl nitrite was injected into the right external jugular vein. There resulted a fall of 70 millimeters of mercury in arterial pressure and a betterment of 4.1 per cent in the height of muscular contraction, requiring fifteen seconds of fatigue (about 60 contractions) to decrease the height of contraction to its former level. In neither case did the blood pressure fall below the critical region (see p. 104).[*]