Abstract
Experiment (I)
If the bulbus arteriosus of the frog is ligated, the heart gradually dilates. In about ten minutes the heart has more than doubled its size. (Fig. 1.) The heart muscle appears more cyanotic. If at the same time the peripheral circulation in the frog's web is observed microscopically, it is seen that the blood keeps moving in the capillaries for 5-10 minutes after aortic ligature. While corpuscular flow is slower, it simulates the normal as far as direction is concerned, going from the arteries to capillaries, then to the veins.
Thus the enlargement of the heart after aortic ligation is associated with the movement of blood from the large arteries to the capillaries, and from these back to the heart. It appears as though co-ordinated contractions of the vessels themselves were capable of circulating the blood along its usual course. This vascular mechanism comes into play when the cardiac output is prevented by ligation of the aorta.
If now the vessels of a second frog are injured quite another reaction takes place following the ligation of the aorta. In order to produce a profound vascular injury, the spinal cord of the animal was destroyed by pithing. This, as is known, has a tremendous
“shock effect.” One of the evidences of this is the cessation of spontaneous arterial contractions in the frog 1 , 2 To further damage the vessels chloroform was applied to the skin of the animal. This caused a marked dilatation of the capillaries, but the corpuscular velocity before aortic ligation did not differ materially from the normal. Now the aorta was ligated. Alniost at once thy bood-flow in the capillaries stopped, the corpuscles became stagnant. There was now no sign of cardiac enlargement, when the functional integrity of the vessels was impaired (Fig. 2). Hence in the animal with damaged Yessels there was neither a peripheral circulation nor an enlargement of the heart after the aorta was clamped. These two effects must therefore be ascribed to the proper functioning of the vessels.
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