Abstract
Multiple synchronous recordings of heart contractile force with strain gauge arches in open-chest dogs have demonstrated that the contractile force measured from any given area of the heart is representative of the contractile activity of the entire syncytium. Control levels of contractile force as well as contractile force responses to heart stimulant drugs were roughly parallel for all areas of the ventricles. Electrically produced increases in heart rate from control levels (65-90/min.) to 210/min. in chronically sympathectomized dogs were associated with only minimal (10%) increases in contractile force; with rates of 210/min. and over contractile force was decreased an avg. of 12%. The increases in heart force associated with increased heart rate were shown to be small as compared with the increase in heart force produced by a moderate dose of l-arterenol. Stimulation of the right accelerator nerve was associated with marked increases in heart force and heart rate but only small increases in diastolic pressure. Progressively increasing the initial length of the muscle segment between the 2 points of attachment of the strain gauge arch to 30% above control resulted in increments in contractile force of up to 145% above control; increasing initial length beyond 30% up to 75% beyond control did not change contractile force. Rapid infusion of 20 cc./kg. of warmed Ringer-Locke soln. produced an increase in heart force of about 15% with an estimated increase in heart size of about 10%; occlusion of the thoracic aorta in sufficient degree to raise the diastolic pressure 60 mm. Hg produced an increase in heart force of about 20%.