Abstract
Cardiac performance was studied in the cat during and after a mimicked shock situation in the small intestine (regional hypotension at 35 mm Hg during nervous vasoconstrictor fibre activation). Aortic blood flow was measured with an electromagnetic flow probe around the ascending aorta and, in some experiments, maximal dP/dt of the left ventricle was also followed. Upon restoration of intestinal perfusion pressure after a 2 h “shock” period a rapid reduction of aortic flow occurred due to a decreased stroke volume. Concomitantly maximal dP/dt was reduced in the face of an unchanged central venous pressure and left end diastolic pressure. This decline of cardiac performance could be prevented by substituting, during the first posthypotensive min, the intestinal venous blood with fresh blood from a healthy donor animal. However, when the shed intestinal venous blood was retransfused, a rapid decline of cardiac performance was evident. The reduced cardiac function was accompanied by an unchanged or slightly elevated total peripheral resistance. It is proposed that substances released front the “shocked” intestine cause a rapid and pronounced depression of cardiac function.