The purpose of this study was to determine how the myocardium can compensate (change O2 supply/consumption parameters) regionally during acute hemorrhagic hypotension. Twenty-one open chest, anesthetized rabbits were subjected to one of three treatments: (1) control (nonhemorrhaged), (2) hemorrhage to 70 mm Hg, (3) hemorrhage to 50 mm Hg. Myocardial blood flows were determined by using radioactive microspheres before and during hemorrhage. At the end of the experiment the hearts were removed and stored in liquid N2 and analyzed for subepicardial and subendocardial arterial and venous O2 saturation by using microspectrophotometry, and from this, O2 consumption was determined. During hemorrhage, blood pressures were significantly depressed for all groups compared to the control group. Myocardial blood flow was depressed 20% in the 70 mm Hg group and coronary resistance fell 15% compared to control. In the 50 mm Hg group, flow was reduced 38% and resistance decreased 31% compared to the 70 mm Hg group. No regional (subepicardial-subendocardial) differences in flow or resistance occurred during hypotension. These decreases in resistance were observed despite a 32% drop in O2 consumption in the 70 mm Hg group and 44% in the 50 mm Hg group compared to the control. O2 extraction remained unchanged for all groups as did the O2 supply/consumption balance. Thus, despite decreases in O2 consumption during acute hemorrhage, rabbit hearts decreased coronary resistance so as to maintain the O2 regional supply/consumption balance constant. Since O2 extraction did not change, these hearts were not ischemic, even in the subendocardium.
|Original language||English (US)|
|Number of pages||10|
|State||Published - 1987|
All Science Journal Classification (ASJC) codes
- Cardiology and Cardiovascular Medicine