Regional cerebral blood flow and oxygen consumption of the canine brain during hemorrhagic hypotension.
The sequential changes in systemic and cerebral hemodynamics, systemic and cerebral oxygen transport and consumption rates, and the regional blood flows (measured with 15 micron microspheres) to the cortical and subcortical brain tissues were determined in nine dogs subjected to graded hemorrhage (10 ml/kg X 4 at 15 min intervals). As hemorrhage progressed, both mean arterial pressure and cardiac output decreased progressively. In contrast to the systemic circulation, the mean cerebral blood flow (mCBF) was well maintained by cerebral vasodilation and the cerebral O2 consumption rate (CMRO2) increased during the first three stages of hemorrhage. At 40 ml/kg of hemorrhage, there were significant reduction in mCBF and CMRO2 despite the increase in O2 extraction, suggesting the occurrence of cerebral hypoxia and decompensation of the cerebral circulation. There were remarkable regional variations in the responses of regional cerebral blood flows (rCBF) to hypovolemia, resulting in a significant redistribution of cerebral blood flow. The fractions of cardiac output supplying the diencephalon (thalamus and hypothalamus), the brain stem (pons and medulla oblongata) and the cervical spinal cord increased after hemorrhage up to 40 ml/kg. The redistribution of rCBF favors those areas where neurons related to cardiovascular control are located. These findings have significant implications relating to hemodynamic regulation during hemorrhagic hypotension.
D000818:Animals; D001809:Blood Viscosity; D001921:Brain / Q000378:metabolism*; D002560:Cerebrovascular Circulation; D004285:Dogs; D007022:Hypotension / Q000209:etiology / Q000378:metabolism* / Q000503:physiopathology; D010101:Oxygen Consumption; D012212:Rheology; D012771:Shock, Hemorrhagic / Q000150:complications / Q000378:metabolism* / Q000503:physiopathology; D014655:Vascular Resistance