Anemic hypoxia in moderate intracerebral hemorrhage: the alterations of cerebral hemodynamics and brain metabolism.
To determine the influence of anemic hypoxia on cerebral hemodynamics and brain metabolism during pathological conditions of the brain, moderate-sized intracerebral hemorrhage (ICH) was created in canines with and without preoperatively inducing chronic anemia. The changes in cerebral perfusion pressure (CPP) and cerebral blood flow velocities (CBFv) were evaluated as well as the determinations for cerebral extraction fraction of oxygen (CEO2), arteriovenous oxygen content difference (AVDO2) and lactate (Lac) concentrations through the arterial and superior sagittal sinus (SSS) samples. Before ICH production, anemic animals (n = 8) showed a significant reduction in cerebral AVDO2 and arteriovenous Lac difference (AVDLac) but had higher CBFv as well as CEO2 than did nonanemic animals (n = 8). The CBFv began to decrease within 30 min after ICH in anemic but not in nonanemic animals, and the difference between the two groups was found to be significant at 2 h (P<0.05). Following ICH, anemic group also showed coupling reductions in CEO2 and AVDO2, indicating a decreased cerebral metabolic rate for oxygen (CMRO2) relative to the baseline data, compared with a constant CMRO2 in nonanemic group in which the CEO2, AVDO2, and CBFv remained relatively normal. Moreover, compared to the baseline data, a significant increase of the AVDLac was found in anemic but not in nonanemic group, although the former had lower Lac concentrations of the SSS than did the latter group throughout the whole observation period. We conclude that, in cases with chronically reduced Hct, cerebral hemodynamics and oxygenation remain in favorable conditions, thus decreasing Lac production of the brain. The findings suggest a lowered metabolic demand of the brain tissue due to reduced cerebral O2-carrying capacity. During the early phase of moderate ICH, the regulation capacity in cerebral hemodynamics and brain oxygenation tend to deteriorate in profound anemic hypoxia, which consequently leads to enhancing at least modest anaerobic glycolysis.
Lee
E J
EJ
Department of Surgery, National Cheng Kung University Medical Center and Medical School, Tainan, Taiwan. ejian@mail.ncku.edu.tw
Hung
Y C
YC
Lee
M Y
MY
D000740:Anemia / Q000150:complications* / Q000378:metabolism / Q000503:physiopathology; D000818:Animals; D001158:Arteries; D001783:Blood Flow Velocity / Q000502:physiology; D001794:Blood Pressure / Q000502:physiology; D001921:Brain / Q000378:metabolism*; D002543:Cerebral Hemorrhage / Q000150:complications* / Q000378:metabolism / Q000503:physiopathology*; D002560:Cerebrovascular Circulation / Q000502:physiology*; D004285:Dogs; D005260:Female; D006439:Hemodynamics / Q000502:physiology; D000860:Hypoxia / Q000150:complications* / Q000378:metabolism / Q000503:physiopathology; D019344:Lactic Acid / Q000097:blood; D008297:Male; D010100:Oxygen / Q000097:blood; D010101:Oxygen Consumption / Q000502:physiology; D014680:Veins
D019344:Lactic Acid; D010100:Oxygen