Abstract
Systemic hypotension in adults results in hypoxic-ischemic injury to the brain, which may be exacerbated by the post-ischemic pattern of cerebral reperfusion. Therefore, we studied cerebral O2 delivery (OD), uptake (CMRO2), and extraction (OE) following nemorrhagic, transient global ischemia in 12 ventilated newborn piglets. We measured cerebral blood flow (CBF) and cardiac output (CO) with microspheres and arteriovenous differences of O2 content and blood gases during control (C), after 15 min of ischemia, and 10 and 90 min after rapid reperfusion (R) with whole blood. Perfusion pressure (mmHg) fell from 81±2 (X̄±SE) to 31±2* during ischemia, and was 80±3 and 77±2 after R. Hemodynamic and metabolic data are:
Percent of CO to the brain was similar during C and R. A fall in OE during R-10 min led to cerebral venous hyperoxia, whereas a lower O2 content at R-90 min led to decreased OD. We conclude that after brain ischemia: 1) R-10 min results in cerebral hyperemia, OD comparable to C but a reduced CMRO2, and 2) although both OD and CMRO2 are reduced at R-90 min, OE is similar to C, demonstrating reestablishment of a match between OD and CMRO2.
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Laptook, A., Porter, A. & Peterson, J. PATTERN OF CEREBRAL REPERFUSION FOLLOWING BRAIN ISCHEMIA. Pediatr Res 18 (Suppl 4), 378 (1984). https://doi.org/10.1203/00006450-198404001-01712
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DOI: https://doi.org/10.1203/00006450-198404001-01712