Abstract
Cerebral microvascular volume loads due to acute increases in arterial transmural pressure (ATMP) are implicated in the genesis of IVH. Previously, we have shown that such volume and pressure loads occur during the hyperemia accompanying acute recovery from asphyxia (AS) in newborn dogs, and that sagittal sinus pressure (SSP) reflects intracranial pressure at all times (CLIN. RES: 31:791, 1983).
We studied AS and volume depletion-repletion (V) in paralyzed anesthetized ventilated NBs<36hrs. AS involved temporary cessation of ventilation (7-10 min); V involved reducing MAP by 40% for 5 minutes, then rapid repletion. Mean arterial pressure (MAP) and SSP were measured, and ATMP calculated as MAP-SSP at I: baseline, II: end asphyxia (AS) or end hypotension (V), and III: peak recovery. The II-III time interval was <30 secs in AS and V. Changes in cerebral vascular volume were inferred from changes in SSP via the cranial compliance. Histopathology was done. All results as mean ± SE.
CONCLUSION: Acute volume loads due to increases in ATMP may not be the cause of IVH.
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McPhee, A., Kotagal, U. & Decourten-Myers, G. 1458 FAILURE OF ACUTE CEREBROVASCULAR STRESSES TO PRODUCE INTRAVENTRICULAR HEMORRHAGE (IVH) IN THE NEWBORN BEAGLE (NB) MODEL. Pediatr Res 19, 353 (1985). https://doi.org/10.1203/00006450-198504000-01482
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DOI: https://doi.org/10.1203/00006450-198504000-01482