• W A Tweed, J Cote, J G Wade, G Gregory, and A Mills.
• Pediatr. Res. 1982 Feb 1; 16 (2): 137-40.

AbstractThe asphyxiated newborn is particularly vulnerable to hypotension, which contributes to hypoxic brain damage by reducing cerebral perfusion. During asphyxia, cerebral blood flow (CBF)( is pressure passive, that is, CBF autoregulation is abolished. It is important to know if the nonasphyxiated fetus and newborn are similarly vulnerable to hypotension. In the present study, we have measured acute responses of organ blood flow to a hypovolemic/hypotensive stress in the normoxic near term sheep fetus. Changes in brain flow were compared to changes in other organs. Eight chronically prepared fetal lambs were studied. Organ blood flows were measured by the microsphere technique during a control period, after a 20% blood volume reduction, and again after reinfusion of that volume. Hypovolemia was accompanied by a 21% decrease in blood pressure and a 4 torr increase in PCO2; after reinfusion blood pressure increased 16% above control. Control measurements of organ perfusion were similar to those reported by other investigators. Cardiac output and flow to all organs, with the exception of the brain, were reduced 30-56% during hypovolemia. Brain blood flow was insignificantly reduced by 9%. If a correction is applied for the increase in PCO2, CBF corrected to control PCO2 would have have been significantly reduced by 18%. After reinfusion, flow to all organs increased to near control levels. We conclude that the normoxic fetal lamb shows evidence of CBF autoregulation, and is able to preserve relative constancy of CBF within a blood pressure range of +/- 20% of normal. However, the evidence presented in this study suggests that autoregulation may be less effective in response to a hypotensive stress, even though CBF is better preserved than flow to most other organs.

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