Studies of cerebral blood flow and oxygen metabolism during acute hypoxic hypoxia in fetal sheep have been confined to late gestation, a time when brain development in this species is largely complete. There is no systematic study of cerebral vascular responses to acute hypoxic hypoxia in immature fetal sheep or, indeed, in immature brains of any species. We studied 13 fetal sheep in utero at 93 +/- 1 days gestation (term = 145-150 days), 48 h after intravascular catheters were placed into the superior sagittal sinus, axillary arteries, and inferior vena cava. We measured brain blood flow by the microsphere method. Cerebral oxygen consumption was calculated with the use of blood flow to the cerebral hemispheres (cerebrum, diencephalon, mesencephalon) and arterial and sagittal sinus values for oxygen content. Fractional oxygen extraction was calculated as the ratio between oxygen consumption and oxygen transport. We altered fetal oxygenation by changing the mother's inspired oxygen concentration. As in the near-term fetus, acute hypoxic hypoxia resulted in increased blood flow to cerebral hemispheres, cerebellum, and pons-medulla; furthermore, the increase in blood flow was sufficient to sustain cerebral oxygen consumption. However, in contrast to near-term fetuses, the increase in blood flow to the cerebral hemispheres was not sufficient to maintain convective oxygen transport. Cerebral oxygen consumption was therefore sustained in part by an increase in fractional extraction. Blunted hypoxic vasodilation in immature fetuses might reflect either immature regulatory mechanisms or an inability of cerebral vessels to respond to the usual stimuli. It is also possible that hypoxic vasodilation was blunted by reflex stimulation of the sympathetic nervous system.
Intrinsic performance limits of noncontacting fiber lever displacement measuring systems are quantitatively described. Generalized relationships linking displacement detection limit, frequency response, dynamic range, linearity, and working distance to fiber diameter, illumination irradiance and coupling angle, photodetector characteristics, and reflection and transmission losses were obtained by analysis and confirmed by measurement. Both procedures showed performance limits to be functions of the square root of the flux density coupled into the target-illuminating fiber(s) by the electroluminescent source. Displacement detection and bandwidth limits achievable with tungsten or LED sources were in the 2 x 10(-11) to 2 x 10(-12) [equation] and MHz, range respectively. A basis for optimizing levers for different applications and determination of intrinsic performance limits is provided.
Studies of cerebral blood flow (CBF) and metabolism in fetal sheep have been largely confined to late gestation, a time when brain development in this species is largely complete. Few studies have been done at a time when the fetal sheep brain is in the midst of rapid differentiation and development. We studied seven fetal sheep in utero at 91 days of gestation (term = 145-150 days) 24 h after catheters were placed into the sagittal sinus, axillary artery, and inferior vena cava. We measured CBF by the microsphere method and used arteriovenous differences of O2, lactate, and glucose to calculate cerebral O2 consumption (CMRo2), fractional O2 extraction, glucose consumption, O2-glucose index (OGI), and cerebral lactate production. Compared with near-term fetal sheep, we found lower CBF (33.9 +/- 5.3 ml.100 g-1.min-1), lower glucose consumption (8.5 +/- 1.25 mumol.100 g-1.min-1), and lower CMRo2 (41.8 +/- 8.8 mumol.100 g-1.min-1). Fractional O2 extraction was 0.29 +/- 0.04, which is similar to near-term fetal sheep. There was consistent cerebral lactate production (2.45 +/- 1.58 mumol.100 g-1.min-1). The OGI was 81 +/- 16%, i.e., oxidative metabolism could account for 81% of glucose uptake. Lactate production accounts for virtually all glucose uptake exceeding that required for oxidation.
Significant variability exists in the retinal appearance of the NCLs, but, in general, ophthalmoscopy and fluorescein angiography distinguish these patients from other more common blinding disorders of childhood such as retinitis pigmentosa and Stargardt disease. Examining retinas of parents of affected children does not aid in the diagnosis of NCL.
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