A new phosphorescence imaging method (Rumsey et al. Science Wash. DC 241: 1649-1651, 1988) has been used to continuously monitor the PO2 in the blood of the cerebral cortex of newborn pigs. A window was prepared in the skull and the brain superfused with artificial cerebrospinal fluid. The phosphorescent probe for PO2, Pd-meso-tetra(4-carboxyphenyl)porphine, was injected directly into the systemic blood. The phosphorescence of the probe was imaged, and the lifetimes were measured using flash illumination and a gated video camera. The PO2 in the blood of the veins and capillary beds of the cortex was calculated from the lifetimes. Systemic blood pressure was continuously monitored while the systemic arterial PCO2, PO2, and blood pH were measured periodically. The PO2 in the blood was quantitated for 60- to 200 microns2 regions within the image (from a total field of approximately 3 mm diam). The PO2 in the microvasculature was not uniform across the viewing field but increased or decreased in each region independently of the other regions. Thus at any point in time the PO2 in a region could be substantially above or below the average value. During hyperventilation, which lowered arterial PCO2 and increased pH of the blood, the average PO2 decreased in proportion to the decrease in arterial PCO2. For example, hyperventilation, which decreased arterial PCO2 from its normal value of 40 Torr to 10 Torr, caused a rapid (within 5 min) decrease in PO2 in the blood of capillaries and veins to approximately one-third of normal.
The effects of a continuous infusion of tris(hydroxymethyl)-aminomethane (THAM) on pH, base excess, p50, serum osmolality, and plasma drug concentration during respiratory acidosis were studied in newborn piglets. Measurements were made during three experimental periods: (1) control period with normal blood gases; (2) hypercapnia period, and (3) hypercapnia plus THAM period (THAM infusion: 1.65 mmol/kg/h). pH decreased and paCO2 increased between control period (7.40 ± 0.05 and 45 ± 3 mm Hg) and hypercapnia period (7.24 ± 0.06 and 59 ± 2 mm Hg; p < 0.001; mean ± SD). pH returned to baseline (7.37 ± 0.04) during the hypercapnia plus THAM period, while paCO2remained elevated (63 ± 4 mm Hg). p50 increased from 30.7 ± 5.9 to 38.3 ± 4.7 (p < 0.05) during hypercapnia and decreased with hypercapnia plus THAM. THAM concentration and base excess increased with time and were linearly related. Serum osmolality was unchanged during the THAM infusion. We conclude that continuous infusion of THAM is effective in normalizing pH during respiratory acidosis in the piglet.
The effect of hypercapnia on brain cell membrane structure and function was studied in anesthetized newborn piglets. Lipid peroxidation products (conjugated dienes and fluorescent compounds), Na+,K(+)-ATPase activity and enzyme affinity to ATP (substrate), K+ and Na+ ions (activators), and strophanthidin (inhibitor) were measured in three groups of animals: controls, those exposed to 90 minutes of PaCO2 > 80 mmHg (hypercapnia) and those exposed the same way, following restoration of normal PaCO2 (recovery). Enzyme activity was unchanged by hypercapnia, but enzyme affinity was altered as indicated by an increase in ATP affinity. Affinities to Na+, K+, and strophanthidin were unchanged. Restoration of normal PaCO2 resulted in an increase in conjugated dienes. The data demonstrate that hypercapnia followed by restoration of normal PaCO2 in healthy term newborn piglets is associated with mild modification of brain cell membrane Na+,K(+)-ATPase, possibly due to lipid peroxidation.
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