PubMed · 4924768
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J A Moncrief. 1970. Topical therapy.. https://doi.org/10.1016/s0039-6109(16)39289-1
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OBJECTIVE: Purpose of this presentation is to show the diagnostic power of fetal pulse oximetry in comparison to the other blood gas parameters from fetal blood samplings (FBS). The distribution of saturation readings in acidotic fetuses and normally oxygenated fetuses should be established. STUDY DESIGN: A fetal pulse oximetry system (N400, FS14) was evaluated in a strictly observational study design based on blinded saturation display and on continuous data storing. The investigation was performed on 170 fetuses with non-reassuring fetal heart rate (FHR)-tracings. Since pulse oximetry readings were not available for decision finding, the clinical management was based on electronic fetal monitoring and fetal blood samplings. The oxygen saturation from FBS or umbilical cord blood was measured by blood gas analysers with an integrated hemoximeter (Bayer 865; ABL 625, Radiometer) and biosensors measuring lactate as metabolic component. Out of the 170 cases 17 cases were defined as group of acidemia (pH(umb.art.) < 7.16 + BD<-9.4). The distribution of saturation readings and the duration of desaturation periods (in minutes and percentage of total monitoring time SPO2 below 30%) were determined. ROC curve analysis from FBS preceding delivery compared the diagnostic power of other blood gas parameters with oxygen saturation. The Wilcoxon test for uneven pairs was used. RESULTS: The distribution of oxygen saturation in the normal group of fetuses differs significantly from the acidemic group. The correlation coefficient between both methods to determine oxygen saturation was r=0.66. A specific evaluation of the distribution of SPO2 shows an overestimation of pulse oximetry in the low range and an underestimation in the high range of saturation. ROC-curve analysis showed a good diagnostic power of lactate in comparison to the oxygen saturation measured by pulse oximetry or by hemoximetry. CONCLUSIONS: The advantage of continuous fetal pulse oximetry surveilling the fetus under suspicion of hypoxia appears limited by the poor diagnostic power of the respiratory parameter saturation itself and by the impairment of the precision of the technology.
Prolonged lithium treatment of humans and rodents often results in hyperchloremic metabolic acidosis. This is thought to be caused by diminished net H+ secretion and/or excessive back-diffusion of acid equivalents. To explore whether lithium treatment is associated with changes in the expression of key renal acid-base transporters, semiquantitative immunoblotting and immunocytochemistry were performed using kidneys from lithium-treated (n = 6) and control (n = 6) rats. Rats treated with lithium for 28 days showed decreased urine pH, whereas no significant differences in blood pH and plasma HCO3- levels were observed. Immunoblot analysis revealed that lithium treatment induced a significant increase in the expression of the H+-ATPase (B1-subunit) in cortex (190 +/- 18%) and inner stripe of the outer medulla (190 +/- 9%), and a dramatic increase in inner medulla (900 +/- 104%) in parallel to an increase in the expression of type 1 anion exchanger (400 +/- 40%). This was confirmed by immunocytochemistry and immunoelectron microscopy, which also revealed increased density of intercalated cells. Moreover, immunoblotting and immunocytochemistry revealed a significant increase in the expression of the type 1 electrogenic Na+-HCO3- cotransporter (NBC) in cortex (200 +/- 23%) and of the electroneutral NBCn1 in inner stripe of the outer medulla (250 +/- 54%). In contrast, there were no changes in the expression of Na+/H+ exchanger-3 or of the Cl-/HCO3- exchanger pendrin. These results demonstrate that the expression of specific renal acid-base transporters is markedly altered in response to long-term lithium treatment. This is likely to represent direct or compensatory effects to increase the capacity for HCO3- reabsorption, NH4+ reabsorption, and proton secretion to prevent the development of systemic metabolic acidosis.
The effects of acidosis were investigated on the resting and precontracted aortas from Wistar and Wistar Kyoto (WKY) rats. Decrease in pH from 7.4 to 6.5, having no effect on the resting tension of Wistar aorta, induced a marked contraction of WKY aorta. Acidic pH markedly relaxed the contraction to 300 nM phenylephrine in Wistar aorta, whereas in WKY aorta, it produced a biphasic response, an initial relaxation followed by potentiation of the contraction. In aortas loaded with fura 2-AM, phenylephrine caused an increase in intracellular Ca2+ ([Ca2+]i) and a contraction in both Wistar and WKY rats. pH 6.5 produced a decrease in [Ca2+]i to a near-basal level and almost abolished the phenylephrine-induced contraction in Wistar rat aorta. However, in WKY aorta, a biphasic response, an initial decline and later a recovery of [Ca2+]i level, was observed. Interestingly, at similar sustained [Ca2+]i, the contractile response to phenylephrine in WKY aorta was potentiated under acidic pH conditions. Acidic pH-induced inhibition of the contraction to phenylephrine was unaffected by iberiotoxin, 4-aminopyridine, and glibenclamide (Ca2+-activated, delayed rectifier and ATP-sensitive K+ channel inhibitors, respectively), in aortas from both Wistar and WKY. Decrease in extracellular pH was associated with a rapid fall in intracellular pH (pHi) and the intracellular acidification profile was not different in both strains. All these results show that acidic pH induces strain-specific inhibitory and excitatory effects on the contractile state of aortas from Wistar and WKY rats, respectively. The sustained and transient relaxant responses to acidic pH in Wistar and WKY aortas, respectively, are due to decrease in [Ca2+]i levels, but this decrease in [Ca2+]i is independent of the activation of K+ channels.