The influence of respiratory-induced acid-base changes on the action of non-depolarizing muscle relaxants in rats.
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The influence of respiratory-induced acid-base changes on the action of non-depolarizing muscle relaxants was investigated using the rat phrenic nerve-hemidiaphragm preparation. Changes in pH were induced by changes in the CO2 concentration aerating Krebs' solution. In the absence of muscle relaxants, an increase in CO2 from 5% to 7.5% decreased (P less than 0.01) indirectly elicited twitch tension by 5.4 +/- 0.7% (mean +/- SEM), while a decrease in CO2 from 5% to 2.5% increased (P less than 0.01) twitch tension by 2.3 +/- 0.7%. With a change in CO2 from 2.5% to 7.5%, partial neuromuscular blockade produced by d-Tc or vecuronium was augmented (P less than 0.01), while that produced by metocurine, pancuronium, or alcuronium was reduced (P less than 0.01). With the change in CO2 from 7.5% to 2.5%, the neuromuscular blockade produced by d-Tc or vecuronium was reduced (P less than 0.01), while that produced by metocurine, pancuronium, or alcuronium was augmented (P less than 0.01). Dose-response study showed that 2.5% CO2 shifted the dose-response curves for d-Tc and vecuronium to the right (P less than 0.01) from those with 5% CO2, whereas 7.5% CO2 shifted them to the left (P less than 0.05). In contrast, neither 2.5% CO2 or 7.5% CO2 significantly shifted the dose-response curves for metocurine or pancuronium from those with 5% CO2. Their dose-response curves with 2.5% CO2 were to the left, instead of to the right, of those with 7.5% CO2 (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS) (+info)
Regulation of net bicarbonate transport in rabbit cortical collecting tubule by peritubular pH, carbon dioxide tension, and bicarbonate concentration.
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The effects of changes in peritubular pH, carbon dioxide tension (PCO2), and HCO3- concentration on net HCO3- transport was examined in in vitro perfused cortical collecting tubules (CCTs) from unpretreated New Zealand white rabbits. Lowering peritubular HCO3- concentration and pH by reciprocal replacement of HCO3- with Cl-, significantly stimulated net HCO3- absorption. Lowering peritubular HCO3- concentration and pH, by substitution of HCO3- with gluconate, while keeping Cl- concentration constant, also stimulated net HCO3- absorption. Raising peritubular HCO3- concentration and pH, by reciprocal replacement of Cl- with HCO3-, inhibited net HCO3- absorption (or stimulated net HCO3- secretion). When the tubule was cooled, raising peritubular HCO3- concentration had no effect on net HCO3- transport, suggesting these results are not due to the passive flux of HCO3- down its concentration gradient. The effect of changes in ambient PCO2 on net HCO3- transport were also studied. Increasing the ambient PCO2 from 40 mmHg to either 80 or 120 mmHg, allowing pH to fall, had no effect on net HCO3- transport. Similarly, lowering ambient PCO2 to 14 mmHg had no effect on net HCO3- transport. Simultaneously increasing peritubular HCO3- concentration and PCO2, without accompanying changes in peritubular pH, i.e., isohydric changes, stimulated net HCO3- secretion to the same degree as nonisohydric increases in peritubular HCO3- concentration. Likewise, isohydric lowering of peritubular HCO3- concentration and PCO2 stimulated net HCO3- absorption. We conclude that: acute changes in peritubular HCO3- concentration regulate acidification in the CCT and these effects are mediated by a transcellular process; acute changes in ambient PCO2 within the physiologic range have no effect on HCO3- transport in the in vitro perfused CCT; and acute in vitro regulation of CCT acidification is independent of peritubular pH. (+info)
Comparison of [125I]HIPDm and [125I]iodoantipyrine in quantifying regional cerebral blood flow in rats.
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We determined regional cerebral blood flow (rCBF) using [125I]HIPDm [N,N,N'-trimethyl-N'-(2-hydroxy-3-methyl-5-iodobenzyl)-1,3-propanediamin e] and [125I]iodoantipyrine autoradiography under control and pathologic conditions (hypercapnia [acidosis], hypocapnia [alkalosis], and disrupted blood-brain barrier) conditions in 35 rats. In control rats, HIPDm rCBF (indicator fractionation method, n = 5) was lower than the corresponding IAP rCBF (diffusible indicator method, n = 4), most notably in the infratentorial regions and subcortical nuclei. In hypercapnia, rCBF increased by 100% and 37% in the HIPDm (n = 5) and IAP (n = 5) groups, respectively. In hypocapnia, IAP rCBF (n = 4) decreased 34% but HIPDm rCBF (n = 4) did not change. Following disruption of the blood-brain barrier by intracarotid infusion of mannitol in eight rats, both radiotracers (HIPDm n = 4, IAP n = 4) showed decreased rCBF to regions of disruption as defined by trypan blue extravasation. Our work indicates that modeling HIPDm uptake to quantify rCBF using the indicator fractionation method will underestimate blood flow and that HIPDm kinetics are influenced by compartmental pH dynamics that will limit the accuracy of this method in quantifying rCBF in pathologic conditions. (+info)
Effects of changes in maternal--fetal pH on the transplacental equilibrium of bupivacaine.
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Increases in the maternal-fetal pH gradient that may occur during labor and delivery may increase the fetal concentration of local anesthetics. The authors evaluated effects of pH changes on the transplacental concentration equilibrium of bupivacaine. They increased the maternal-fetal pH gradient in each of six pregnant ewes from a control value of 0.15 to 0.54 by hyperventilating the lungs of the ewe and infusing lactic acid into her fetus. After infusion of bupivacaine, 0.15 mg/kg, intravenously into the mother, the drug rapidly appeared in fetal blood, with values significantly increased over control values at 1 and 5 min. The fetal/maternal (f/m) ratios were increased significantly at 5, 15, and 30 min. The f/m ratios had stabilized by 15 min in both control and experimental states, suggesting that equilibrium had been achieved. The consistently low f/m ratios are explained by the presumed similarity of the ovine maternal and fetal protein binding rates to those of man. It is concluded that the maternal and fetal pH values are major factors in the determination of the f/m ratios. (+info)
Mixed acid-base disorders.
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Mixed acid-base disorders, the occurrence of two or more primary acid-base disturbances in the same patient, are common in the hospital population, but are usually misdiagnosed because of lack of knowledge of the consequences of the primary disturbances. This paper describes seven examples of these disorders recently seen in the authors' hospital, and provides a logical approach to their diagnosis. (+info)
Fentanyl concentrations in brain and serum during respiratory acid--base changes in the dog.
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It is a clinical impression that less fentanyl is needed for anesthesia during hyperventilation and hypocarbia. If true, it might be due to both increased penetration of fentanyl, a highly lipid-soluble agent, into the brain and increased brain tissue binding. Serum and brain concentrations of fentanyl were determined in dogs anesthetized with halothane during normocarbia, hypocarbia by hyperventilation, and hypercarbia by addition of CO2 to the inspired mixture. Fentanyl, 12.5 micrograms/kg, was injected iv, and serum and brain samples were taken for fentanyl analysis by radioimmunoassay. Brain fentanyl values peaked latest (15--20 min) and were highest during hypocarbia; brain fentanyl values peaked earliest (0--5 min) and were lowest during hypercarbia; values during normocarbia were intermediate in time to peak (10--15 min) and concentration. Thereafter, brain levels declined, but during hypocarbia were significantly higher and during hypercarbia were significantly lower than during normocarbia. Interestingly, serum fentanyl levels were also significantly higher during hypocarbia. The brain--blood fentanyl ratios for each of the three CO2 levels increased for 30 min and thereafter stayed relatively constant. The brain--blood ratios were highest with hypocarbia and lowest with hypercarbia. At 35 min, when clinical analgesia may be considered terminated, hypocarbic brain levels were double those of normocarbia. The authors feel this reflects, to a large extent, higher serum fentanyl concentrations and delayed cerebral wash-out because of decreased blood flow. To a small but unknown extent the higher brain fentanyl levels result from increased brain--blood penetration due to increased lipid solubility, and increased brain tissue binding of fentanyl during respiratory alkalosis. (+info)
Diabetic ketoalkalosis.
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The usual metabolic derangement in uncontrolled diabetes mellitus is metabolic acidosis, with an increase in the anion gap because of increased ketoacids and lactate. However, diabetic ketoalkalosis may occasionally be encountered, the prominent clinical feature of which is vomiting, with depletion of potassium, chloride, and hydrogen ions. Self-medication with absorbabe alkali may also contribute to the alkalosis. It would be dangerous to treat hyperlgycemic patients with alkali if their condition is ketoalkalosis instead of ketoacidosis. (+info)