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PubMed1975

Propanidid for anaesthetic induction at Caesarean section.

In 50 healthy mothers scheduled for elective Caesarean section, anaesthesia was induced with propanidid (7 mg/kg body weight). Thereafter, ventilation was controlled with nitrous oxide, oxygen and muscle relaxants. A further dose of propanidid (1 mg/kg body weight) was administered 3 minutes after the initial injection of this drug, as a means of preventing maternal awareness during equilibration with the anaesthetic gas mixture. The acid-base status of the mothers before the induction of anaesthesia, and at delivery, revealed a mild degree of respiratory alkalosis with a compensatory metabolic acidosis. Umbilical cord blood gas results indicated the presence of significant fetal acidosis, both respiratory (mean pCO2 Uv 46,3 torr (SD 11,3) and Ua 54,3 torr (SD 12,0)), and metabolic (mean base excess Uv-9 mEq/l (SD 4,2) and Ua-11,8 mEq/l, (SD 5,0)) in origin. The average umbilical cord blood oxygen tensions were Uv 25,9 torr (SD 10), and Ua 15,4 torr (SD 8,5); mean maternal to fetal base-excess gradients were Ma-Uv 4,1 mEq/l (SD 2,8) and Ma-Ua 6,5 mEq/l (SD 3,5). Five mothers (10%) offered convincing evidence of factual recall during surgery, and 3 of these were aware of pain. Nausea and vomiting occurred in 5 patients and in 4 there were clinical signs of postoperative chest infection. The degree of fetal biochemical asphyxia, and the incidence of maternal awareness during surgery, were significantly greater than previously reported when thiopentone was used for the induction of anaesthesia for Caesarean section. The results obtained are discussed, and the conclusion is drawn that propanidid for anaesthesia appears to offer no advantage over thiopentone in obstetric practice.

Acidosis↗
PubMed1990

Relationship between intracellular pH and ammonia metabolism in LLC-PK1 cells.

Previous studies from our laboratory have confirmed that cultures of LLC-PK1 cells exhibit pH-responsive alterations in ammonia metabolism produced by changes in media bicarbonate concentration. To further elucidate the mechanism of ammonia regulation, studies were carried out using parallel cultures of still and rocked LLC-PK1 cells subjected to acute alterations in media pH by either metabolic or respiratory acid-base manipulations. When media pH was altered by modifying PCO2 levels, the response of ammonia and alanine production by rocked culture was identical to the changes observed with metabolic acid-base maneuvers. Furthermore, both metabolic and respiratory acute acidosis resulted in a fall of intracellular alpha-ketoglutarate concentrations in these cells. In contrast, standard still cultures subjected to acute acidosis/alkalosis by metabolic and respiratory manipulations did not exert any significant change in ammonia and alanine production or in intracellular alpha-ketoglutarate concentration. Measurements of intracellular pH (pHi) by the 5,5-[2-14C]dimethyloxazolidine-2,4-dione method in rocked cells demonstrated changes in pHi parallel to media pH changes induced by both metabolic and respiratory acid-base maneuvers. Despite the absence of pH-responsive ammonia-genesis in still cultured cells the pHi values were altered in a fashion similar to their rocked counterparts, indicating the lack of an effect of the pHi signal on ammonia metabolism.

Acidosis↗
PubMed1987

Respiratory and cardiovascular effects of halothane, isoflurane and enflurane delivered via a Jackson-Rees breathing system in temperature controlled and uncontrolled rats.

We studied the respiratory and cardiovascular effects of 1.25 MAC halothane, isoflurane and enflurane in oxygen delivered via the Jackson-Rees breathing system in 10 rats. Mean arterial pressure, heart rate and respiratory rate were depressed significantly (P less than 0.05) in rats (n = 5) whose body temperature was not controlled after 2 hr of anesthesia regardless of the inhalational agent. Respiratory and metabolic acidosis developed. The respiratory and cardiovascular depression was most marked under enflurane anesthesia. In normothermic rats (n = 5) the initial cardiovascular depression stabilized after 30 min of halothane and isoflurane anesthesia. Moderate respiratory depression developed (PCO2 48.42 +/- 2.48 torr with halothane vs. 41.02 +/- 1.68 torr with isoflurane). Because the cardiovascular and respiratory changes caused by halothane and isoflurane were far less than changes produced by enflurane, halothane or isoflurane is preferable to enflurane for maintaining anesthesia in rats. Maintenance of constant temperature minimizes the cardiovascular and respiratory disturbances.

Anesthesia, Inhalation↗
PubMed1978

Acid-base balance and neostigmine antagonism of pancuronium neuromuscular blockade.

In 40 cases anesthetized with chloralose and urethane, pancuronium was infused i.v. at a constant rate to produce and maintain 90% depression twitch tension of the anterior tibialis muscle following supramaximal stimulation of the peroneal nerve. Neither respiratory alkalosis nor metabolic acidosis influenced the infusion rate required to produce 90% depression of twitch tension or antagonism of this depression yb neotigmine. Respiratory acidosis (pH 7.15; PaCO2 10 kPa) did not alter the required infusion rate but did prevent complete antagonism by neostigmine. Metabolic alkalosis (pH 7.65; PaCO2 4.8 kPa) reduced both the required infusion rate and prevented complete restoration of twitch tension by neostigmine. The duration of neostigmine antagonism was shortened by metabolic alkalosis. We conclude that respiratory acidosis and metabolic alkalosis prevent antagonism of pancuronium by neostigmine.

Acid-Base Equilibrium↗
PubMed1964

FOETAL ACIDOSIS.

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Acidosis↗
PubMed1984

Influence of in vitro lactic acidosis and hypercapnia on respiratory activity of isolated rat brain mitochondria.

Respiratory activity and the ADP/O ratio of isolated rat brain mitochondria were measured following incubation with varying concentrations of lactic acid in reaction media buffered either with bicarbonate and CO2 or with phosphate alone, at a pH of 7.1. Increasing lactic acid levels caused a progressive decrease in substrate-, phosphate-, and ADP-stimulated (State 3) respiration and ADP/O ratios. Fifteen millimolar lactic acid, pH 6.4, caused approximately 50% inhibition of State 3 respiration (with malate + glutamate as substrate). At lower pH values (5.3-6.1), addition of ADP caused little or no increase in O2 consumption; i.e., ATP formation ceased. Addition of lactic acid at constant pH moderately affected respiratory control ratios but did not change State 3 respiration or ADP/O ratios. Thus, the effect of lactic acid was related to the pH change. Increasing CO2 concentrations in the reaction medium had similar effects on mitochondrial respiration, indicating that changes in extramitochondrial pH rather than in transmembrane H+ gradients determined the respiratory alterations. Following a 5-min incubation of mitochondria with lactic acid, pH 6.1, there was an incomplete recovery of State 3 respiration and respiratory control ratios. It is concluded that mitochondrial respiration is inhibited by a decrease in pH which, if excessive, may lead to a permanent suppression of ATP production. These results may, at least partly, explain the deleterious effects of enhanced lactic acidosis in brain ischemia.

Acidosis↗