PubMed · 5765967
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J Lumley, P Renou, W Newman, C Wood. 1969-03-15. Hyperventilation in obstetrics.. https://doi.org/10.1016/0002-9378(69)90585-7
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The hysteroscopic approach to the correction of congenital anomalies in utero may be helped by the temporary introduction of clear, electrically neutral fluids (liquids or gases) into the amniotic cavity. Accordingly, the authors determined the effects of three candidate fluids (helium, carbon dioxide, and water) on the oxygenation, acid-base balance, electrolyte concentrations, and hemodynamic function of nine sheep fetuses at 120 days' gestation (full term 145 days). Each fetus was exposed, in random order, to each of the three fluids, at an intraamniotic pressure of 15 mm Hg. The authors found that helium produced no changes in any of the measurements and was well tolerated by the fetus and the mother. Carbon dioxide decreased fetal arterial pH, and increased both arterial PCO2 and PO2. Although the decrease in pH was explained entirely by the increase in PCO2, the increase in arterial PO2 may have resulted from vasodilatation of the placental circulation or vasoconstriction of the fetal circulation with a redistribution of blood flow to the placenta. Water caused mild fetal hyponatremia and hypochloremia, without significant changes in acid-base balance or oxygenation. The results suggest that both helium and water may represent viable alternatives for amniotic fluid replacement during hysteroscopic surgery.
Tracheal instillation of perfluorochemical liquid (PFC) lowers surface tension in the lung and thus might reduce barotrauma commonly associated with conventional gas ventilation (GV) in highly immature and hypoplastic lungs. It could be a promising alternative treatment for congenital diaphragmatic hernia (CDH) when GV alone is proving inefficient. The authors compared data for eight newborn lambs with surgically induced CDH. The animals had GV and were studied (in 2 groups) for up to 3.5 hours. Group 1 (GV, n = 4) had gas ventilation only. In group 2 (PFC, n = 4), after 30 minutes of GV, 10 to 12 mL/kg of warmed, oxygenated PFC liquid (LiquiVent) was instilled into the lung via the trachea under pressure-volume curve monitoring. Arterial pressure, blood chemistry, and pulmonary mechanics were evaluated serially; histological analysis was performed. One preassigned animal in group 1 died after 15 minutes. After 30 minutes of life, the cardiopulmonary profile of survivors was indicative of severe respiratory distress (Pao2 < 72 mm Hg with FIO2 at 1.0, PaCO2 > 90 mm Hg, compliance < 0.10 mL/cm H2O/kg) and not different between groups; the severity of pulmonary hypoplasia was further confirmed postmortem; the ratio of lung weight to body weight was 41% of that observed in control lambs, in both gas-only and combined gas/PFC-ventilated animals, compared with their respective controls. After instillation of PFC, there were dramatic improvements in acid-base status and pulmonary compliance in group 2. Survival at 3.5 hours also was markedly different (4 of 4 PFC animals and 1 of 3 GV animals).(ABSTRACT TRUNCATED AT 250 WORDS)
The effect of prostaglandin E2 (PGE2), on the intracellular pH (pHi) in BCECF-loaded Madin Darby Canine Kidney (MDCK) cells was investigated. PGE2 elevated the pHi. Under resting conditions, pHi of MDCK cells suspended in PBS at pH 7.4 was 7.11 +/- 0.08; PGE2 increased pHi with an EC50 of 0.16 microM. PGF2 alpha elicited a similar response to PGE2, with an EC50 of 0.24 microM. Amiloride (0.4 mM) reversed the response to PGE2 (control 7.18 +/- 0.05; PGE2 7.26 +/- 0.05; after amiloride 7.18 +/- 0.05). In MDCK cells exposed to a Na(+)-free solution, alkalinization induced by this eicosanoid was blocked (Ringer-choline 7.16 +/- 0.03; PGE2 7.16 +/- 0.02). PGE2 increased by 100% the rate of recovery after an acidification pulse with ammonium chloride. In the presence of Ringer-HCO3- (pH 7.4), there was a delay in the maximal response to this prostaglandin (PBS 2.2 +/- 0.27, Ringer-bicarbonate 3.4 +/- 0.55 min) and the pHi increment was less marked than in PBS (0.09 pH units in HCO3- versus 0.16 pH units in PBS; P < 0.001). This effect of PGE2 was not blocked by 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid (1.0 mM). PMA (100 nM), activator of protein kinase C, mimicked the response to PGE2, suggesting the participation of this kinase on the effect of the prostanoid. As expected, two inhibitors of protein kinase C, staurosporine and sphingosine, abolished the response to PGE2. Staurosporine (0.10 microM), an inhibitor of protein kinase C, blocked the response to PGE2 (control 7.02 +/- 0.04; PGE2 and staurosporine 7.03 +/- 0.04, n = 9, not significant). Sphingosine, another inhibitor of protein kinase C, also blocked the response to PGE2. Two analogues of cAMP did not modify the pHi. In summary, PGE2 induced an intracellular alkalinization via stimulation of a Na+/H+ exchanger, with the participation of protein kinase C, in MDCK cells.