PubMed · 5752079
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D Michaeli. 1968. Heatstroke.. https://doi.org/10.1136/bmj.1.5647.844-c
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UNLABELLED: Pulmonary aspiration of gastric acid is a complication that occurs during anesthesia. The effects of the often used anesthetics on the inflammatory response after aspiration of acid are not known. We examined the effects of three different inhaled anesthetics--halothane, enflurane, and isoflurane--as well as parenteral ketamine, on the associated immediate mortality, alveolar protein leakage, and morphometric changes after intrapulmonary instillation of acidic solution in rats. Animals in deep state of anesthesia had a higher mortality after the instillation of acidic solutions than those in lighter stages (82.5% vs 31.6%). Protein leakage over 5 h was greater in the animals receiving volatile anesthetics (range 0.9-1.2) compared with those receiving ketamine (0.6 +/- 0.05). Desferoxamine did not decrease protein leakage in acid-injured animals (1.1 +/- 0.06 vs 1.02 +/- 0.08). Furthermore, volatile anesthetics resulted in an increase in the acute inflammatory response and leukocytic infiltration compared with ketamine in acid-injured lungs. We conclude that the administration of inhaled anesthetics was associated with exacerbation of an acute inflammatory response after aspiration of acidic solution. Lung injury was not increased with ketamine anesthesia. This difference was the result of the hypotensive effects of inhaled anesthetics. IMPLICATIONS: This study reveals that the use of inhaled anesthetics aggravates inflammation secondary to gastric aspiration and should be avoided on diagnosis of the situation.
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We evaluated the contribution of cytochrome P-450 (CYP450)-dependent arachidonic acid (AA) metabolites and prostanoids to the renal hemodynamic and tubular effects of endothelin-1 (ET-1) in anesthetized rats. Either ET-1 (0.3, 1.0, and 3 pmol.kg-1.min-1) or vehicle was infused intravenously during two to three 30-min clearance experimental periods. Only high-dose ET-1 increased mean arterial pressure: control, 75 +/- 3 mmHg vs. experimental, 84 +/- 4 mmHg. A dose-dependent diuretic-natriuretic response to ET-1 occurred despite progressive declines in glomerular filtration rate (GFR) and renal blood flow. In the face of a 36% reduction in GFR in response to the highest dose of ET-1, urinary sodium excretion (UNaV) increased threefold from 0.57 +/- 0.11 to 1.6 +/- 0.10 mumol.100 g-1.min-1. Indomethacin (5 mg/kg) decreased basal GFR from 1.2 +/- 0.3 ml.100 g-1.min-1 to 0.8 +/- 0.1 ml.100 g-1.min-1 and potentiated the GFR lowering action of ET-1 associated with reductions in UNaV and urine volume. Cobalt chloride (CoCl2) and dibromododec-11-enoic acid (DBDD), which diminish CYP450-dependent AA metabolism through different mechanisms, were used to identify CYP450 products mediating the renal functional actions of ET-1. DBDD (12.5 micrograms/min) reduced urinary excretion of 20-hydroxyeicosatetraenoic acid from 3.4 +/- 0.9 (control) to 1.1 +/- 0.6 ng/h and abolished the negative effects of ET-1 on GFR while decreasing the diuretic-natriuretic action of ET-1. Similar effects were produced by CoCl2. Clotrimazole, an inhibitor of epoxygenase activity, was without effect on ET-1-induced renal functional changes. Thus the capacity of ET-1 to enhance prostaglandin production was primarily expressed in terms of positive effects on renal hemodynamics. In contrast, CYP450 products promoted sodium excretion despite negative effects on renal hemodynamics.