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Query: UMLS:C0242706 (hyperoxia)
 5,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of HCl infusion on multipoint mean pulmonary arterial pressure (PAP)/cardiac index (CI) plots in pentobarbital-anesthetized dogs whose lungs were ventilated alternately in hyperoxia (fraction of inspired O2 [FIO2], 0.4) and hypoxia (FIO2, 0.1) were investigated. Over the range of CI studied (1 to 5 l.min-1.m-2), hypoxia increased PAP in 22 dogs (responders) and did not affect PAP in 16 other dogs (nonresponders). In eight nonresponders, two repetitions of alternated 0.4 and 0.1 FIO2 exposures did not restore hypoxic pulmonary vasoconstriction (HPV), defined as a hypoxia-induced increase in PAP at a given flow. Intravenous infusion of 2 M HCl (2 mmol.kg-1.h-1) decreased arterial pH from normal to around 7.20 in eight responders and eight nonresponders. This metabolic acidosis increased PAP at all levels of CI in hyperoxia and in hypoxia in all the dogs, enhanced HPV in the responders, and restored HPV in the nonresponders. In eight responders, 2 M HCl infusion (2 mmol.kg-1.h-1) together with a 7% sodium bicarbonate infusion (adjusted to maintain arterial pH unchanged) did not affect hyperoxic or hypoxic PAP/CI plots. Pretreatment with 1 g acetylsalicylic acid iv (6 dogs) did not affect the pulmonary vasoreactivity to HCl-induced (2 M HCl, 2 mmol.kg-1.h-1) metabolic acidosis. It was concluded that in intact dogs: 1) metabolic acidosis enhances HPV; 2) at the given dose, HCl does not produce pulmonary vascular effects unrelated to the circulating blood pH; and 3) it is unlikely that the pulmonary vasoreactivity to metabolic acidosis is mediated by products of the cyclooxygenase pathway.
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PMID:Enhancement of hypoxic pulmonary vasoconstriction by metabolic acidosis in dogs. 216 53

We studied the effects of metabolic and respiratory acidosis (pH 7.20) and alkalosis (pH 7.60) on pulmonary vascular tone in 32 pentobarbital-anesthetized dogs ventilated with hyperoxia (inspired oxygen fraction, FIO2 0.40) and with hypoxia (FIO2 0.10). Ventilation, pulmonary capillary wedge pressure (Ppw), and cardiac output (3 l.min-1.m-2) were maintained constant to prevent passive changes in pulmonary arterial pressure (Ppa). Metabolic acidosis and alkalosis were induced with HCl (2 mmol.kg-1.h-1) and NaHCO3-Na2CO3 (5 mmol.kg-1.h-1) infusions, respectively, and respiratory acidosis and alkalosis by modifying the inspiratory CO2 fraction. The hypoxia-induced rise in Ppa-Ppw gradient increased from 5 to 9 mmHg in metabolic acidosis (P less than 0.001), decreased from 6 to 1 mmHg in metabolic alkalosis (P less than 0.001), remained unchanged in respiratory acidosis, and decreased from 5 to 2 mmHg in respiratory alkalosis (P less than 0.001). Linear relationships were found between pH and Ppa-Ppw gradients. These data indicate that in intact anesthetized dogs, metabolic acidosis and alkalosis, respectively, enhance and reverse hypoxic pulmonary vasoconstriction (HPV). Respiratory acidosis did not affect HPV and respiratory alkalosis blunted HPV, which suggests an pH-independent vasodilating effect of CO2.
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PMID:Effects of acidosis and alkalosis on hypoxic pulmonary vasoconstriction in dogs. 230 2

The hypothesis that severe lung damage generated by acid aspiration or a 50-hour exposure to 100% oxygen aggravates ethanol-induced hemorrhagic mucosal lesions in the stomach was examined in the rat. Animals were either given intratracheally with pyrogen-free saline or HCl (pH 1.75) or exposed for 50 h to 100% oxygen before the intragastric application of 1 ml of 50 or 75% ethanol. All rats receiving 50% ethanol were also given 3% monastral blue, 3 min before ethanol administration as a vascular tracer. Lung acid damage and inflammation as assessed by bronchopulmonary lavage were severe. We observed a significant increase in extracellular lactate dehydrogenase beta-glucosaminidase, albumin and the number of polymorphonuclear leukocytes in the lavage fluid. The number of resident macrophages decreased significantly. Blood gas analysis was not influenced. Hemorrhagic gastric mucosal lesions after 50 or 75% ethanol increased from 4.4 or 8.2% to 9.8 or 13.1% after HCl and from 6.7 or 18.2% to 10.6 or 21.6% of the glandular stomach following oxygen exposure. The area of mucosal vascular damage caused by 50% ethanol as revealed by monastral blue labelling was 3.3 and 2.6 times larger in rats with lung damage induced by HCl or hyperoxia, respectively. Thus, severe lung damage predisposes to microvascular damage and aggravates chemically induced hemorrhagic mucosal lesions.
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PMID:Lung damage aggravates gastric mucosal lesions induced by ethanol in the rat. 765 45

1. The object of this study was to investigate the effect of central chemoreceptor stimulation on the ventilatory responses to peripheral chemoreceptor stimulation. 2. The level of central chemoreceptor stimulation was varied by performing experiments at two different levels of end-tidal CO2 pressure (PCO2). Variations in peripheral chemoreceptor stimulus were achieved by varying arterial pH (at constant end-tidal PCO2) and by varying end-tidal O2 pressure (PO2). 3. Two protocols were each performed on six human subjects. In one protocol ventilatory measurements were made during eucapnia, when the arterial pH was lowered from 7.4 to 7.3. The variation in pH was achieved by the progressive infusion of acid (0.1 M HCl). In the other protocol ventilatory measurements were made during hypercapnia, when the arterial pH was increased from 7.3 to 7.4. The variation in pH was achieved by the progressive infusion of 1.26% NaHCO3. In each protocol ventilatory responses were measured during euoxia (end-tidal PO2, 100 Torr), hypoxia (end-tidal PO2, 50 Torr) and hyperoxia (end-tidal PO2, 300 Torr), with end-tidal PCO2 held constant. 4. The increase in ventilatory sensitivity to arterial pH induced by hypoxia (50 Torr) was not significantly different between protocols (acid protocol, -104 +/- 31 l min-1 (pH unit)-1 vs. bicarbonate protocol, -60 +/- 44 l min-1 (pH unit)-1; mean +/- S.E.M.; not significant (n.s.)). The ventilatory sensitivity to hypoxia at an arterial pH of 7.35 was not significantly different between protocols (acid protocol, 14.7 +/- 3.3 l min-1 vs. bicarbonate protocol, 15.6 +/- 2.4 l min-1; mean +/- S.E.M.; n.s.). The results provide no evidence to suggest that peripheral chemoreflex ventilatory responses are modulated by central chemoreceptor stimulation.
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PMID:An assessment of central-peripheral ventilatory chemoreflex interaction using acid and bicarbonate infusions in humans. 766 75

Marked morphological responses occur in the gills of freshwater rainbow trout in response to experimental acid-base disturbance and these responses play an important role in acid-base correction. Compensated respiratory acidosis induced by 70h exposure to environmental hyperoxia (elevated water PO2) caused a 33% decrease in branchial chloride cell fractional surface area (CCFA). Metabolic alkalosis induced by normoxic recovery (6h) from hyperoxia (72h) caused a 50% increase in CCFA, whereas metabolic alkalosis induced by infusion (19h) of NaHCO3 caused a 70% rise. However, the largest increase (135%) in CCFA was seen in response to infusion (19h) of HCl. NaCl infusion had no effect. A particular goal was to assess the relative importance of changes in CCFA vs. changes in internal substrate (HCO3 (-)) availability in regulating the activity of the branchial Cl(-)/HCO3 (-) exchange system. For each of the experimental treatments, the accompanying blood acid-base status and branchial transport kinetics (Km, Jmax) for Cl(-) uptake had been determined in earlier studies. In the present study, a positive linear relationship was established between CCFA and J(Cl-) max in individual control fish in the absence of an acid-base disturbance. By reference to this relationship, observed changes in J(Cl-) max during metabolic acid-base disturbances were clearly due to changes in both CCFA and internal substrate levels (plasma [HCO3 (-)]) with the two factors having approximately equal influence.
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PMID:Morphological responses of the rainbow trout (Oncorhynchus mykiss) gill to hyperoxia, base (NaHCO3) and acid (HCl) infusions. 2420 8