Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

---

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

Ventilatory regulation of intact, unrestrained lugworms Arenicola marina living in glass-tube artificial burrows was examined for values of inspired seawater PO2, PIO2, from 20 to 700 torr, at constant ambient pH and PCO2 values. The water ventilation rate and the respiratory characteristics of the ventilated seawater were measured. The water convection requirement and the corresponding specific rates of O2 uptake and CO2 production were calculated. The mean ventilatory water flow was a complex function of PIO2: decrease in hyperoxia, increase in hypoxia, decrease in extreme hypoxia. Compared to the normoxic responses, hyperoxia led to a hypercapnia (and acidosis) and moderate hypoxia to a hypocapnia (and alkalosis) in the expired water, variations which presumably reflect blood acid-base balance changes. Thus, as in other water breathers, the regulation of the organism's oxygenation may override the regulation of its acid-base balance. The lugworm's oxygen exchanger is highly efficient. However, below a critical partial pressure, PIO2 ca 120 torr, values of O2 consumption and ventilation decreased. A second critical O2 partial pressure appeared at PIO2 values between 80 and 40 torr; a 'switch-on' of anaerobic metabolism. These phenomena may be viewed as features of an adaptative respiratory strategy selected for in relation with the lugworm's particular peristaltic ventilatory mechanism and its intertidal mode of life.
...
PMID:Ventilation and respiratory gas exchanges of the lugworm Arenicola marina (L.) as functions of ambient PO2 (20-700 torr). 644 Dec 15

In normotensive Wistar rats of a random-bred strain and in spontaneously hypertensive rats (SHR) of the Okamoto-Aoki-strain, the mean systemic arterial blood pressure, the pO2, pCO2, pH-values and the base excess of the arterial blood were measured during ventilating normal air as well as hypoxic (12.6% O2 in N2) and hyperoxic (100% O2) gas mixtures. The animals were anaesthetized and breathed spontaneously; they aged 5-6, 15-20, 30-40, and 50-70 weeks. The volume of their carotid bodies was determined morphometrically. When compared with the age-matched normotensive controls at an age of 5-6 weeks the SHR already exhibited slightly but significantly elevated blood pressures but had equal carotid body size and arterial carbon dioxide tension. In contrast, hypertensive animals in the established phase of hypertension (older than 15 weeks) showed greater carotid bodies and a highly significant respiratory alkalosis when compared with the corresponding age-group of the normotensive rats. The reactions of the mean systemic arterial blood pressure and the arterial pCO2 provoked by hypoxia and hyperoxia proved to be age-dependent in both the normotensive and hypertensive animals but this influence of age was different in the two strains of rats. The data support the concept that alterations of arterial chemoreceptor structures and reflex effects found in the established phase of hypertension are the result of this disease. Furthermore they indicate that, when interpreting arterial chemoreceptor reflex effects in hypertensive humans and animals, the stage of hypertension must be taken into account.
...
PMID:Influence of age on carotid body size and arterial chemoreceptor reflex effects in spontaneously hypertensive (SHR) and normotensive rats. 673 56

If 100% O2 produces hyperventilation by increasing central CO2 due to cerebral vasoconstriction or dimished reduction of oxyhemoglobin, then, there should be a parallel decrease in alveolar and CSF PCO2 during O2 breathing in neonates. To test this hypothesis, we measured ventilation, alveolar PCO2 and CSF PCO2, pH and HCO2 before and 10-20 min after infants began breathing 100% O2. With 100% O2, minute ventilation increased from 0.193 +/- (SE) 0.013 (n = 7) to 0.252 +/- 0.013 liter/min/kg (p less than 0.015), PACO2 decreased from 42 +/- 2 to 38 +/- 2 mm Hg (p less than 0.005), CSF PCO2 decreased from 51 +/- 1 to 44 +/- 1 mm Hg (p less than 0.015), and pH increased from 7.308 +/- 0.013 to 7.354 +/- 0.013 (p less than 0.05). CSF bicarbonate decreased, but not significantly. These findings, showing a trend toward alkalosis, suggest that the neonate, like the adult man, induces hyperventilation during hyperoxia via an increase in PCO2 at the central level.
...
PMID:Effect of inhaling 100% O2 on ventilation and acid-base balance in cerebrospinal fluid of neonates. 677 Sep 13

Pulmonary ventilation and pattern, arterial blood gases, and [H+] were studied in 15 highly trained runners [maximum O2 consumption (VO2 max) 53--82 ml . kg-1 . min-1] during road racing (24 km, n = 5) and 60--70 min of treadmill running (70--75% VO2 max, n = 13). The predominant response throughout prolonged treadmill running and especially road running was a tachypneic, respiratory alkalosis (-5 to -12 Torr PaCO2) that was evident early in the exercise. Time-dependent increases in breathing frequency (10--40%, 6--60 min work), expired ventilation, and dead space ventilation were common in prolonged work; these were especially evident in two subjects even as VO2 fell during road racing under hot humid conditions. The tachypneic hyperventilation was 1) most often accompanied by alkaline [H+]a, 2) associated with time-dependent elevation in rectal temperature (1--1.5 degrees C) and circulating norepinephrine (5--20 x rest), 3) quickly alleviated via hyperoxia after 60--70 min of exercise, and 4) was shown to result from increased running velocity in separate experiments that compared walking vs. running at similar CO2 excretion and [HCO-3]a. In highly trained runners competing under favorable environmental conditions and optional pace selection, we view the net effects of the hyperventilatory response to be truly advantageous, whereby the benefits to pulmonary gas exchange and [H+] regulation outweigh the expense of some inefficiency in ventilatory work and pattern and a departure from steady-state homeostasis.
...
PMID:Determinants and consequences of ventilatory responses to competitive endurance running. 680 87

To determine the influence of altered carotid body drive on exercise ventilatory kinetics, five subjects performed four repetitions of constant-load cycle ergometer exercise during air and O2 breathing under each of the following conditions: 1) metabolic acidosis, (NH4Cl, 0.3 g . kg-1 . day-1); 2) metabolic alkalosis (NaHCO3, 0.7 g . kg-1 . day-1); and 3) control (CaCO3, 0.1 g . kg-1 . day-1). Ventilatory and gas exchange variables were computed, breath-by-breath, and the time constant of the ventilatory response in each condition was determined by a least-squares technique. While breathing air, metabolic acidosis caused the magnitude of the ventilatory response to increase and the time constant of the ventilatory kinetics to decrease. With metabolic alkalosis the increase in ventilation caused by exercise tended to be smaller and time constant larger although these changes were not statistically significant. Hyperoxia slowed the ventilatory response in the three acid-base conditions to a similar value. Thus hyperoxia slowed the ventilatory kinetics to a greater degree during acidosis than during control or alkalosis. We conclude that ventilatory dynamics during moderate exercise can be appreciably influenced by the acid-base status with acidosis significantly speeding the response dynamics. And, as these effects are abolished by hyperoxia, they appear to be mediated via the carotid bodies, in the human.
...
PMID:Effect of acid-base status on the kinetics of the ventilatory response to moderate exercise. 708

To determine if angiotension converting enzyme activity is altered by acute pathophysiological insults, we assessed angiotensin I conversion using a blood pressure response technique in anesthetized dogs studied during acute 100% O2 breathing and acute acid-base derangements. Also, we determined systemic vascular reactivity to angiotensin II by measuring the magnitude and duration of the arterial blood pressure response to intra-arterial injections of angiotensin II under these same conditions. Angiotensin I conversion found in normoxia [91 +/- 7 (SD)%] was unchanged by acute acidosis, alkalosis, and hyperoxia. During acute hyperoxia the mean half time of the hypertensive response increased from 68 +/- 25 (SD) s at a PaO2 of 112 +/- 18 (SD) Torr to 100 +/- 34 (SD) s at a PaO2 of 491 +/- 47 (SD) Torr (P less than 0.01). No other pathophysiological condition studied had any effect on reactivity of systemic vasculature to angiotensin II. We conclude that, except during acute hypoxia as previously shown, converting enzyme activity is resistant to other pathophysiological insults and that vascular responsiveness to angiotensin II is enhanced by hyperoxia.
...
PMID:Angiotensin I conversion and vascular reactivity in pathophysiological states in dogs. 736 17

Estimates of the proportional contribution of the peripheral chemoreceptors (i.e., the carotid bodies) to human ventilatory control during moderate exercise (i.e., below the lactate threshold, theta L) suggest that they: (a) exert no discernible influence on the initial (usually rapid) phase I component; (b) provide significant modulation of the slower, exponential phase II dynamics, therefore contributing to the tightness of arterial PCO2 regulation and the magnitude of the transient hypoxemia in this phase; and (c) account for approximately 20% of the steady-state phase III drive, which can rise to over 50% in hypoxia (PaO2 approximately 50 mm Hg). Above theta L, the carotid bodies constrain the transient fall in arterial pH by mediating much (but not all) of the compensatory hyperventilation for the metabolic acidemia. The carotid body contribution above theta L, estimated by Dejours O2 testing, is not appreciably different from subthreshold estimates, suggesting that: (a) the respiratory alkalosis in blood and cerebrospinal fluid resulting from the hyperventilation may suppress carotid chemosensitivity; (b) an artifact resulting from secondary hyperoxia-induced stimulation of central chemoreceptors may lead to underestimation of the carotid body contribution; or (c) the carotid bodies may not be entirely "silenced" by hyperoxia during a metabolic acidemia.
...
PMID:Peripheral chemoreceptor control of exercise hyperpnea in humans. 818 98

Supplemental oxygen and alkalosis are the most effective treatments used to lower pulmonary arterial pressure in children with pulmonary hypertensive disorders. However, their mechanisms of action are unknown. Endothelium-derived nitric oxide (EDNO) is an important mediator of pulmonary vascular tone and produces potent pulmonary vasodilation during pulmonary hypertension. In vitro evidence suggests that EDNO may mediate the vasodilating effects of oxygen. To investigate whether EDNO synthesis mediates the pulmonary vasodilation produced by hyperoxia [normocarbic ventilation with 100% oxygen, arterial oxygen tension > 450 torr (60 kPa)] or alkalosis (hyperventilation with 21% oxygen, pH > 7.55) in vivo, eight intact newborn lambs were studied during similar degrees of pulmonary hypertension induced either by the infusion of U46619 (a thromboxane A2 mimic) or N omega-nitro-L-arginine (an inhibitor of EDNO synthesis). The lambs were sedated, paralyzed, and mechanically ventilated. Meclofenamic acid was infused to inhibit prostaglandin synthesis. During pulmonary hypertension induced by U46619, pulmonary arterial pressure and pulmonary vascular resistance were significantly decreased by acetylcholine (an EDNO-dependent vasodilator) (23.1 +/- 3.4% and 43.3 +/- 14.5%, respectively), hyperoxia (26.8 +/- 7.8% and 32.9 +/- 10.6%), and alkalosis (32.1 +/- 10.3% and 36.1 +/- 17.0%) (p < 0.05). During pulmonary hypertension induced by N omega-nitro-L-arginine, the decreases in pulmonary arterial pressure and pulmonary vascular resistance produced by acetylcholine (9.6 +/- 6.4% and 23.9 +/- 14.1%, respectively) were significantly attenuated (p < 0.05), but the decreases produced by hyperoxia or alkalosis were unchanged. Therefore, hyperoxia and alkalosis can produce pulmonary vasodilation independent of EDNO synthesis in the intact newborn lamb.
...
PMID:Hyperoxia and alkalosis produce pulmonary vasodilation independent of endothelium-derived nitric oxide in newborn lambs. 847 13

We used extracorporeal perfusion of the vascularly isolated carotid sinus region to determine the effects of specific carotid body chemoreceptor hypocapnia-alkalosis on ventilatory control in the unanesthetized dog. Eight female dogs were studied during wakefulness, non-rapid-eye-movement (NREM) sleep, and rapid eye movement (REM) sleep. Carotid body perfusions lasted from 1 to 2 min, and each trial was preceded by a 1-min control period. Two levels of carotid body hypocapnia were employed, approximately 7 and 14 Torr below eupneic levels in a given dog. We found that 1) During wakefulness and NREM sleep, carotid body hypocapnia caused reduced tidal volume (VT) but not apnea or expiratory time prolongation. 2) The inhibition of ventilation in response to carotid body hypocapnia was graded below normocapnia, showing the highest sensitivity at carotid body PCO2 near 7 Torr below eupneic values. Inhibition reached a maximum near 14 Torr below the eupneic level; VT, inspiratory minute ventilation (VI), and VT-to-inspiratory time ratio fell 31, 23, and 27% in wakefulness and 30, 23, and 30% in NREM sleep. 3) Reductions in ventilation in response to carotid body hypocapnia are lessened but still persist throughout perfusion (up to at least 130 s) despite significant systemic hypercapnia. 4) During REM sleep, carotid body hypocapnia had no consistent inhibitory effect on ventilation until carotid body PCO2 was reduced to values near 14 Torr below the eupneic level, at which point ventilation was similar to wakefulness and NREM. 5) Moderate carotid body hypocapnia was as effective as carotid body hyperoxia in reducing VT and VI. We conclude that carotid body hypocapnia-alkalosis can significantly inhibit eupneic VT and ventilation during wakefulness and NREM sleep and, if the hypocapnia is severe enough, during REM sleep.
...
PMID:Ventilatory effects of specific carotid body hypocapnia in dogs during wakefulness and sleep. 856 4

Ventilatory acclimatization to hypoxia is associated with an increase in ventilation under conditions of acute hyperoxia (VEhyperoxia) and an increase in acute hypoxic ventilatory response (AHVR). This study compares 48-h exposures to isocapnic hypoxia (protocol I) with 48-h exposures to poikilocapnic hypoxia (protocol P) in 10 subjects to assess the importance of hypocapnic alkalosis in generating the changes observed in ventilatory acclimatization to hypoxia. During both hypoxic exposures, end-tidal PO2 was maintained at 60 Torr, with end-tidal PCO2 held at the subject's prehypoxic level (protocol I) or uncontrolled (protocol P). VEhyperoxia and AHVR were assessed regularly throughout the exposures. VEhyperoxia (P < 0.001, ANOVA) and AHVR (P < 0.001) increased during the hypoxic exposures, with no significant differences between protocols I and P. The increase in VEhyperoxia was associated with an increase in slope of the ventilation-end-tidal PCO2 response (P < 0.001) with no significant change in intercept. These results suggest that changes in respiratory control early in ventilatory acclimatization to hypoxia result from the effects of hypoxia per se and not the alkalosis normally accompanying hypoxia.
...
PMID:Changes in respiratory control during and after 48 h of isocapnic and poikilocapnic hypoxia in humans. 984 35


<< Previous 1 2 3 Next >>

---