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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Intensive care medicine 22 (1996), S. 813-817 
    ISSN: 1432-1238
    Keywords: Key words Alternating ventilation ; Cardiac output ; Central venous pressure ; Intrathoracic pressure ; Lung volume ; Pericardial pressure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract   Objective: We tested the hypothesis that mean thoracic expansion (and mean lung volume) is lower during alternating ventilation (AV), i.e. ventilation of both lungs with a phase shift of half a ventilatory cycle, compared to synchronous ventilation (SV) of both lungs. As a consequence, intrathoracic pressure will be lower, causing lower, central venous pressure and higher cardiac output. Design: In eight anaesthetized and paralysed piglets, differential ventilation was established by fixation of an endobronchial tube in the left main bronchus. SV and AV were sequentially applied for four and three periods, respectively, of 10 minutes each. Minute ventilation was the same during AV and SV and adapted to normocapnia. Two series of observations were performed: series 1 with intact thorax and monitoring of oesophageal pressure; series 2 after perforation of the sternum, airtight closure of the thorax and monitoring of pericardial pressure. Results: In both series, mean lung volume was 16±4% lower and central venous, oesophageal (series 1) and pericardial pressures (series 2) were 0.5–0.7 mmHg lower during AV compared to SV (all p〈0.001). In series 1, aortic pressure was 5 mmHg and cardiac output 8% higher (both p〈0.001). In series 2, cardiac output was 5% higher during AV (p〈0.001), but aortic pressure did not change (p=0.07). Conclusion: Our data verified the hypothesis. The lower oesophageal (series 1), pericardial (series 2) and central venous pressures during AV compared to SV could be explained by the smaller thoracic expansion due to the lower mean lung volume, which was attributed to compression of the opposite lung by the expansion of the inflated lung.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Intensive care medicine 22 (1996), S. 813-817 
    ISSN: 1432-1238
    Keywords: Alternating ventilation ; Cardiac output ; Central venous pressure ; Intrathoracic pressure ; Lung volume ; Pericardial pressure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Objective We tested the hypothesis that mean thoracic expansion (and mean lung volume) is lower during alternating ventilation (AV), i.e. ventilation of both lungs with a phase shift of half a ventilatory cycle, compared to synchronous ventilation (SV) of both lungs. As a consequence, intrathoracic pressure will be lower, causing lower, central venous pressure and higher cardiac output. Design In eight anaesthetized and paralysed piglets, differential ventilation was established by fixation of an endobronchial tube in the left main bronchus. SV and AV were sequentially applied for four and three periods, respectively, of 10 minutes each. Minute ventilation was the same during AV and SV and adapted to normocapnia. Two series of observations were performed: series 1 with intact thorax and monitoring of oesophageal pressure; series 2 after perforation of the sternum, airtight closure of the thorax and monitoring of pericardial pressure. Results In both series, mean lung volume was 16±4% lower and central venous, oesophageal (series 1) and pericardial pressures (series 2) were 0.5±0.7 mmHg lower during AV compared to SV (allp〈0.001). In series 1, aortic pressure was 5 mmHg and cardiac output 8% higher (bothp〈0.001). In series 2, cardiac output was 5% higher during AV (p〈0.001), but aortic pressure did not change (p=0.07). Conclusion Our data verified the hypothesis. The lower oesophageal (series 1), pericardial (series 2) and central venous pressures during AV compared to SV could be explained by the smaller thoracic expansion due to the lower mean lung volume, which was attributed to compression of the opposite lung by the expansion of the inflated lung.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Intensive care medicine 16 (1990), S. 33-40 
    ISSN: 1432-1238
    Keywords: Intrinsic PEEP ; Ventilatory pattern ; Lung volume ; Lung stretch ; piglets
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We studied the influence of ventilatory frequency (1–5 Hz), tidal volume, lung volume and body position on the end-expiratory alveolar-to-tracheal pressure difference during high-frequency jet ventilation (HFJV) in Yorkshire piglets. The animals were anesthetized and paralysed. Alveolar pressure was estimated with the clamp off method, which was performed by a computer controlled ventilator and which had been extensively tested on its feasibility. The alveolar-to-tracheal pressure difference increased with increasing frequency and with increasing tidal volume, the common determinant appearing to be the mean expiratory flow. The effects in prone and in supine position were similar. Increasing thoracic volume decreased the alveolar-to-tracheal pressure difference indicating a dependence of this pressure difference on airway resistance. We concluded that the main factors determining the alveolar-to-tracheal pressure difference (ΔP) during HFJV are expiratory flow (V′E) and airway resistance (R), ΔP≃V′E×R.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Intensive care medicine 12 (1986), S. 26-32 
    ISSN: 1432-1238
    Keywords: Ventilatory pattern ; PEEP ; Lung volume ; Respiratory drive ; EMG diaphragm ; Piglets
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Conditions which suppress spontaneous breathing activity during high-frequency jet ventilation (HFJV) were analysed in Yorkshire piglets under pentobarbital anesthesia. The highest PaCO2 at which the animals did not breathe against the ventilator (apnea point) was established during different patterns of ventilation, either by changing the minute volume or by adding CO2 to the inspiratory gas. Arterial oxygen tension was maintained throughout the study above 80 mm Hg. An elevation of ventilatory rate increased the apnea point, suggesting a progressive suppression of spontaneous breathing. This suppression did not depend on the amount of lung stretch during insufflation, because at higher rates lower tidal volumes were used. Suppression also appeared to be independent of insufflatory flow, i.e. the velocity of lung stretch. At higher frequencies end-expiratory airway pressure (PEE) increased and there appeared to be a positive relationship between the apnea point and PEE. In a separate series this positive relationship between the apnea point and PEE was confirmed. A hysteresis effect in this relationship, however, suggests that other than jet frequency, lung volume rather than positive end-expiratory pressure (PEEP) is a major determinant of suppression of spontaneous breathing activity during HFJV.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1432-1041
    Keywords: Nifedipine ; omeprazole ; absorption ; gastric pH ; pharmacokinetic ; drug interaction ; adverse effects
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary The effects of single dose (20 mg) and short-term (20 mg/day for 8 days) oral treatment with omeprazole on the pharmacokinetics and effects of oral nifedipine (10 mg capsule) and on gastric pH have been investigated in a randomized, double-blind, placebo-controlled cross-over study in 10 non-smoking healthy male subjects. The single dose of omeprazole had no significant effect on any pharmacokinetic parameter of nifedipine, nor on gastric pH, or blood pressure or heart rate. Short-term omeprazole treatment increased the AUC of nifedipine by 26% (95% confidence interval 9–46%), but all other pharmacokinetic parameters of nifedipine, including elimination half-life, Cmax, tmax, and recovery of the main urinary metabolite, were not significantly changed. The median gastric pH during the absorption phase of nifedipine was increased by short-term omeprazole (pH 4.2) compared to placebo treatment (pH 1.4). Blood pressure and heart rate did not differ between treatments. The interaction between nifedipine and omeprazole is not likely to be of major clinical relevance.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1432-1041
    Keywords: omeprazole ; pepsinogen A ; pepsinogen C ; fasting serum gastrin ; pentagastrin ; gastric-acid ; healthy volunteers
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary A study has been done in 10 male healthy volunteers of the effect of oral omeprazole 20 mg daily for 3 days on the serum concentrations of Pepsinogens A and C in relation to changes in fasting serum gastrin and basal and pentagastrin stimulated gastric acid output. The concentrations of Pepsinogens A and C showed concomitant and variable but significant increases, and the Pepsinogen A, C ratio did not change during the 3-day course of omeprazole. The increments were also significantly correlated with the increase in fasting serum gastrin and with the reduction in pentagastrin stimulated acid output. The correlations were mainly due to the marked inhibition of gastric acid secretion and the corresponding increases in serum gastrin and Pepsinogens A and C in two subjects, as in the other 8 subjects the changes were only modest. There appears to be a relationship, therefore, between the degree of inhibition of acid by omeprazole and the parallel increases in both serum pepsinogens and fasting gastrin.
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1573-2568
    Keywords: prostaglandin E2 analog ; enprostil ; omeprazole ; gastrin ; pepsinogen A ; pepsinogen C
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract This study was undertaken to determine whether the synthetic prostaglandin E2 analog enprostil is able to inhibit basal and postprandial hypergastrinemia induced by omeprazole. We also studied the effect of omeprazole, enprostil, and the combination of both drugs on serum pepsinogen A and C levels. Eight normal subjects received in random order five-day courses of 40 mg omeprazole once a day, 35 µg enprostil three times a day, the combination of both drugs, and placebo. Omeprazole induced significant increases in basal and postprandial serum gastrin and in pepsinogen A and C levels. These increments persisted on the day after stopping treatment. Coadministration of enprostil inhibited omeprazole-induced basal hypergastrinemia and postprandial integrated serum gastrin, but not basal serum pepsinogen A and C, while the inhibition on the day after the treatment courses only reached statistical significance for the postprandial integrated serum gastrin concentration. It is concluded that enprostil inhibits omeprazole-induced basal and postprandial hypergastrinemia, with a tendency to protracted inhibition after stopping the drugs, and that enprostil does not significantly influence omeprazole-induced increases in pepsinogen A and C level. Coadministration of enprostil may be helpful in preventing pronounced hypergastrinemia in the few patients who show large serum gastrin increases during treatment with omeprazole.
    Type of Medium: Electronic Resource
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