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  • Articles: DFG German National Licenses  (12)
  • Cardiac output  (5)
  • pancreatic polypeptide  (4)
  • omeprazole  (3)
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  • Articles: DFG German National Licenses  (12)
Material
Years
  • 1
    ISSN: 1432-0428
    Keywords: Islet of Langerhans ; transplantation ; metabolism ; dog ; glucose-dependent insulinotropic polypeptide ; pancreatic polypeptide
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Successful transplantation of isolated islets of Langerhans has been reported in large mammals, including man, but metabolic control has not been well-established. We studied the glucose and islet hormone response to fasting, i. v. glucose bolus infusion, i.v. arginine bolus infusion during a 35-mmol/l hyperglycaemic clamp, mixed meals, and i. v. insulin-induced hypoglycaemia up to 3 years after intrasplenic islet autotransplantation in six pancreatectomised dogs. The individual postprandial insulinogenic index (ratio of 2-h postprandial insulin to glucose levels) at 1 month post-transplant, predicted (r=0.99) the time to functional graft failure (6–175 weeks). Metabolic studies at 6 months post-transplant in four dogs demonstrated normal fasting glucose and hormone levels, except for reduced pancreatic polypeptide levels. Intravenous glucose and arginine-stimulated insulin were reduced to 15% of preoperative values. In contrast, postprandial normoin-sulinaemia was observed — albeit with moderate hyperglycaemia (approximately 10 mmol/l). Postprandial glucagon and glucose-dependent insulinotropic polypeptide (GIP) had increased. Comparison of the post-transplant insulin responses to a meal and to intravenous challenges demonstrated maximal stimulation of the graft by the meal. Post-transplant pancreatic polypeptide responses to a meal and i.v. arginine were severely reduced, and no pancreatic polypeptide response to i.v. insulin-induced hypoglycaemia was observed — indicating absence of cholinergic reinnervation. Thus, glucose regulation and both the insulin secretory capacity and life expectancy of islet grafts were best documented by meal testing. Tentatively, a postprandial hyperglycaemia-enhanced incretin effect of glucose-dependent insulinotropic polypeptide and other gut hormones may account for the difference in the insulin response to i. v. glucose and a meal. Aside from the reduced insulin secretory capacity, both a deranged pulsatile delivery of insulin, hyperglucagonaemia, and pancreatic polypeptide deficiency may have been conducive to glucose intolerance.
    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: 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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  • 3
    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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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Intensive care medicine 12 (1986), S. 71-79 
    ISSN: 1432-1238
    Keywords: Cardiac output ; Flow modulation ; Mechanical ventilation ; Thermodilution method
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The reliability of cardiac output estimation by thermodilution during artificial ventilation was studied in anesthetized pigs at the right side of the heart. The estimates exhibited a cyclic modulation related to the ventilation. The amplitude of the modulation was independent of the level of positive end-expiratory pressure, ventilatory pattern and volemic loading of the animals. However, a non-constant phase relation existed between the ventilatory cycle and the modulation. Single observations at a fixed moment in the ventilatory cycle are therefore not appropriate for estimation of mean cardiac output nor for studying its relative changes. The averaging of estimates spread equally over the ventilatory cycle led to a much larger reduction in the deviation of the averages from the mean cardiac output than an averaging procedure of randomly selected estimates. The accracy of estimation of mean cardiac output by two estimates equally spread in the ventilatory cycle was equal to the accuracy obtained by averaging five randomly selected estimates. Averaging four estimates, equally spread in the cycle, appeared to be the optimal procedure. For 89% of all averages an accuracy of 5% around the mean was obtained and for 99% an accuracy of ±10%.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1432-1238
    Keywords: Cardiac output ; Mechanical ventilation ; Multiple injections ; Thermodilution
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The application of the thermodilution method in conditions associated with variations in blood flow implies a misuse of the Stewart Hamilton equation. Therefore, we studied the reliability of the thermodilution method for the estimation of mean cardiac output (CO) during mechanical ventilation in patients (n=9). Variation of the injection moment in the ventilatory cycle elicited a cyclic variation of CO estimates. This variation was not the same for all patients neither in phase nor in amplitude. Therefore, no specific phase in the ventilatory cycle could be selected for an accurate estimation of mean CO. Averaging CO estimates randomly distributed in the ventilatory cycle led to an improvement of accuracy with the square root of the number of observations. The averaging of CO estimates spread equally over the ventilatory cycle led to a much better result, e.g., the variation in the average of two estimates equally spread in the ventilatory cycle was similar to the variation in the average of four random estimates. We conclude that averaging of 3 or 4 estimates spread equally over the ventilatory cycle is an adequate strategy to estimate mean cardiac output in patients reliably.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Intensive care medicine 21 (1995), S. 1009-1015 
    ISSN: 1432-1238
    Keywords: Alternating ventilation ; Cardiac output ; Central venous pressure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Objective We tested whether alternating ventilation (AV) of each lung (i.e. with a phase difference of half a ventilatory cycle) would decrease central venous pressure and so increase cardiac output when compared with simultaneous ventilation (SV) of both lungs. Theory If, during AV, the inflated lung expands partly via compression of the opposite lung, mean lung volume will be smaller during AV than SV. As a consequence, mean intrathoracic pressure (as cited in the literature), and therefore, central venous pressure will be smaller. Design The experiments were performed in seven anaesthetized and paralyzed piglets using a double-piston ventilator. Minute ventilation was the same during AV and SV. Starting at SV, we alternated three times between AV and SV for periods of 10 min. Results During AV, central venous pressure was decreased by 0.7 mmHg and cardiac output was increased by 10±4.4% (mean, ±SD) compared with SV. AV also resulted in increased arterial pressure. During one-sided inflation with closed outlet of the opposite lung, a pressure rise occurred in the opposite lung, indicating compression. Conclusion The higher cardiac output during AV than SV can be explained by the fact that central venous pressure is lower during AV. This lower central venous pressure is very probably due to the lower mean intrathoracic pressure caused by compression of the opposite lung during unilateral inflation.
    Type of Medium: Electronic Resource
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  • 7
    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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  • 8
    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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  • 9
    ISSN: 1573-2568
    Keywords: hyperglycemia ; amino acids ; parenteral nutrition ; gallbladder motility ; cholecystokinin ; pancreatic polypeptide
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The present study was undertaken to investigate the effect of acute hyperglycemia on the gallbladder contraction induced by intravenous administration of high doses of amino acids (Vamin 18, 250 mg protein/kg/hr). Six healthy volunteers were studied in random order on two occasions during normoglycemia and hyperglycemia with blood glucose levels stabilized at 15 mmol/liter. Gallbladder volumes, measured with ultrasonography, were studied for 60 min before and for 120 min during intravenous infusion of amino acids (IVAA). Administration of IVAA resulted in a significant reduction (P〈0.05) in gallbladder volume from 32±5 cm3 to 17±2 cm3 during normolgycemia. During hyperglycemia no significant changes in gallbladder volume were observed in response to IVAA. No significant changes in plasma CCK concentration, the major hormonal stimulus for gallbladder contraction, occurred in response to IVAA. During hyperglycemia, pancreatic polypeptide (PP) secretion, as an indirect measure of vagal cholinergic tone, in response to IVAA was significantly (P〈0.05) reduced compared to normoglycemia. It is concluded that: (1) administration of high doses of IVAA results in significant gallbladder contraction, (2) high doses of IVAA do not stimulate CCK secretion, (3) acute hyperglycemia inhibits IVAA-induced gallbladder contraction, and (4) acute hyperglycemia inhibits basal and stimulated plasma PP secretion, suggesting impaired vagal-cholinergic tone during hyperglycemia.
    Type of Medium: Electronic Resource
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  • 10
    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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