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Biomedical subjects

O Wagner

Publications and source records attributed to O Wagner.

At least 73 records · Page 4Linked to original sources
PubMed1996

Big endothelin in patients with complicated Plasmodium falciparum malaria.

Plasma concentrations of big endothelin-1 were determined by ELISA in 18 patients with complicated Plasmodium falciparum malaria in Bangkok. Before therapy, elevated levels were recorded (21 +/- 12 vs. 2.9 +/- 1.1 pmol/L in age- and sex-matched healthy subjects; P < .001). Even 7 days after therapy, elevated concentrations were seen (25 +/- 14 pmol/L). Plasma endothelin levels were correlated with levels of tumor necrosis factor-alpha (r = .632, P < .01), and a negative correlation with platelet counts was seen (r = .783, P < .005). No relation between plasma endothelin concentrations and parasitemia, fever, or other indices of severe infection (hypotension, renal, hepatic or pulmonary impairment, cerebral malaria) existed. During and after complicated malaria, increased levels of plasma endothelin could contribute to malarial pathology or reflect endothelial damage or both.

Antimalarials↗
PubMed1996

Anterior pituitary function in patients with newly diagnosed rheumatoid arthritis.

Hormonal dysfunction involving the hypothalamic-pituitary-adrenal (HPA) axis, prolactin (PRL) secretion and sex hormone status has been supposed to contribute to the development or persistence of rheumatoid arthritis (RA). In addition, a reduced number of glucocorticoid receptors on circulating lymphocytes has been found in patients with RA. However, so far most studies have been performed in pre-treated patients. A combined test for total anterior pituitary reserve was performed in 10 patients with newly diagnosed untreated RA. Before and after stimulation with the respective hypothalamic releasing hormones, RA patients showed no difference in plasma concentrations of adrenocorticotrophic hormone (ACTH), cortisol, prolactin (PRL) and thyroid-stimulating hormone (TSH) when compared to healthy controls. In contrast, the growth hormone (GH) response to growth hormone-releasing hormone (GHRH) was blunted in RA patients. The hypothalamic-pituitary-thyroid/gonadal and adrenal axes seem to be unaltered in RA. However, if one considers the presence of chronic inflammation, normal plasma ACTH and cortisol concentrations must be considered as inappropriately low. The observed blunted GH release could be mediated by cytokines (e.g. IL-1), which are known to be elevated in RA.

Adrenocorticotropic Hormone↗
PubMed1996

Influence of angiotensin II on circulating adhesion molecules and blood leukocyte count in vivo.

The mechanism of the beneficial effect of angiotensin converting enzyme inhibitors in patients with myocardial infarction is not clear. Recent in vitro data indicate that angiotensin II (AII) stimulates the expression of adhesion molecules and thus activates leukocyte endothelial interactions. In eight healthy volunteers we investigated the influence of exogenous AII on circulating adhesion molecules and on the blood leukocyte count. A systemically effective and a systemically ineffective dose of AII were administered intravenously over 4 h in a single blind crossover design. Examination of the time course of circulating intercellular and vascular adhesion molecules and E-selectin (cICAM-1, cVCAM-1, cE-selectin-1) in response to the AII infusion revealed increases of up to 11% (especially in cVCAM-1 levels) at single time points, but no significant sustained elevation or trend that can be interpreted as a drug-induced effect. The systemically effective dose, which induced an increase in mean arterial blood pressure from 80 to 108 mmHg (1 mmHg = 133.3 Pa), resulted in a significant increase in blood leukocytes, from 4.8 +/- 0.3 to 5.5 +/- 0.3 g/L (p < 0.05); the systemically ineffective AII dose did not alter blood leukocyte count significantly. Although we did not find an influence of AII on circulating adhesion molecules in vivo, we observed an increase in the blood leukocyte count; thus it may be intriguing to assess whether renin-angiotensin system modulating drugs might exert their favorable effect in ischemic diseases at least in part via an influence on leukocytes.

Adult↗
PubMed1995

Effects of cisplatin on urinary thromboxane B2 excretion.

PURPOSE: Thromboxane A2 (TxA2) is implicated in the pathogenesis of various forms of drug-induced renal damage. Based on previous functional studies, we postulated that cis-dichlorodiammineplatinum (cisplatin) induces intrarenal TxA2 synthesis. To test this hypothesis, we measured urinary excretion of thromboxane B2 (TxB2), the stable inactive metabolite of TxA2, during and after cisplatin administration. PATIENTS AND METHODS: The study included 16 patients with malignant disease who were scheduled to receive cisplatin (100 mg/m2) and 11 healthy subjects who received the same amount of fluid loading and the same concomitant medication as the patients but no cisplatin. Total urine output was collected in seven intervals from 24 hours before until 72 hours after the start of prehydration. Urinary immunoreactive TxB2 was measured. RESULTS: There was a marked increase (4.5 +/- 1.6-fold; mean +/- SEM) in urinary TxB2 excretion in patients during and immediately after cisplatin infusion. This increase was significant compared with baseline and the control group. CONCLUSION: High-dose cisplatin causes an acute increase in urinary excretion of TxB2. This likely represents enhanced intrarenal synthesis of TxA2, in response to an acute damaging effect of cisplatin on the kidneys. These findings warrant further studies to evaluate the renoprotective effect of anti-TxA2 intervention in patients receiving high-dose cisplatin.

Acetylglucosaminidase↗
PubMed1995

Stress response to tracheal intubation: direct laryngoscopy compared with blind oral intubation.

Haemodynamic and hormonal responses to tracheal intubation can be profound and associated with serious cardiovascular and cerebral side effects. The Augustine Guide, a device enabling blind oral intubation, has been introduced recently. The aim of our study was to compare the haemodynamic and hormonal stress response of this method with direct laryngoscopy. Thirty five patients (ASA 1 and 2) were randomly assigned to undergo either direct laryngoscopy (n = 17), or blind oral intubation (n = 18). Haemodynamic responses and concentrations of adrenaline, noradrenaline and prolactin were determined prior to induction, before intubation and 5 min after intubation. The median duration of intubation was 22s for direct laryngoscopy vs 46s for blind oral intubation (p < 0.05). Between the groups, no significant differences were observed for heart rate, systolic or mean arterial blood pressure. Serum levels of adrenaline decreased slightly after induction and remained unaltered after intubation in both groups. Noradrenaline (1.01 vs 0.66 nmol.l-1) and prolactin (5.2 vs 2.9 nmol.l-1) levels were significantly higher after direct laryngoscopy compared to blind oral intubation. Although blind oral intubation took significantly longer to perform than direct laryngoscopy, hormonal stress response was less pronounced. Blind oral intubation should therefore not be withheld from patients with impaired cardiovascular reserve.

Adolescent↗
PubMed1995

Metabolic effect of sodium selenite: insulin-like inhibition of glucagon-stimulated glycogenolysis in the isolated perfused rat liver.

Selenium, an essential trace element, has been shown to decrease plasma glucose concentrations of diabetic rats. To study the short-term effects of selenium on hepatic carbohydrate metabolism, isolated perfused livers of fed Sprague-Dawley rats were continuously infused with sodium selenite for 90 minutes. This resulted in an immediate elevation of selenium in the effluent perfusate (3.3 +/- 0.1, 16.1 +/- 0.4, 30.3 +/- 1.6, and 118.9 +/- 0.8 mumol/L at infusion of 10, 50, 100, and 500 mumol/L sodium selenite, respectively). Basal hepatic glucose production decreased in a dose-dependent manner within 60 minutes of low-dose sodium selenite infusion (10: 0.60 +/- 0.20, 50: 0.21 +/- 0.40, and 100 mumol/L: 0.21 +/- 0.09 mumol.min-1.g-1 liver; P < .05 vs. zero time), while it was transiently increased by 500 mumol/L sodium selenite (1.11 +/- 0.18 mumol.min-1.g-1 liver; P < .05). Glucagon-stimulated glycogenolysis was suppressed by 50% (P < .05) at 1.8 nmol/L insulin and by 90% (P < .001) at 10 mumol/L sodium selenite. That selenium concentration did not affect glutathione peroxidase activities in liver and perfusate erythrocytes within 60 minutes. Toxic effects of high-dose selenite (500 mumol/L), but not of low-dose selenite (10 mumol/L) infusion, were indicated by increased hepatic glucose (P < .05), lactate (P < .01), and lactate dehydrogenase (P < .001) release as well as histologically by degeneration and necrosis of periportal hepatocytes. In conclusion, low-dose selenite exerts a potent insulinlike effect on hepatic glycogenolysis in vitro by counteracting glucagon action, whereas high-dose selenite may severely impair liver function.

Animals↗
PubMed1994

Stimulation of endothelin-1 production by thrombin, but lack of interference by high ambient glucose in vitro.

Diabetic vascular disease is associated with a state of hypercoagulability and altered endothelial properties, leading to elevated plasma levels of endothelium-derived peptides and proteins, e.g. endothelin-1, von Willebrand factor or fibronectin. This study determined dynamic immunoreactive endothelin-1 secretion by human umbilical vein endothelial cells exposed to thrombin (5 x 10(6) mU/l) in the presence (40 mmol/l) and absence (5.5 mmol/l) of excessive glucose in the cell culture medium. Exposure to high glucose and thrombin concentrations was initiated after cell confluency and applied for 24 h for measurements of endothelin-1 and for 2 and 5 h for the determination of preproendothelin-1, von Willebrand factor and fibronectin messenger ribonucleic acid. Comparisons were made versus cells incubated with normal glucose concentrations or with high mannose or NaCl concentrations as osmotic control. Neither preproendothelin-1, fibronectin and von Willebrand factor messenger ribonucleic acid expression nor endothelin-1 release was affected by high concentrations of glucose, mannose or sodium chloride.

Cells, Cultured↗
PubMed1993

Determinants of survival after rodent cardiac arrest: implications for therapy with adrenergic agents.

Coronary perfusion pressure and its relation with the expired carbon dioxide concentration (end-tidal CO2) was examined in a rodent model of sustained ventricular fibrillation and subsequent cardiopulmonary resuscitation. Equipressor dosages of the pure alpha 1-agonist methoxamine, the mixed alpha/beta-agonists epinephrine and norepinephrine were randomly compared with 0.9% NaCl. Thirty two Sprague-Dawley rats were anesthetized and catheters were advanced into the aorta, right ventricle, right atrium and inferior vena cava. After 4 min of untreated ventricular fibrillation external chest compression was initiated and defibrillation was attempted after 8 min. Drugs were infused for 3 min during cardiopulmonary resuscitation into the inferior vena cava. A 60-min survival period followed methoxamine administration in 7 of 8 (P < 0.019 vs. NaCl), after epinephrine in 4 of 8, after norepinephrine in 5 of 8, and after NaCl in only 2 of 8 animals. Resuscitation success was determined by coronary perfusion and mean aortic pressures generated during cardiopulmonary resuscitation but not by arterial or venous blood gases. Adrenergic agents increased coronary perfusion and mean aortic pressures but decreased end-tidal CO2 which failed to correlate with these pressures. Accordingly, alpha-adrenergic agents mitigated the accuracy of end-tidal CO2 as a non-invasive hemodynamic monitor and predictor of survival after rodent cardiopulmonary resuscitation.

Acid-Base Equilibrium↗
PubMed1993

Coronary perfusion pressure, end-tidal CO2 and adrenergic agents in haemodynamic stable rats.

Coronary perfusion pressure (CPP) determines myocardial perfusion during low flow. CPP correlates with end-tidal CO2 (PetCO2) during cardiac arrest. Recent studies have demonstrated that after adrenaline, increased CPP was associated with decreased PetCO2. Intravenous infusions (4 min, N = 10) or bolus (10 s, N = 6) of methoxamine (60 micrograms/kg), isoproterenol (10 micrograms/kg), adrenaline and noradrenaline (3 micrograms/kg) were compared with saline placebo (0.2 ml/min) during spontaneous circulation in anaesthetized Sprague-Dawley rats. Infusion and bolus of methoxamine, adrenaline and noradrenaline increased CPP between 39 and 46% above baseline. Isoproterenol decreased CPP by 67%. PetCO2 decreased by 27% after bolus and only 10% after infusion of methoxamine but increased after infusion (7%) and bolus (10%) of isoproterenol and after infusion of adrenaline (11%) and noradrenaline (17%). Equipressor bolus of methoxamine, adrenaline and noradrenaline reduced PetCO2 between 10 and 27%. Bolus application induced more alpha-effects and drug infusion more beta-effects in the pulmonary vasculature. Thus, changes in pulmonary vascular resistance and associated increases in dead space were responsible for differences in PetCO2. Alpha-effects increased CPP, decreased P(et)CO2 and conversely, beta-effects decreased CPP but increased PetCO2 indicating caution when P(et)CO2 is used as non-invasive monitor of perfusion, especially after alpha-adrenergic agents.

Animals↗
PubMed1992

Clinical evaluation of a new lipid-based delivery system for intravenous administration of amphotericin B.

In a retrospective study a new lipid-based delivery system for administration of amphotericin B was evaluated in 26 treatment courses in 22 patients. Amphotericin B was given by infusion diluted in either the lipid solution (1 mg/kg/d; 13 courses) or dextrose (0.92 mg/kg/d; 13 courses). No differences were noted in the serum pharmacokinetics. Fever or rigors were observed in 6 of 13 courses in the conventional amphotericin B group versus none in the lipid amphotericin B group (p = 0.007). Four of 13 courses of treatment were discontinued due to adverse effects in the conventional amphotericin B group compared to none in the other group (p = 0.048). In the lipid amphotericin B group the decrease in creatinine clearance was significantly lower on the fourth day of treatment (p = 0.04) and significantly fewer patients had a decrease of more than 25% in creatinine clearance on the sixth day (4/12 vs 9/11 p = 0.02). These preliminary findings suggest that this lipid amphotericin B formulation is well tolerated with few nephrotoxic effects.

Adult↗
PubMed1992

Adenosine during cardiac arrest and cardiopulmonary resuscitation: a placebo-controlled, randomized trial.

UNLABELLED: BACKGROUND AND HYPOTHESIS TESTED: The effects of adenosine (100 micrograms/kg/min; n = 7) were examined during rodent cardiopulmonary resuscitation (CPR). Change in coronary artery perfusion pressure, end-tidal PCO2, and arterial acid-base status of anesthetized, male, Sprague-Dawley rats were compared with CPR controls (0.9% sodium chloride; n = 7) and with sham controls (n = 9). Sustained ventricular fibrillation was induced and precordial chest compression was followed by defibrillation. RESULTS: After 6 mins of cardiac arrest, six (86%) of seven adenosine-treated animals were resuscitated after adenosine infusion and four (57%) of seven control animals were resuscitated after sodium chloride infusion. During chest compression, coronary artery perfusion pressure was 7 +/- 2 mm Hg after adenosine, but was 22 +/- 3 mm Hg in the controls (p less than .01). Parallel decreases were observed in mean aortic pressure. Arterial and end-tidal PCO2 significantly (p less than .01) decreased after adenosine. These changes contrasted with a second control group of nine identically prepared animals which, in the absence of ventricular fibrillation and subsequent chest compression, demonstrated no changes in hemodynamic, respiratory, or blood gas variables. CONCLUSIONS: Adenosine decreased coronary artery perfusion pressure. However, despite marked reductions in coronary artery perfusion pressure, survival was not compromised after adenosine infusion in this rodent model of CPR.

Acid-Base Equilibrium↗
PubMed1991

Arterial baroreflex sensitivity and blood pressure variabilities before and after carotid surgery.

Carotid surgery is frequently associated with postoperative blood pressure alterations. The role of baroreceptors with regard to these alterations was assessed in 50 patients by determining the pre- and postoperative mechanoreceptor sensitivity after Valsalva maneuver and intravenous injections of angiotensin and nitroglycerine as described by Smyth, Sleight and Pickering. In addition, blood pressure was monitored perioperatively and renin and aldosterone levels were measured. In patients with arterial hypertension a postoperative increase of receptor reactivity can be seen necessitating a reduction of antihypertensive therapy in more than 50% of cases. In normotensive patients no uniform response can be observed. A possible explanation for this effect might be the local increase of pressure in the operated vascular segment. The postoperative reintegration of receptor areas which had been adjusted to a reduced pressure level might induce a more sensitive response than can be seen for the remaining receptors, which usually are less responsive in hypertensive patients.

Aged↗