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Biomedical subjects

P Christensen

Publications and source records attributed to P Christensen.

At least 37 records · Page 2Linked to original sources
PubMed2001

Harmonisation and dosimetric quality assurance in individual monitoring for external radiation.

The current situation amongst Member States is that there are widely differing national requirements for dosimetric services and for dosemeter performance. It is clear that with the free movement of workers within the European Union (EU) and the requirements for individual dosimetry given in Council Directive 96/29 EURATOM, a degree of harmonisation of requirements and procedures of EU Member States would be desirable. A EURADOS action group, made up of members from each of the EU Member States plus Switzerland, was set up with the overall objectives of consolidating within the EU the quality of individual monitoring using personal dosemeters and assisting movement towards harmonised procedures. An outline of the work of the action group is given and the term 'harmonisation' is discussed.

Europe↗
PubMed2000

GM-CSF regulates bleomycin-induced pulmonary fibrosis via a prostaglandin-dependent mechanism.

To characterize the role of GM-CSF in pulmonary fibrosis, we have studied bleomycin-induced fibrosis in wild-type mice vs mice with a targeted deletion of the GM-CSF gene (GM-CSF-/- mice). Without GM-CSF, pulmonary fibrosis was worse both histologically and quantitatively. These changes were not related to enhanced recruitment of inflammatory cells because wild-type and GM-CSF-/- mice recruited equivalent numbers of cells to the lung following bleomycin. Interestingly, recruitment of eosinophils was absent in GM-CSF-/- mice. We investigated whether the enhanced fibrotic response in GM-CSF-/- animals was due to a deficiency in an endogenous down-regulator of fibrogenesis. Analysis of whole lung homogenates from saline- or bleomycin-treated mice revealed that GM-CSF-/- animals had reduced levels of PGE2. Additionally, alveolar macrophages were harvested from wild-type and GM-CSF-/- mice that had been exposed to bleomycin. Although bleomycin treatment impaired the ability of alveolar macrophages from wild-type mice to synthesize PGE2, alveolar macrophages from GM-CSF-/- mice exhibited a significantly greater defect in PGE2 synthesis than did wild-type cells. Exogenous addition of GM-CSF to alveolar macrophages reversed the PGE2 synthesis defect in vitro. Administration of the PG synthesis inhibitor, indomethacin, to wild-type mice during the fibrogenic phase postbleomycin worsened the severity of fibrosis, implying a causal role for PGE2 deficiency in the evolution of the fibrotic lesion. These data demonstrate that GM-CSF deficiency results in enhanced fibrogenesis in bleomycin-induced pulmonary fibrosis and indicate that one mechanism for this effect is impaired production of the potent antifibrotic eicosanoid, PGE2.

Animals↗
PubMed2000

Antiemetic efficacy of combination therapy with granisetron plus prednisolone plus the dopamine D2 antagonist metopimazine during multiple cycles of moderately emetogenic chemotherapy in patients refractory to previous antiemetic therapy.

Effective antiemetic treatment of patients who have previously experienced chemotherapy-induced nausea and vomiting is difficult. The aim of this study was to evaluate the antiemetic efficacy of a single intravenous dose of granisetron plus a 3-day oral treatment with prednisolone 25 mg once a day plus metopimazine 30 mg four times a day in patients refractory to previous antiemetic treatment with granisetron or with prednisolone plus metopimazine. The study population was made up of 25 consecutive women with stage I or II breast cancer, who were treated with multiple cycles of adjuvant cyclophosphamide, fluorouracil plus methotrexate or cyclophosphamide, epirubicin plus fluorouracil given i.v. every 3 weeks. Patients received the three-drug combination of antiemetics during a total of 113 cycles of chemotherapy. No emetic episodes were reported in 88.9% cycles on day 1, in 94.7% cycles on days 2 through 5 and in 85.8% cycles on days 1 through 5 after chemotherapy. No nausea was reported in 43.4% cycles on day 1, in 49.6% cycles on days 2 through 5 and in 34.5% cycles on days 1 through 5. Nineteen patients (76.0%) completed the scheduled nine cycles of chemotherapy, 1 being withdrawn because of > or =5 emetic episodes and 5, because they were not satisfied with the antiemetic treatment. The treatment was well tolerated. In conclusion, granisetron plus prednisolone plus metopimazine is a highly effective antiemetic treatment in patients receiving moderately emetogenic chemotherapy refractory to antiemetic therapy with granisetron or prednisolone plus metopimazine.

Adult↗
PubMed2000

Neurogenic colorectal dysfunction - use of new antegrade and retrograde colonic wash-out methods.

OBJECTIVES: To evaluate results of the Enema Continence Catheter (ECC) and the Malone Antegrade Continence Enema (MACE) applied in patients with severe neurogenic colorectal dysfunction. METHODS: The ECC was offered to 21 patients (mean age 39.9, range 7 - 72 years). The MACE was used in eight patients (mean age 32.8 years, range 15 - 66 years). All patients still using the ECC or the MACE at follow-up were interviewed. Results from patients not available for follow-up were drawn from hospital records. RESULTS: Overall success with the ECC was found in 12 of 21 patients (57%). In patients with faecal incontinence, the ECC was successful in eight out of eleven patients (73%), while four out of ten patients (40%) with constipation were successfully treated. Overall success with the MACE was found in seven out of eight patients (87%). Successful treatment with the ECC or the MACE was followed by significant improvement in quality of life. CONCLUSION: The ECC is a simple therapeutic method in severe neurogenic colorectal dysfunction. If the ECC fails the MACE, as a minor and reversible operation, is a suitable alternative to more extensive procedures.

Adolescent↗
PubMed2000

Thermodilution versus inert gas rebreathing for estimation of effective pulmonary blood flow.

OBJECTIVE: To compare measurements of the effective pulmonary blood flow (Qep, i.e., nonshunted fraction of cardiac output, Qt) by the inert gas rebreathing (RB) method and the thermodilution (TD) technique in critically ill patients. DESIGN: Prospective, comparative study of a noninvasive method and an established invasive technique. SETTING: An 11-bed general intensive care unit in a university hospital. PATIENTS: A total of 14 critically ill patients, all mechanically ventilated and monitored with systemic and pulmonary artery catheters. MEASUREMENTS AND MAIN RESULTS: Qep was determined in duplicate by RB using a mass spectrometer for gas analysis. For each determination, Qt was measured in triplicate by the cold water bolus TD technique and averaged. Simultaneously mixed venous and arterial blood samples were analyzed to calculate the intrapulmonary shunt fraction and thereby convert estimates of Qt to Qep. Mean difference between paired estimates (RB - TD) was 0.01 L/min, so for differences was 1.19 L/min, and 95% confidence interval for the bias was -0.45 to 0.47 L/min. Coefficients of variation for repeated Qep estimates were 8% (RB) and 12% (TD), respectively. Coefficients of variation for RB estimates of functional residual capacity and lung tissue volume were 6% and 17%, respectively. CONCLUSIONS: The RB method is a promising method for simultaneous noninvasive estimation of Qep and functional residual capacity in mechanically ventilated patients. However, further investigations are needed to evaluate potential problems of the method before it can be recommended for clinical purposes.

Adult↗
PubMed1999

Cardiovascular, endocrine, and renal effects of urodilatin in normal humans.

Effects of urodilatin (5, 10, 20, and 40 ng. kg-1. min-1) infused over 2 h on separate study days were studied in eight normal subjects with use of a randomized, double-blind protocol. All doses decreased renal plasma flow (hippurate clearance, 13-37%) and increased fractional Li+ clearance (7-22%) and urinary Na+ excretion (by 30, 76, 136, and 99% at 5, 10, 20, and 40 ng. kg-1. min-1, respectively). Glomerular filtration rate did not increase significantly with any dose. The two lowest doses decreased cardiac output (7 and 16%) and stroke volume (10 and 20%) without changing mean arterial blood pressure and heart rate. The two highest doses elicited larger decreases in stroke volume (17 and 21%) but also decreased blood pressure (6 and 14%) and increased heart rate (15 and 38%), such that cardiac output remained unchanged. Hematocrit and plasma protein concentration increased with the three highest doses. The renin-angiotensin-aldosterone system was inhibited by the three lowest doses but activated by the hypotensive dose of 40 ng. kg-1. min-1. Plasma vasopressin increased by factors of up to 5 during infusion of the three highest doses. Atrial natriuretic peptide immunoreactivity (including urodilatin) and plasma cGMP increased dose dependently. The urinary excretion rate of albumin was elevated up to 15-fold (37 +/- 17 micrograms/min). Use of a newly developed assay revealed that baseline urinary urodilatin excretion rate was low (<10 pg/min) and that fractional excretion of urodilatin remained below 0.1%. The results indicate that even moderately natriuretic doses of urodilatin exert protracted effects on systemic hemodynamic, endocrine, and renal functions, including decreases in cardiac output and renal blood flow, without changes in arterial pressure or glomerular filtration rate, and that filtered urodilatin is almost completely removed by the renal tubules.

Absorption↗
PubMed1998

Tachykinins mediate changes in ion transport in porcine jejunum through release of prostaglandins and neurotransmitters.

In the present study, we investigated the mediators involved in substance P (SP) and neurokinin A (NKA) induced ion transport. Stripped preparations of porcine jejunal tissue were mounted in Ussing-chambers and short-circuited. The cyclo-oxygenase inhibitor, piroxicam (10 microM) and the neuronal conduction blocker, tetrodotoxin (TTX) (0.1 microM) both significantly decreased the SP (0.1 microM) (66% and 36%, respectively) and NKA (1 microM) (64% and 31%, respectively) induced increase in short-circuit current (SCC). Pretreatment with both piroxicam and TTX totally abolished the SP and NKA response. SP (0.1 microM) caused a significant release of prostaglandin E2 (PGE2), whereas the release of PGE2 induced by NKA was not significant. Experiments were performed to clarify if vasoactive intestinal polypeptide (VIP) was mediating SP or NKA responses. VIP caused a TTX-insensitive and a concentration-dependent increase in SCC. Two VIP antagonists did not change the response to VIP (10 nM and 0.1 microM). Thus, these antagonists could not be used to further elucidate the role of VIP. We were unable to measure a significant release of VIP after SP or NKA treatment. These results indicate, that SP and NKA regulate ion transport in porcine jejunum, entirely through the release of prostaglandins and enteric neurotransmitters.

Animals↗
PubMed1998

Effects of receptor blockade on metabolism and renal actions of vasopressin in conscious dogs.

Vasopressin--but not the V2 receptor agonist [deamino-cis1,D-Arg8]-vasopressin (dDAVP)--may mediate natriuresis in dogs. The present study investigated this phenomenon by use of nonpeptide antagonists to V1a and V2 receptors 1-¿1-[4-(3-acetylaminopropoxy)benzoyl]-4-piperidyl¿-3,4-dihydro-2 (1H)-quinolinone (OPC-21268) and 5-dimethylamino-1-¿4-(2-methylbenzoylamino)-benzoyl¿-2,3,4,5-tetra hydro-1 H-benzazepine (OPC-31260), respectively) hypothesising that only V1a inhibition would reduce the natriuresis. In conscious dogs vasopressin secretion was suppressed by water loading (2% body weight) and replaced by infusion of vasopressin (50 pg min-1 kg-1) resulting in physiological plasma concentrations (plasma levels of AVP (pAVP) = 2.0 +/- 0.1 pg mL-1). In this setting, OPC-21268 did not change the rate of sodium excretion. OPC-31260 increased water excretion 12-fold without significant changes in sodium excretion. Heart rate, mean arterial blood pressure, glomerular filtration rate, and clearance of endogenous Li+ were unchanged. During vasopressin infusion, both antagonists increased pAVP, OPC-21268 by 20% and OPC-31260 by 100% (2.0 +/- 0.2-4.0 +/- 0.3 pg mL-1). In the absence of vasopressin infusion, OPC-31260 did not increase pAVP. Thus, the increase in pAVP appeared to be due to a decrease in metabolic clearance rate. The results indicate that the present dose of V1a receptor inhibitor OPC-21268 does not reduce sodium excretion and that both vasopressin antagonists inhibit vasopressin metabolism.

Animals↗
PubMed1998

Mechanism of vasopressin natriuresis in the dog: role of vasopressin receptors and prostaglandins.

Renal effects of physiological amounts of vasopressin were studied in conscious dogs during servocontrolled overhydration (2% body wt). During infusion of vasopressin (50 pg . min-1 . kg body wt-1), plasma vasopressin concentration increased to 2.30 +/- 0.20 pg/ml compared with 0.12 +/- 0.03 pg/ml during control (water diuresis). With vasopressin infusion, urine flow was significantly lower (0.30 +/- 0.10 ml/min) and sodium excretion (UNaV) was significantly higher (58.0 +/- 15.8 micromol/min) than without vasopressin (4.6 +/- 0.4 ml/min and 14.4 +/- 4.1 micromol/min, respectively). Deamino-[Cys1,D-Arg8]vasopressin, a V2 receptor agonist (4 pg . min-1 . kg-1), mimicked the antidiuretic response (0.20 +/- 0.03 ml/min) without changing UNaV (9.7 +/- 4.4 micromol/min). Indomethacin given during arginine vasopressin (AVP) infusion suppressed prostaglandin E2 excretion, intensified the antidiuresis (0.10 +/- 0.02 ml/min), and abolished the natriuresis (13.4 +/- 3.7 micromol/min). During AVP infusion, UNaV was highly correlated (r = 0.85) with prostaglandin E2 excretion. Blood pressure, glomerular filtration rate, plasma atrial natriuretic peptide concentration, and the rate of proximal tubule reabsorption (derived from lithium clearance) were similar in all series. The data indicate that, in the dog, physiological amounts of vasopressin can induce natriuresis, probably through activation of non-V2 receptors and the intrarenal synthesis of prostaglandins.

Animals↗
PubMed1998

Osmoregulatory control of renal sodium excretion after sodium loading in humans.

The hypothesis that renal sodium handling is controlled by changes in plasma sodium concentration was tested in seated volunteers. A standard salt load (3.08 mmol/kg body wt over 120 min) was administered as 0.9% saline (Isot) or as 5% saline (Hypr) after 4 days of constant sodium intake of 75 (LoNa+) or 300 mmol/day (HiNa+). Hypr increased plasma sodium by approximately 4 mmol/l but increased plasma volume and central venous pressure significantly less than Isot irrespective of diet. After LoNa+, Hypr induced a smaller increase in sodium excretion than Isot (48 +/- 8 vs. 110 +/- 17 micromol/min). However, after HiNa+ the corresponding natriureses were identical (135 +/- 33 vs. 139 +/- 39 micromol/min), despite significant difference between the increases in central venous pressure. Decreases in plasma ANG II concentrations of 23-52% were inversely related to sodium excretion. Mean arterial pressure, plasma oxytocin and atrial natriuretic peptide concentrations, and urinary excretion rates of endothelin-1 and urodilatin remained unchanged. The results indicate that an increase in plasma sodium may contribute to the natriuresis of salt loading when salt intake is high, supporting the hypothesis that osmostimulated natriuresis is dependent on sodium balance in normal seated humans.

Adult↗