bluuebunny/crossref_metadata_2025_split huggingface dataset:
Blood flow to the haemopoietic bone marrow
Authors: IVERSEN P. O. 
Published: October 2003

IVERSEN, P. O. 1997. Blood flow to the haemopoietic bone marrow. Acta Physiol Scand159, 269–276. Received 25 September 1996, accepted 14 October 1996. ISSN 0001–6772. Department of Physiology, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway.In order to maintain an adequate haemopoiesis, the bone marrow is dependent on a sufficient blood supply. Our understanding of the regulation of marrow perfusion remained patchy for several decades, mainly because of technological difficulties. Recent advances in methodology have permitted more detailed analyses of bone marrow perfusion.Enhanced stimulation of erythropoietic or leucopoietic activity leads to increased blood flow to the bone marrow. There is evidence that this vasodilatory effect is mediated by the cytokines erythropoietin and granulocyte colony‐stimulating factor; however, a direct link has yet to be firmly established. The presence of receptors for several other cytokines on vascular endothelial and smooth muscle cells suggests that these may also have a regulatory role. The vasodilating factor nitric oxide (NO) regulates bone marrow blood flow both under normal conditions and during accelerated haemopoiesis, and NO is possibly induced via activation of cytokine receptors. There are conflicting reports as to how catecholamines affect marrow vascular tone. Although there is firm evidence that the bone marrow vasculature is innervated, no definite role of this innervation in vasoregulation has been documented.Advances in bone marrow/blood stem cell transplantation technology and the development of other therapeutic strategies for bone marrow failure may in part be dependent on optimization of the blood supply to the haemopoietic bone marrow.
Effects of reduced muscle temperature on the oxygen uptake kinetics at the start of exercise
Authors: SHIOJIRI T. , SHIBASAKI M. , AOKI K. , KONDO N. , KOGA S. 
Published: October 2003

SHIOJIRI, T., SHIBASAKI, M., AOKI, K., KONDO, N. & KOGA, S. 1997. Effects of reduced muscle temperature on the oxygen uptake kinetics at the start of exercise. Acta Physiol Scand 159, 327–333. Received 25 September 1995, accepted 5 November 1996. ISSN 0001–6772. Laboratory of Exercise and Sports Science, Yokohama City University; Division of Intelligence Science, Graduate School and Technology, Division of Education, Graduate School, Faculty of Human Development, Kobe University; and Applied Physiology Laboratory, Kobe Design University, Japan.The purpose of this study was to examine the effects of reduced muscle temperature (Tm ) on gas exchange kinetics and haemodynamics at the start of exercise. Six male subjects performed moderate cycle exercise under reduced (C) and normal (N) Tm conditions. Tm and rectal temperature were significantly reduced by immersion in cold water (by 6.6 °C and 1.8 °C, respectively). The increases in oxygen uptake (V˙o2) and oxygen pulse (V˙o2/HR) during phase 1 (abrupt increase after the start of exercise) were significantly lower under C than under N. The time constant for O2 under C (36.0 ± 7.7 (SD) s) was significantly greater than under N (27.5 ± 4.4 s); however, the time constants of cardiac output under C (38.3 ± 16.6 s) and N (33.7 ± 18.5 s) were similar. These results suggest that the slower V˙o2 on‐response under reduced Tm conditions is caused by decreased O2 extraction in working muscle and/or by impairment of oxidative reactions by reduced muscle temperature.
Mechanisms of cutaneous vasoconstriction during upright posture
Authors: VISSING S. F. , SECHER N. H. , VICTOR R. G. 
Published: October 2003

The cutaneous circulation is thought to participate in the neurocirculatory adjustments during orthostatic stress, but the underlying mechanisms mediating such reflex cutaneous vasoconstriction are poorly understood. The aim of this study was to assess the relative importance of baroreceptor (cardiopulmonary and arterial) and positional (vestibular, exercise, veno‐arteriolar and myogenic) reflexes in triggering cutaneous vasoconstriction during upright posture.First, hypotensive lower body negative pressure (LBNP) was compared with actual postural changes to assess the relative contributions of baroreceptor reflexes and positional reflexes. Then changes in body position were compared with changes in limb position in the absence or presence of proximal (axillary) or distal (local cutaneous) nerve blocks, to assess the relative contributions of vestibular, exercise, veno‐arteriolar and myogenic reflexes. Skin sympathetic nerve activity was determined by microneurography, and skin blood flow was determined by laser Doppler velocimetry.LBNP of –50 mmHg (cardiopulmonary + arterial baroreceptors) had no effect on skin sympathetic nerve activity or skin vascular resistance. In contrast, an upright posture with the arms dependent (baroreceptor+vestibular+exercise+veno‐arteriolar reflexes) caused a two‐ to threefold increase in skin vascular resistance. In the supine position, passive movement of the arm into a dependent position to activate veno‐arteriolar reflexes alone evoked an increase in skin vascular resistance which approximated the response to normal upright posture.Blocking central sympathetic nerve impulses by application of an axillary blockade did not influence the cutaneous vasoconstrictor response to an upright posture or changes in limb position. In contrast, application of a distal nerve block by local cutaneous surface anaesthesia completely blocked vasoconstrictor responses evoked by these manoeuvres.In conclusion, these experiments in human subjects identify a primary role for veno‐arteriolar reflexes in triggering vasoconstriction in the cutaneous circulation during upright posture.
Influence of sympathetic stimulation on the mechanical properties of the aorta in humans
Authors: SONESSON B. , VERNERSSON E. , HANSEN F. , LÄNNE T. 
Published: October 2003

The mechanical properties of the aorta play a major role in the regulation of blood pressure and cardiac performance. The effect of sympathetic stimulation on the mechanical properties of the human abdominal aorta was studied in 19 healthy volunteers, divided into young (25±2 years) and elderly individuals (69±2 years) of both sexes. A non‐invasive ultrasonic echo‐tracking system for measurement of systolic/diastolic variation of aortic diameter in combination with intra‐aortic pressure measurements was used to determine wall mechanics. The pressure–diameter (P–D) relationship and the distensibility indices, stiffness (β) and pressure strain elastic modulus (Ep) of the abdominal aorta were obtained. Measurements were made at rest and during sympathetic stimulation induced by lower body negative pressure (LBNP).As a sign of sympathetic activation, the peripheral resistance increased by 74–96% (P<0.001) during LBNP. However, the mechanical properties of the abdominal aorta remained unaltered, as estimated either from the P–D relationship or from the indices Ep and β, both in the young (rest: Ep=0.53±0.18, β=4.5±1.5; LBNP: Ep=0.51±0.15, β=4.5 ±1.2, NS) and in the elderly (rest: Ep=2.17±0.70, β=17.6 ±5.8; LBNP: Ep=2.11±0.60, β=16.9±3.9, NS).In conclusion, this investigation shows that LBNP‐induced sympathetic activation does not change aortic wall mechanics. Thus, sympathetic modulation of the aortic smooth muscle contractile activity seems to be unimportant in the blood pressure regulation.
Gender and age differences in transthoracic bioimpedance
Authors: METRY G. , WIKSTRÖM B. , LINDE T. , DANIELSON B. G. 
Published: October 2003

Thoracic impedance consists of a constant baseline component Z0 and a time‐variable component ΔZ which represents the impedance change related to the cardiac cycle. The maximum part of ΔZ [
(dZ/dt)max] represents the peak of the ascending aortic blood flow. Measurements of basal thoracic impedance are affected by structural and anatomical differences in the thorax related to sex and ageing. This component is a variable in the denominator of Sramek's formula which is used for calculating stroke volume. The aim of this study was to elucidate the question as to whether the age‐ and sex‐related variation in basal impedance may affect bioimpedance measurements of stroke volume.The study comprised 111 healthy subjects (55 males and 56 females) of ages between 20 and 69 years, divided according to age decades into five groups each of males and females. Stroke volume index (SI), Z0 and (dZ/dt)max were measured in every subject, using transthoracic bioimpedance cardiography. Z0 and (dZ/dt)max had significantly higher values in females than in males in every age group except the oldest one in the case of Z0 and the oldest two groups in the case of (dZ/dt)max. Stroke index showed no significant sex difference, although the higher Z0 in females may underestimate the values of stroke index. Elevation of (dZ/dt)max in females may therefore reflect a positive relation to Z0 rather than higher flow rates. Since Z0 and (dZ/dt)max are variants in opposite positions in Sramek's formula (denominator and numerator, respectively), this functional relationship may keep the bioimpedance measurements from being affected by the sex‐ and age‐related changes in Z0.
Long‐term treatment with lansoprazole for patients with Zollinger–Ellison syndrome
Authors: HIRSCHOWITZ B. I. , MOHNEN J. , SHAW S. 
Published: October 2003

Background: Normalization of gastric secretion and cure of associated upper gastrointestinal lesions by resection of gastrinoma is possible in ≈20% of patients with Zollinger–Ellison syndrome, leaving ≈80% dependent on medical treatment with proton pump inhibitors for acid suppression. Methods: Lansoprazole was given for 3–48 months (median 28 months) to 26 Zollinger–Ellison syndrome patients with peptic ulcer manifestations in all and oesophagitis in 13. Starting with 60 mg/day, the dose was individualized to lower basal acid output to less than 5 mmol/h for those with intact stomachs and less than 1 mmol/h in those who had prior gastrectomy or with oesophagitis. The patients were studied every 3 months for 1 year and then every 6 months with gastric analysis (basal and maximal acid and pepsin output) and endoscopy with biopsy for enterochromaffin‐like (ECL) cells. Results: Lansoprazole inhibited basal acid output by 95%, pepsin output by 65% and remained effective at the initial mean (66±4.3 mg/day) or smaller doses (56±12 mg/day) at 48 months. Mucosal lesions healed and symptoms (ulcer‐type pain, diarrhoea, heartburn, weight loss) resolved rapidly, usually within a few weeks. Serum gastrin and ECL cell populations, which were elevated before treatment, remained statistically unchanged but one of the three multiple endocrine neoplasia I (MEN‐I) patients developed a small carcinoid. Of the three patients with metastatic gastrinoma at diagnosis one has died and one has progressed, while the third has had stable liver metastases for 26 years. Ulcer‐type relapses occurred in three of the five post‐gastrectomy patients, one with fatal jejunal ulcer perforation despite adequate acid suppression. No biochemical or clinical adverse events due to lansoprazole were encountered. Conclusion: Lansoprazole effectively inhibits acid and pepsin secretion in Zollinger–Ellison syndrome patients without any demonstrated side‐effects. Despite strict acid control, post‐gastrectomy Zollinger–Ellison syndrome patients were more liable to ulcer relapse, while oesophagitis was not a marker for therapeutic difficulty.
Effects of rebamipide on bile acid‐induced inhibition of gastric epithelial repair in a rabbit cell culture model
Authors: WATANABE S. , WANG X.‐E. , HIROSE M. , YOSHIZAWA T. , IWAZAKI R. , OIDE H. , KITAMURA T. , MIWA H. , A.  , SATO N. 
Published: October 2003

Background: Anti‐ulcer agents exert various functional effects on gastric epithelial cells. Aim: The effects of a novel gastro‐cytoprotective agent (rebamipide) on epithelial restoration following bile acid damage were assessed using primary cultured rabbit gastric epithelial cells. Methods: Rebamipide was added to complete confluent cell sheets with deoxycholic acid just after creating a cell‐free wound (2 mm2). The restoration was monitored and analysed by phase contrast microscopy and an image analyser for 48 h. The migration speed was measured during the initial 3 h after wounding. Cell proliferation was detected by staining for bromodeoxyuridine (BrdU) at 12‐h intervals. The labelling index was calculated per unit area. The major cytoskeletal protein actin was detected by immunohistochemical staining. Results: In the controls, restoration was completed 48 h following wounding. Deoxycholic acid retarded this process. The addition of rebamipide to deoxycholic acid abolished the bile acid‐induced retardation. The migration speed was 26 μm/h in the controls, 15 μm/h in the deoxycholic acid group and 27 μm/h in the deoxycholic acid plus rebamipide group. In the controls, BrdU‐positive cells, which were rarely detected in the initial 24 h, were maximal at 36 h (labelling index 1.7%). In the deoxycholic acid group, proliferation was inhibited (peak labeling index; 0.5% at 48 h). Actin‐containing stress fibres were detected throughout the cells and the periphery of the lamellipodia in the controls, and were disrupted in the deoxycholic acid‐treated group. Rebamipide prevented these effects. Conclusions: Deoxycholic acid significantly retarded restoration by the inhibition of both cell migration and proliferation, potentially through an effect on the cytoskeleton. Rebamipide protected the mucosal cells from bile acid mediated injury.
Prescribing patterns for dyspepsia in primary care: a prospective study of selected general practitioners
Authors: BODGER K. , DALY M. J. , HEATLEY R. V. 
Published: October 2003

Aim: To define prescribing patterns for symptomatic dyspeptic patients in a cross‐section of general practitioners in Leeds, United Kingdom. Methods: Nine general practitioners from a range of practices took part in a prospective observational study of prescribing patterns for dyspepsia. All consultations with symptomatic dyspeptic patients were recorded over a 4‐month period. Symptoms were recorded as ulcer‐like, reflux‐like, or nonspecific, and details of recent therapy, previous investigations and any prescription issued were noted. Results: 257 consecutive consultations were recorded (new patients 23%, consulted before but not investigated 33%, previously investigated 44%). 93% of consultations resulted in a prescription (antacids 24%, prokinetic/motility agent 8%, H2‐receptor antagonist 36%, proton pump inhibitor 24%, Helicobacter pylori eradication therapy 8%). 42.5% of new patients received an acid‐suppressing drug as first‐line therapy, of which only 32% had tried over‐the‐counter remedies. Symptom‐type (ulcer‐like, reflux‐like or nonspecific) significantly influenced choice of empiric therapy (P<0.001), though prescribing was still variable. Although around 60% of patients with previously negative investigations or only minor disease received acid‐suppressing drugs, such patients were six times more likely to receive ‘less potent’ treatments (no prescription, antacid or motility agent) than those with known acid‐peptic disease (odds ratio 6.23, P<0.01). Only 30% of patients with previously documented peptic ulcer received H. pylori eradication therapy, yet patients with a wide range of other diagnoses received this form of treatment. Conclusions: Management guidelines may help to promote a more consistent and selective use of newer treatments, and promote more cost‐effective patient care.
Implication of nitric oxide synthase activity in the genesis of water immersion stress‐induced gastric lesions in rats: the protective effects of FK506
Authors: HISANAGA Y. , GOTO H. , TACHI K. , HAYAKAWA T. , SUGIYAMA S. 
Published: October 2003

Background: Nitric oxide (NO) is a potent cytoprotective substance of gastric mucosa. FK506, an immunosuppressive drug, shows anti‐gastric ulcer effects equivalent to famotidine, an H2 blocker, in rats. This study was designed to evaluate the cytoprotective mechanism of FK506 on gastric mucosa in relation to the changes in NO synthase activity. Methods: Gastric lesions were induced in rats by water immersion stress. Changes in NO synthase activity during water immersion stress treatment, and effects of FK506 on NO synthase activity were determined enzymatically. Gastric mucosal interleukin (IL)‐1β and IL‐2 were measured by immunoradiometric assay. Gastric mucosal blood flow was measured by hydrogen gas clearance technique. Results: FK506 mitigated gastric lesions developed by water immersion stress. Stress‐induced lesions were exacerbated by NG‐monomethyl‐L‐arginine (L‐NMMA), a specific inhibitor of NO synthase, while sodium nitroprusside, a NO donor, mitigated the lesions. Water immersion stress increased NO synthase activity in the early phase (0.5 h after stress treatment) and decreased it in the late phase (6 h after). Decrease in NO synthase activity in the late phase was significantly mitigated by FK506, though it did not affect changes in NO synthase activity in the early phase. Water immersion stress increased gastric mucosal IL‐1β and IL‐2 contents 6 h after stress treatment, and these increases were prevented by FK506. FK506 itself did not affect gastric mucosal blood flow. L‐NMMA treatment significantly decreased gastric mucosal blood flow. In contrast, gastric mucosal blood flow was significantly increased by sodium nitroprusside. Conclusions: Increase in NO synthase activity might contribute to cytoprotection, and a decrease in activity might be a harmful factor for the gastric mucosa. Preservation of NO synthase activity by FK506 might be involved in FK506's protective effects on the gastric mucosa.
safety of bismuth in the treatment of gastrointestinal diseases
Authors: TILLMAN L. A. , DRAKE F. M. , DIXON J. S. , WOOD J. R. 
Published: October 2003

Bismuth preparations are commonly used to treat a variety of gastrointestinal disorders, including peptic ulcers and dyspepsia. The safety profile of currently approved bismuth preparations, such as tripotassium dicitrato bismuthate (De‐Nol), bismuth subsalicylate (Pepto‐Bismol) and ranitidine bismuth citrate (Pylorid, Tritec), is excellent. Adverse reactions to these agents are mild, transient and infrequent, and reports of serious adverse reactions are rare. This, in part, reflects the low systemic bioavailability of bismuth from these medicines: less than 1% of the bismuth dose administered is absorbed.During repeated dosing with ranitidine bismuth citrate 200, 400 or 800 mg b.d. trough plasma bismuth concentrations remain well below 50 μg/L. After 4 weeks of treatment median concentrations of 3.4 μg/L or less were reported amongst 1210 duodenal ulcer patients receiving this new chemical entity, while mean concentrations of 5.1 μg/L (plasma) and 12.3 μg/L (blood) have been reported in two studies of patients receiving tripotassium dicitrato bismuthate 120 mg q.d.s. for 4 weeks. Transient peak plasma bismuth concentrations greater than 50 μg/L are observed 30–60 min after dosing with tripotassium dicitrato bismuthate in some patients, but are not associated with any toxic effects. After discontinuation of treatment with bismuth preparations its excretion in urine may continue for up to 3 months, by which time blood bismuth concentrations have declined to pre‐treatment values.
Megestrol acetate therapy for anorexia and weight loss in children with malignant solid tumours
Authors: AZCONA C. , CASTRO L. , CRESPO E. , JIMÉNEZ M. , SIERRASESÚMAGA L. 
Published: October 2003

Background: Malnutrition is very frequent in childhood cancer. Its main cause is inadequate intake for energy demands owing to lack of appetite. Megestrol acetate is a synthetic progestin that has been used for reversing anorexia in adult cancer. Objectives: To assess megestrol acetate efficacy and side‐effects in treating anorexia in childhood cancer. Methods: Thirty‐five children with solid tumours were receiving antitumour therapy. Nutritional assessment was by anthropometry. Megestrol acetate efficacy was assessed by evaluating grade of appetite, energy intake and well‐being. Side‐effects were evaluated by means of clinical history, physical examination, lipid profile, coagulation tests and cortisol rhythm. Results: When compared to baseline all the anthropometric measurements increased (P<0.05) from the first month of megestrol acetate therapy, as well as appetite and energy intake. No significant side‐effects were found. Conclusion: Megestrol acetate therapy is a powerful appetite stimulant which led to weight gain, composed of both fat mass and fat‐free mass. Megestrol acetate is well tolerated, with few and mild side‐effects. If megestrol acetate therapy is started at the onset of anorexia, the use of more expensive, invasive and complicated techniques of nutritional support may be avoided.
Omeprazole prevents indomethacin‐induced gastric ulcers in rabbits
Authors: LEE M. , KALLAL S. M. , FELDMAN M. 
Published: October 2003

Background: The role of gastric acid in the development of non‐steroidal anti‐inflammatory drug (NSAID)‐induced gastric ulcers is unclear. The aim of this study was to determine the effect of the proton pump inhibitor omeprazole on the formation of indomethacin‐induced gastric ulcers in a rabbit model. Methods: Twenty‐four rabbits were randomly divided into four groups and treated as follows: vehicle for indomethacin; vehicle for omeprazole; indomethacin (20 mg/kg b.d. subcutaneously for seven doses); and indomethacin plus omeprazole (both at 20 mg/kg b.d. subcutaneously for seven doses). On day 4 (after the seventh injection), rabbits were sacrificed, and gastric mucosal injury and prostaglandin formation were assessed. Results: Subcutaneous administration of 20 mg/kg omeprazole b.d. caused a profound suppression of gastric acidity (i.e. pH above 5.0 continuously). This same dose of omeprazole significantly reduced gastric ulcer formation induced by indomethacin despite significant (>80%) inhibition of gastric mucosal prostaglandin E2 (PGE2) formation. Conclusion: We conclude from these observations that gastric acid plays a critical role in the formation of indomethacin‐induced gastric ulcers in rabbits.