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Biomedical subjects

Henning Bay Nielsen

Publications and source records attributed to Henning Bay Nielsen.

12 recordsLinked to original sources
PubMed2007

Advanced quantitative echocardiography in arrhythmogenic right ventricular cardiomyopathy.

BACKGROUND: Arrhythmogenic right ventricular (RV) cardiomyopathy (ARVC) is a regional disease of the RV myocardium with variable degrees of left ventricular involvement. Three-dimensional echocardiography and Doppler tissue imaging (DTI) are new echocardiographic modalities for the evaluation of global and regional function, but the diagnostic potential remains to be assessed. METHODS: Twenty patients with previously established ARVC were evaluated by 3-dimensional echocardiography and DTI, and compared with 32 age- and sex-matched control subjects. RESULTS: Using 3-dimensional echocardiography, patients with ARVC had a decreased RV ejection fraction (0.47 +/- 0.08 vs 0.53 +/- 0.05, P < .01), and a decreased peak lateral systolic annular velocity by pulsed wave imaging of both the RV (11.9 +/- 2.6 vs 15.1 +/- 3.7 cm/s, P < .01) and the left ventricle (7.0 +/- 2.6 vs 9.5 +/- 1.9 cm/s, P < .01). DTI showed decreased regional systolic strain, but with wide variation in the measurements. CONCLUSION: Three-dimensional echocardiography identifies decreased RV ejection fraction in ARVC. Assessment of regional contractility by DTI is limited by wide variation. Echocardiographic evaluation of the longitudinal motility appears to be a sensitive marker of preclinical left ventricular involvement.

Adult↗
PubMed2006

[Patient injuries in response to anaesthetic procedures: cases evaluated by the Danish Patient Insurance Association--secondary publication].

We investigated the Danish Patient Insurance Association files of patients, who were given financial compensation, because of an injury caused by an anaesthetic procedure. In the six-year-period 1996-2002, 374 patients were compensated in total 8.0 million euros for an injury caused by an anaesthetic procedure. Some anaesthetic complications may result in severe disability, whereby the financial compensation to the suffering patients is high. We estimate that approximately 0.2 per 1,000 of all patients receiving anaesthesia may develop complications that entitle them to financial compensation.

English Abstract↗
PubMed2006

[Obesity in Denmark--why has it not gone so badly?].

In the Western world the number of obese people is increasing, but in Denmark the incidence is not on the same scale as in the USA. Although several factors may be of importance, Danes are more physically active and their intake of beverages with added sugar is less than in the American population.

Denmark↗
PubMed2005

Maintained cerebral and skeletal muscle oxygenation during maximal exercise in patients with liver cirrhosis.

BACKGROUND/AIMS: In cirrhotic patients, insufficient redistribution of blood from splanchnic organs to the central circulation could limit blood supply to skeletal muscles and the brain during exercise. METHODS: Eight cirrhotic patients performed incremental cycling to exhaustion (74 (49-123) W; median with range). RESULTS: Heart rate increased from 68 (62-88)beats/min at rest to 142 (116-163)beats/min, cardiac output from 5.1 (3.3-7.2) to 12.9 (8.5-15.9)l/min, and mean arterial pressure from 89 (75-104) to 115 (92-129)mmHg (P<0.05), while the indocyanine green elimination determined hepatosplanchnic blood flow declined from 0.97 (0.55-1.46) to 0.62 (0.36-1.06)l/min (P<0.05). As assessed by near-infrared spectrophotometry, cerebral oxygenation (NIRS) was 61% (48-85%) and increased to 72% (57-86%) during exercise (P<0.05). The NIRS determined oxygenation of the vastus lateralis muscle also increased: the concentrations of oxygenated haemoglobin by 5.9 (0.57-9.47)micromol/l, deoxygenated haemoglobin by 7.2 (1.8-12.0)micromol/l, and thus total haemoglobin by 12.1 (3.6-21.5)micromol/l (P<0.05). CONCLUSIONS: In patients with cirrhosis, exercise reduces hepatosplanchnic blood flow, while O(2) supply to muscle and brain appears to increase indicating that blood redistribution from splanchnic organs does not limit blood flow to working muscles and the brain.

Adult↗
PubMed2004

Effect of smoking and abstention on oxidative burst and reactivity of neutrophils and monocytes.

BACKGROUND: Smoking is associated with surgical wound infections, impaired wound healing, and tissue-destructive disorders. The mechanisms are largely unknown, but changes in the function and activity of inflammatory cells may be involved. METHODS: Seventy healthy volunteers (54 smokers and 16 never smokers) were included. The smokers were studied while they smoked and after 20 days of abstinence. After the first 10 days of abstinence, they were randomized to double-blind treatment with transdermal nicotine patch 25 mg per day or placebo. Venous blood neutrophils and monocytes were sampled and isolated. In 22 randomly selected smokers and in all never smokers, the oxidative burst and chemotaxis were determined by a chemiluminescence response assay and a modified Boyden chamber technique, respectively. Stimulants were opsonized zymosan, formyl-Met-Leu-Phe, and zymosan-activated serum. RESULTS: The neutrophil and monocyte oxidative burst was 50% and 68% lower, respectively, in smokers compared to never smokers (P < .05). Neutrophil chemotaxis was 93% higher in smokers (P < .05). Monocyte chemotaxis was lower in smokers compared to never smokers (P < .05). After 20 days of abstinence, neutrophil oxidative burst increased to the level of never smokers (P < .05); monocyte oxidative burst increased by 50% (P < .05). Chemotaxis was only marginally affected. The changes induced by abstinence were less pronounced in the transdermal nicotine patch group compared to the placebo group. CONCLUSIONS: Smoking attenuates the oxidative burst of inflammatory cells and increases chemotaxis. Three weeks of abstinence normalize the oxidative burst, but affect chemotaxis only marginally.

Administration, Cutaneous↗
PubMed2003

Cerebral oxygenation determined by near-infrared spectrophotometry in patients with fulminant hepatic failure.

BACKGROUND/AIMS: In severe cases of acute liver failure (ALF), cerebral hyperperfusion may result in high intracranial pressure and brain damage. The aim of this study was to determine if near-infrared spectrophotometry (NIRS) could detect a raise in cerebral blood flow and oxygenation induced by noradrenaline (NA) infusion. METHODS: In seven ALF patients (five females and two males; median age 49 years (range 20-70)) changes in cerebral concentration of oxy-(deltaHbO(2)) and total-haemoglobin (deltaHbT) were compared to the jugular bulb saturation (SvjO(2)) and cerebral blood flow velocity (Vmean) during NA infusion. RESULTS: Mean arterial pressure increased from 68 (64-86) to 103 (87-118) mmHg and the cerebral perfusion pressure from 61 (53-79) to 95 (74-110) mmHg (P<0.05), while the intracranial pressure (7 (6-15) mmHg) was not significantly changed. In six patients cerebral deltaHbO(2) and deltaHbT increased 2.7 (0.3-9.6) and 2.0 (0.3-14.8) micromol l(-1), respectively, but cerebral oxygenation decreased in one patient. SvjO(2) increased from 68 (55-76) to 74 (64-78) % (P<0.05) concomitant with an increase in Vmean from 47 (34-65) to 68 (50-86) cm s(-1) (P<0.05). deltaHbO(2) covariated with changes in SvjO(2) during NA in all but one patient. CONCLUSIONS: In ALF patients, a change in cerebral perfusion was detected by NIRS. The combination of NIRS and transcranial Doppler sonography may be valuable non-invasive techniques to detect cerebral hyperperfusion before intracranial hypertension becomes manifest.

Adult↗
PubMed2003

Arterial desaturation during exercise in man: implication for O2 uptake and work capacity.

Exercise-induced arterial hypoxaemia is defined as a reduction in the arterial O2 pressure (PaO2) by more than 1 kPa and/or a haemoglobin O2 saturation (SaO2) below 95%. With blood gas analyses ideally reported at the actual body temperature, desaturation is a consistent finding during maximal ergometer rowing. Arterial desaturation is most pronounced at the end of a maximal exercise bout, whereas the reduction in PaO2 is established from the onset of exercise. Exercise-induced arterial hypoxaemia is multifactorial. The ability to maintain a high alveolar O2 pressure (PAO2) is critical for blood oxygenation and this appears to be difficult in large individuals. A large lung capacity and, in turn, diffusion capacity seem to protect PaO2. A widening of the PAO2-PaO2 difference does indicate that a diffusion limitation, a ventilation-perfusion mismatch and/or a shunt influence the transport of O2 from alveoli to the pulmonary capillaries. An inspired O2 fraction of 0.30 reduces the widened PAO2-PaO2 difference by 75% and prevents a reduction of PaO2 and SaO2. With a marked increase in cardiac output, diffusion limitation combined with a fast transit time dominates the O2 transport problem. Furthermore, a postexercise reduction in pulmonary diffusion capacity suggests that the alveolo-capillary membrane is affected. An antioxidant attenuates oxidative burst by neutrophilic granulocytes, but it does not affect PaO2, SaO2 or O2 uptake (VO2), and the ventilatory response to maximal exercise also remains the same. It is proposed, though, that increased concentration of certain cytokines correlates to exercise-induced hypoxaemia as cytokines stimulate mast cells and basophilic granulocytes to degranulate histamine. The basophil count increases during maximal rowing. Equally, histamine release is associated with hypoxaemia and when the release of histamine is prevented, the reduction in PaO2 is attenuated. During maximal exercise, an extreme lactate spill-over to blood allows pH decrease to below 7.1 and according to the O2 dissociation curve this is critical for SaO2. When infusion of sodium bicarbonate maintains a stable blood buffer capacity, acidosis is attenuated and SaO2 increases from 89% to 95%. This enables exercise capacity to increase, an effect also seen when O2 supplementation to inspired air restores arterial oxygenation. In that case, exercise capacity increases less than can be explained by VO2 and CaO2. Furthermore, the change in muscle oxygenation during maximal exercise is not affected when hyperoxia and sodium bicarbonate attenuate desaturation. It is proposed that other organs benefit from enhanced O2 availability, and especially the brain appears to increase its oxygenation during maximal exercise with hyperoxia.

Adolescent↗
PubMed2003

Hepatosplanchnic clearance of interleukin-6 in humans during exercise.

The cytokine interleukin (IL)-6 can increase markedly in the circulation during exercise, but whether the liver is a source of this increase is unknown. The aim of this study was to measure IL-6 flux across the hepatosplanchnic tissues in humans. To elevate systemic concentrations of IL-6, six healthy male subjects performed 120 min of semirecumbent cycling, and blood samples were simultaneously obtained from a brachial artery and the hepatic vein before and during exercise for the analysis of IL-6. Hepatosplanchnic blood flow (HBF) was measured using the indocyanine green infusion technique. Net hepatosplanchnic IL-6 balance was calculated from these measures. HBF was 1.3 +/- 0.1 l/min at rest and was not reduced throughout exercise, averaging 1.1 +/- 0.2 l/min. Arterial plasma IL-6 markedly increased (P < 0.05) from 1.8 +/- 0.6 ng/l at rest to 14.3 +/- 3.2 ng/l after 120 min of exercise. The hepatosplanchnic viscera did not contribute to this increase, since there was a net hepatosplanchnic IL-6 uptake (0.8 +/- 0.3 vs. 5.5 +/- 1.9 ng/min, rest vs. 120 min; P < 0.05). These data demonstrate that the hepatosplanchnic viscera remove IL-6 from the circulation in humans. This removal may constitute a mechanism limiting the negative chronic metabolic action of chronically elevated circulating IL-6.

Adult↗
PubMed2003

Lymphocyte responses to maximal exercise: a physiological perspective.

Exercise affects lymphocytes as reflected in total blood counts and the lymphocyte proliferative response. In addition, the production of immunoglobulins is impaired and during exercise the natural killer cell activity increases followed by suppression in the recovery period. Cardiopulmonary adjustments play a major role in lymphocyte response to physical activity. During intense exercise, the activated sympathetic nervous system increases blood flow to muscle as blood flow to splanchnic organs decreases. After exercise, sympathetic tone and blood pressure becomes reduced. The spleen contains lymphocytes and blood resides in gut vessels. A change in blood flow to these organs could affect the number of circulating lymphocytes. Reduced production of immunoglobulins results from suppressed B-cell function and, in response to exercise, mucosal immunity appears to decrease. Pulmonary hyperventilation and enhanced pressure in pulmonary vessels induce increased permeability of airway epithelium and stress failure of the alveolar-capillary membrane during intense exercise. A physiological perspective is of importance for evaluation of the exercise-induced change in lymphocyte function and, in turn, to post-exercise increased susceptibility to infections.

Blood Volume↗
PubMed2002

Exercise induces hepatosplanchnic release of heat shock protein 72 in humans.

Physical exercise results in the appearance of heat shock protein (HSP) 72 in the circulation that precedes any increase in gene or protein expression in contracting skeletal muscle. In rodents, exercise increases liver HSP72 expression and the hepatosplanchnic viscera are known to release many acute phase proteins. In the present study, we tested the hypothesis that the splanchnic tissue beds release HSP72 during exercise. Seven male subjects performed 120 min of semi-recumbent cycling at 62 +/- 2 % of maximal oxygen uptake. Blood samples were obtained simultaneously from a brachial artery, a femoral vein and the hepatic vein prior to and at 30, 60 and 120 min of exercise. Leg blood flow (LBF) was measured by thermodilution in the femoral vein, and hepatosplanchnic blood flow (HBL) was measured using indocyanine green dye. Net leg and net hepatosplanchnic HSP72 balance were calculated as the product of LBF and femoral venous-arterial HSP72 difference and the product of HBF and hepatic venous-arterial HSP72 difference, respectively. Arterial plasma HSP72 was only detected in one subject at rest but progressively appeared in the arterial samples throughout exercise such that at 120 min it was detected in all subjects (0.88 +/- 0.35 pg l(-1); P < 0.05 compared with rest). The contracting muscle did not, however, contribute to this increase since there was no difference in the femoral venous-arterial HSP72 concentration at any time. Rather, the increase in arterial HSP72 was accounted for, at least in part, by release from the hepatosplanchnic viscera with values increasing (P < 0.05) from undetectable levels at rest to 5.2 +/- 0.2 pg min(-1) after 120 min. These data demonstrate that the splanchnic tissues release HSP72 during exercise and this release is responsible, in part, for the elevated systemic concentration of this protein during exercise.

Adult↗
PubMed2002

Cerebral oxygenation during exercise in patients with terminal lung disease.

STUDY OBJECTIVES: In patients with terminal lung disease who were exercising, we assessed whether improved arterial O2 saturation with an increased fraction of inspired oxygen (FIO2) affects cerebral oxygenation. DESIGN: Randomized, crossover. PATIENTS AND METHODS: The cerebral changes in oxyhemoglobin (DeltaHbO2) and changes in deoxyhemoglobin (DeltaHb) levels were evaluated using near-infrared spectrophotometry and the middle cerebral artery (MCA) mean velocity (V(mean)) was determined by transcranial Doppler ultrasonography in 13 patients with terminal lung disease (New York Heart Association class III-IV). Patients were allocated to an FIO2 of either 0.21 or 0.35 during incremental exercise with 15 min between trials. RESULTS: Peak exercise intensity (mean [+/- SE], 26 +/- 4 W) reduced the arterial O2 pressure (at rest, 64 +/- 3 mm Hg; during exercise, 56 +/- 3 mm Hg) and the arterial oxygen saturation (SaO2) [at rest, 92 +/- 2%; 87 +/- 2%; p < 0.05], while the arterial CO2 pressure was not significantly affected. The MCA V(mean) increased from 49 +/- 5 to 63 +/- 7 cm/s (p < 0.05) as did the DeltaHb, while the DeltaHbO2 remained unaffected by exercise. With an elevated FIO2, the SaO2 level (at rest, 95.8 +/- 0.7%; during exercise, 96.0 +/- 1.0%) and arterial O2 pressure (at rest, 102 +/- 11 mm Hg; during exercise, 100 +/- 8 mm Hg) were not significantly affected by exercise, and the levels of blood oxygenation remained higher than the values established at normoxia (p < 0.05). The MCA V(mean) increased to a level similar to that achieved during control exercise (ie, to 70 +/- 11 cm/s). In contrast to control exercise, DeltaHb decreased while DeltaHbO2 increased during exercise with 35% O2 (p < 0.05). CONCLUSION: An O2-enriched atmosphere enabled patients with terminal lung disease to maintain arterial O2 saturation during exercise. An exercise-induced increase in cerebral perfusion was not affected by hyperoxia, whereby the enhanced availability of oxygenated hemoglobin increases cerebral oxygenation. The clinical implication of the study is that during physical activity patients with terminal lung disease are recommended to use an elevated FIO2 to protect cerebral oxygenation.

Adult↗