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Biomedical subjects

J H Henriksen

Publications and source records attributed to J H Henriksen.

At least 19 recordsLinked to original sources
PubMed1998

[Scientific activities in departments of clinical physiology/nuclear medicine in Denmark during the period 1989-1994. A bibliometric analysis of the "impact" and citation frequency].

This study reports a bibliometric analysis of 860 scientific publications of which 763 are papers in scientific journals emanating from departments of clinical physiology and nuclear medicine in Denmark in the years 1989-1994. The number of publications decreased significantly over time. The 763 papers were published in 239 different scientific journals, 80% in journals with an official "impact factor". The average impact per paper remained almost constant over time and was significantly above the national average. A close relationship was found between the number of papers from a department and its cumulated impact. In an analysis of 217 papers a direct relation was found between the journal impact factor and the citation factor. A linear relation was found between cumulated citations and time, and the number of citations per year reached a maximum 3-7 years after publication, whereas the general maximum for all medical specialties is 2-3 years. It is concluded that the total number of scientific papers from Danish departments of clinical physiology & nuclear medicine fell in the years 1989-1991, but the impact per paper was almost constant and above the national average. There seems to be a good agreement between journal impact factor and overall citation frequency in papers from clinical physiology & nuclear medicine.

Bibliometrics↗
PubMed1998

[Decompensation].

Fluid and sodium retention with peripheral oedema and ascites are often seen in decompensated patients with diseases of the liver, kidney and heart and in malignancies. Despite a careful clinical examination including relevant biochemical tests, decompensation is associated with diagnostic challenges. Two cases are presented where a haemodynamic investigation of the splanchnic and systemic circulation contributed to the establishment of a correct diagnosis, and the advantages of this diagnostic tool are discussed.

Ascites↗
PubMed1998

Neurohumoral fluid regulation in chronic liver disease.

Impaired homeostasis of the blood volume, with increased fluid and sodium retention, is a prevailing element in the deranged systemic and splanchnic haemodynamics in patients with liver disease. In this review, some basic elements of the circulatory changes that take place and of neurohumoral fluid regulation are outlined in order to provide an update of recent investigations on the neuroendocrine compensation of circulatory and volume dysfunction in chronic liver disease. The underlying pathophysiology is a systemic vasodilatation in which newly described potent vasoactive substances such as nitric oxide and vasodilating peptides seem to play an important role. The development of central hypovolaemia and activation of potent vasoconstricting systems such as the renin-angiotensin-aldosterone system and the sympathetic nervous system lead to a hyperdynamic circulation with increased heart rate and cardiac output. Moreover, patients exhibit an autonomic dys- and hyperfunction with vascular hyporeactivity to pressor stimuli. The circulatory dysfunction may be part of a multiorgan failure with disturbed haemodynamics of various vascular beds, including those of the splanchnic system, kidneys, brain and lungs. It is still an enigma why patients with chronic liver disease are at the same time overloaded and functional hypovolaemic with a hyperdynamic, hyporeactive circulation. Further research is needed to find the solution to this apparent haemodynamic conflict concerning the abnormal neurohumoral fluid regulation in chronic liver disease.

Adrenomedullin↗
PubMed1998

Arterial hypoxaemia in cirrhosis: fact or fiction?

BACKGROUND: Although low arterial oxygen tension (Po2) has been claimed to occur in one to two thirds of patients with cirrhosis, hypoxaemia appears to be rare in clinical practice. AIMS: To assess the frequency of arterial hypoxaemia in cirrhosis in relation to clinical and haemodynamic characteristics. PATIENTS: One hundred and forty two patients with cirrhosis without significant hepatic encephalopathy (grades 0-I) (41 patients in Child class A, 57 in class B, and 44 in class C) and 21 patients with hepatic encephalopathy. RESULTS: Mean Po2 in kPa was 11.3 in Child class A, 10.8 in class B, 10.6 in class C, and 10.6 in patients with encephalopathy (p < 0.05). The fraction of patients with Po2 below the lower normal limit of 9.6 kPa was 10%, 28%, 25%, and 43%, respectively in class A, B, C, and in patients with encephalopathy (p < 0.05). Oxygen saturation (So2) in these groups was respectively: 96%, 96%, 96%, and 93% (NS). So2 was below the lower limit of 92% in 0%, 9%, 7%, and 24% (p < 0.05). In patients without hepatic encephalopathy, a multivariate regression analysis revealed that independent determinants of a low Po2 were a high arterial carbon dioxide tension, a low systemic vascular resistance, and a low indocyanine green clearance (p < 0.0001). CONCLUSION: The prevalence of arterial hypoxaemia in cirrhosis is about 22% in patients without encephalopathy, but it varies from 10-40% depending on the degree of hepatic dysfunction. Arterial hypoxaemia in patients with cirrhosis of differing severity seems lower than previously reported, and patients with severe arterial hypoxaemia are rare.

Adult↗
PubMed1998

Haemodynamics and fluid retention in liver disease.

Patients with cirrhosis and portal hypertension exhibit characteristic haemodynamic changes with a hyperkinetic systemic circulation, an abnormal distribution of the blood volume and neurohumoral dysregulation. Their plasma and noncentral blood volumes are increased, but the central and arterial blood volume and systemic vascular resistance are decreased. A systemic and splanchnic vasodilatation is of pathogenic importance to the low systemic vascular resistance and abnormal volume distribution. These are important elements in the development of the low arterial blood pressure and hyperkinetic circulation in cirrhosis. Various vasodilators such as nitric oxide, calcitonin gene-related peptide, and adrenomedullin are among potential candidates in the vasodilatation in cirrhosis. Besides reflex induced enhanced sympathetic nervous activity, activation of the renin-angiotensin-aldosterone system, and elevated circulation vasopressin, endothelin-1 may also be implicated in the haemodynamic counter-regulation in cirrhosis. Recent research has focused on the assertion that the haemodynamic and neurohumoral abnormalities in cirrhosis are part of a general circulatory dysfunction, influencing the course of the disease with reduction of kidney function and sodium-water retention as the outcome.

Animals↗
PubMed1997

Carbohydrate deficient transferrin (CDT) in alcoholic cirrhosis: a kinetic study.

BACKGROUND/AIMS: Carbohydrate deficient transferrin has been introduced as a marker of excessive alcohol intake. The present study was undertaken in order to measure the circulating level of carbohydrate deficient transferrin in patients with alcoholic cirrhosis and to assess arteriovenous kinetics of carbohydrate deficient transferrin in liver and kidney. METHODS/RESULTS: The median value of serum carbohydrate deficient transferrin was 16.0 U/l in patients with alcoholic cirrhosis (n = 41), and this value was not significantly different from that of a normal control group (median 17.4 U/l, n = 55, ns). Carbohydrate deficient transferrin was significantly higher in patients with cirrhosis and high current alcohol intake than in abstaining patients (20 vs. 14 U/l, p < 0.05). Similarly, controls with a high current alcohol intake (> 50 g/day) had a significantly higher carbohydrate deficient transferrin concentration than controls with a low alcohol intake (< 10 g/day) (36 vs. 14.9 U/l, p < 0.005). No significant differences were detected between carbohydrate deficient transferrin in artery and liver vein or artery and renal vein, either in patients with alcoholic cirrhosis (n = 11) or in controls (n = 8), which indicates a slow turnover rate of carbohydrate deficient transferrin. Food ingestion did not affect the circulating level of carbohydrate deficient transferrin, and the analysis of carbohydrate deficient transferrin was almost unaffected by the presence of ethanol in plasma within the biological range (ethanol 0-100 mmol/l). CONCLUSIONS: Our results suggest that measurement of carbohydrate deficient transferrin may be used in patients with alcoholic cirrhosis. High current alcohol intake is associated with higher carbohydrate deficient transferrin levels than in those with low alcohol intake, but the overlap is substantial in patients with cirrhosis. Carbohydrate deficient transferrin has a low turnover rate in both patients with cirrhosis and normals.

Adult↗
PubMed1997

Effect of octreotide on systemic, central, and splanchnic haemodynamics in cirrhosis.

BACKGROUND/AIMS: Cirrhosis with portal hypertension is associated with changes in the splanchnic and systemic haemodynamics, and subsequent complications, such as bleeding from oesophageal varices, have led to the introduction of long-acting somatostatin analogues in the treatment of portal hypertension. However, reports on the splanchnic and systemic effects of octreotide are contradictory and therefore the aim of the present study was to assess the effects of continuous infusion of octreotide on central and systemic haemodynamics, portal pressures, and hepatic blood flow. METHODS: Thirteen patients with cirrhosis underwent liver vein catheterisation. Portal and arterial blood pressures were determined at baseline and 10, 30, and 50 min after a bolus injection of octreotide 100 micrograms, followed by continuous infusion of octreotide 100 micrograms/ h for 1 h. Hepatic blood flow, cardiac output, central and arterial blood volume, and central circulation time were determined at baseline and 50 min after the start of the octreotide infusion. RESULTS: The mean arterial blood pressure increased during the first 10 min (p < 0.0005), but returned to baseline after 50 min. The central and arterial blood volume (-16%, p < 0.005) and the central circulation time (-8%, p < 0.05) were significantly decreased after 50 min, whereas the cardiac output did not change significantly. The hepatic venous pressure gradient and the hepatic blood flow did not change significantly at any time after infusion of octreotide. CONCLUSIONS: Octreotide does not affect the portal pressure or hepatic blood flow, whereas it may further contract the central blood volume and thereby exert a potentially harmful effect on central hypovolaemia in patients with cirrhosis. However, these early effects do not exclude the possibility that administration of longacting somatostatin analogues over a longer period may have a beneficial effect.

Adult↗
PubMed1997

Continuous blood pressure monitoring in cirrhosis. Relations to splanchnic and systemic haemodynamics.

BACKGROUND/AIMS: Low arterial blood pressure is recognised as a distinctive factor in the hyperdynamic circulation in cirrhosis. 24-hour monitoring of the blood pressure and heart rate has recently revealed a reduced circadian variation with relation to liver function. However, associations with other clinical and haemodynamic characteristics have not been investigated and the aim of the present study was to identify splanchnic and systemic determinants of the 24-h blood pressure and heart rate in cirrhosis. METHODS: The variables were measured by an automatic ambulant device for monitoring blood pressure and related to the results of an invasive haemodynamic investigation, including measurements of intra-arterial blood pressure (9.00-11.00 h) in 37 patients with cirrhosis. RESULTS: The 24-h blood pressures were significantly lower and the heart rate was significantly higher in patients with cirrhosis than in matched controls (p < 0.05-0.001). To identify determinants of 24-h or intra-arterial blood pressures and heart rate, pertinent variables were included in a multivariate regression model. This model revealed that independent determinants of a low 24-h arterial blood pressure were a high post-sinusoidal resistance, a low plasma volume, a short central circulation time, and the presence of ascites. In contrast, a low intra-arterial blood pressure was determined by a low serum sodium, a low haemoglobin, and a high cardiac output. Diuretic treatment did not influence this model. CONCLUSIONS: Although the 24-h blood pressure and the intra-arterial blood pressure were determined by different variables, the overall results indicate that abnormalities in both splanchnic and central haemodynamics and sodium-water retention are important in the pathophysiology of arterial hypotension in patients with portal hypertension.

Adult↗
PubMed1997

Plasma YKL-40: a new potential marker of fibrosis in patients with alcoholic cirrhosis?

BACKGROUND: YKL-40 (human cartilage glycoprotein-39, or 38-kDa heparin-binding glycoprotein) is a mammalian member of a protein family that includes bacterial chitinases. YKL-40 mRNA is expressed by human liver and may play a role in tissue remodelling. The aims were to assess whether circulating YKL-40 is released or extracted in the hepatosplanchnic system and to localize YKL-40 in liver tissue. METHODS: Plasma YKL-40 was determined by radioimmunoassay in 25 patients with liver diseases (alcoholic cirrhosis (n = 20), chronic active hepatitis (n = 2), cirrhosis of unknown aetiology (n = 2), and fatty liver (n = 1) and in 18 subjects with normal liver function during a haemodynamic investigation with catheterization of liver vein and the femoral artery. Immunohistochemical studies of the localization of YKL-40 in cryostal liver biopsy specimens were obtained from eight other patients with alcoholic liver disease. RESULTS: Plasma YKL-40 was significantly increased in patients with alcoholic cirrhosis (median, 523 micrograms/l; P < 0.001) compared with controls (106 micrograms/l), and plasma YKL-40 in the hepatic vein was higher (P < 0.01) than that of the artery in both the patients and controls, showing release of YKL-40 from the hepatosplanchnic area. The release rate of YKL-40 from the hepatosplanchnic area was higher in patients with liver disease than in controls (11.0 versus 2.1 micrograms/min, P < 0.05). Furthermore, the highest plasma YKL-40 levels were found in patients with a moderate or severe degree of liver fibrosis, and immunohistochemical studies showed positive staining for YKL-40 antigen in areas of the liver biopsy with fibrosis. CONCLUSIONS: The increased plasma YKL-40 in patients with alcoholic cirrhosis may reflect the remodelling of liver fibrosis.

Adipokines↗
PubMed1997

Circulatory abnormalities in cirrhosis with focus on neurohumoral aspects.

Patients with cirrhosis exhibit characteristic hemodynamic changes with a hyperkinetic circulation and an abnormal distribution of the blood volume and neurohumoral regulation. Their plasma and noncentral blood volumes are increased, and the central and arterial blood volume and systemic vascular resistance are decreased. A peripheral arterial vasodilatation may be of pathogenic importance to the low systemic vascular resistance as it directly correlates to the degree of central hypovolemia. It may therefore be an important element in the development of the low arterial blood pressure and hyperkinetic circulation in cirrhosis. Various vasodilators such as atrial natriurectic peptide, calcitonin gene-related peptide, adrenomedullin, and nitric oxide are among potential candidates in the arterial vasodilatation in cirrhosis. Besides enhanced sympathetic nervous activity, activation of the renin-angiotensin-aldosterone system, and elevated circulating vasopressin, endothelin-1 may also be implicated in the hemodynamic counter-regulation in cirrhosis. Recent research has focused on the assertion that the hemodynamic and neurohumoral abnormalities in cirrhosis are part of a general circulatory dysfunction influencing the course of the disease.

Blood Circulation↗
PubMed1996

[Determination of diurnal blood pressure variations in cirrhosis].

Cirrhotic patients have disturbed systemic haemodynamics with reduced arterial blood pressure, but this has not been investigated during daily activity and sleep. Systolic (SBP), diastolic (DBP), and man arterial blood pressure (MAP), and heart rate (HR) were measured by an automatic ambulatory device for monitoring blood pressure in 35 patients with cirrhosis and 35 healthy matched controls. During the day-time, SBP, DBP and MAP were significantly lower in the patients than in the controls (median 118 vs 127; 70 vs 78; 86 vs 94 mmHg, p < 0.0001 to p < 0.05). The night-time blood pressures were almost similar in the two groups (108 vs 110; 65 vs 67; 78 vs 82 mmHg, NS). Conversely, HR was significantly higher in the patients both in the day-time (86 vs 72 min-1, p < 0.0001) and night (80 vs 64 min-1, p < 0.0001). Consequently, the reduction in blood pressure and HR from day-time to night-time was significantly lower in the patients than in the controls (p < 0.0001 to p < 0.01). Multiple regression analysis revealed HR, serum albumin, serum sodium, and clotting factors 2, 7 and 10 as significant independent predictors of SBP in cirrhosis. In conclusion, cirrhotic patients have elevated HR, but surprisingly normal arterial blood pressure during the night-time, and the circadian variation in blood pressure and HR is diminished probably due to an almost unaltered cardiac output during the 24 hours. These results may reflect a major defect in the ability of optimal regulation of blood pressure in cirrhotic patients.

Adult↗