Biomedical subjects

J P Bagger

Publications and source records attributed to J P Bagger.

8 recordsLinked to original sources

PubMed1992

Enhanced urinary excretion of albumin in congestive heart failure: effect of ACE-inhibition.

Urinary excretion of albumin and beta 2-microglobulin were measured in 13 patients with congestive heart failure, NYHA class II-IV, before and after captopril treatment for 4 weeks, and in 13 healthy control subjects. The urinary excretion of albumin was enhanced in heart failure patients compared to control subjects (12.0 micrograms min-1 vs 2.8 micrograms min-1; medians, p less than 0.01), whereas beta 2-microglobulin excretion was normal. No significant change in urinary excretion of albumin was observed after captopril. Using Spearmann's test the urinary excretion of albumin was correlated to the NYHA class (Px = 0.681, p less than 0.05, plasma renin (Px = 0.886, p less than 0.01) and plasma angiotensin II (Px = 0.5840, p less than 0.05). Correlations with atrial natriuretic peptide (rho = 0.412, p = 0.153) and aldosterone (Px = 0.487, p = 0.106) did not reach significance. By multiple linear regression analysis only plasma renin activity was correlated to albumin excretion. In conclusion, patients with congestive heart failure had an increased urinary excretion of albumin. It is suggested that the enhanced transglomerular passage of albumin in congestive heart failure is partly due to an increased intra-renal angiotensin II generation, but elevated plasma level of atrial natriuretic peptide and increased renal venous pressure may also be important pathogenetic factors.

Adult↗

PubMed1991

Antiischemic and metabolic effects of glutamate during pacing in patients with stable angina pectoris secondary to either coronary artery disease or syndrome X.

The effects of glutamate on anginal threshold, cardiac metabolism and hemodynamics were studied in 11 patients with stable angina pectoris, positive stress test results, and pacing-induced myocardial lactate release due to coronary artery disease (CAD) (n = 9) or syndrome X (n = 2). Data were obtained before, during and after 2 identical periods of coronary sinus pacing, the second being preceded by an intravenous injection of monosodium glutamate 1.2 (n = 7) or 2.5 (n = 4) mg/kg body weight. After glutamate administration, pacing time to onset of angina increased from mean +/- standard deviation 103 +/- 53 to 166 +/- 71 seconds (p less than 0.01) and ST-segment depression after pacing decreased from 2.3 +/- 1.0 to 1.6 +/- 1.1 mm (p less than 0.01). Arterial glutamate concentration increased 60% (p less than 0.01) after the low dose and 150% (p less than 0.01) after the high dose of glutamate. Regardless of dose, myocardial glutamate uptake increased by 25% (p less than 0.01). Pacing-induced cardiac release of lactate diminished 50% (p less than 0.05), whereas the releases of xanthine and hypoxanthine were unchanged by glutamate. Arterial free fatty acids decreased 20% (p less than 0.01). Circulating levels and cardiac exchanges of alanine, glucose and citrate were unchanged. Glutamate did not influence heart rate, arterial blood pressure, coronary blood flow, coronary vascular resistance or myocardial oxygen consumption. One patient complained of short-lasting burning sensations after receiving the high glutamate dose. In conclusion, augmented provision of glutamate enhances pacing tolerance in stable angina, presumably by a metabolic improvement of cardiac energy production during ischemia.

Adult↗

PubMed1991

Effects of intravenous glutamate on substrate availability and utilization across the human heart and leg.

To study the effect of monosodium glutamate on hemodynamics and on substrate metabolism in cardiac and skeletal muscle, an intravenous (IV) dose of 1.2, 2.5, or 5.0 mg/kg body weight was administered to 27 patients during arterial-coronary sinus catheterization (15 patients) or arterial-femoral vein catheterization (13 patients). Data were obtained for 25 minutes after the injection. Arterial glutamate concentrations increased 2.5-5 fold in a dose-related manner. Glutamate administration reduced arterial levels of free fatty acids by 25% (P less than .001), of lactate by 13% (P less than .05), and of alanine by 6% (P less than .05). Arterial glucose increased by 10% (P less than .001) and arterial insulin was increased threefold (P less than .01). Myocardial uptake of free fatty acids decreased by 25% (P less than .001), whereas uptakes of glutamate and glucose increased by 60% (P less than .001) and 100% (P less than .001), respectively. Cardiac release of citrate increased transiently (P less than .05), whereas consumption of lactate and releases of alanine were unchanged by the glutamate. Across the leg, the arteriovenous differences of glutamate were elevated threefold to eightfold (dose-related) (P less than .001), and that of glucose was doubled (P less than .01). The release of citrate increased (P less than .01). Arterial-femoral vein gradients of free fatty acids, lactate, and alanine remained unchanged. Heart rate, blood pressure, coronary sinus flow, coronary vascular resistance, and cardiac oxygen uptake were unmodified by glutamate. Six patients complained of short-lasting burning sensations after the highest glutamate doses. In conclusion, glutamate administration stimulates insulin secretion and changes substrate availability and utilization in human cardiac and skeletal muscle from free fatty acids toward glucose and glutamate.

Adult↗

PubMed1991

Attenuated renal excretory response to atrial natriuretic peptide in congestive heart failure in man.

The renal and hormonal effects of atrial natriuretic peptide given as a bolus injection (2.0 micrograms/kg) were studied in 12 patients with congestive heart failure before and after treatment with captopril for 4 weeks and in 13 healthy control subjects. Atrial natriuretic peptide caused a rise in urinary excretion of sodium and urinary flow in the controls, whereas no increases were observed in the patients. Both proximal and distal fractional reabsorption of sodium, as evaluated by the lithium clearance technique, decreased less in the patients than in the controls. Basal plasma concentrations of atrial natriuretic peptide and cyclic guanosine monophosphate (cGMP), and the basal urinary excretion of cGMP, were elevated in the patients. The increases in both plasma and urinary cGMP after administration of atrial natriuretic peptide were blunted in heart failure. Basal glomerular filtration rate and renal plasma flow were reduced, and filtration fraction increased, in the patients. A positive correlation (r = 0.958, P less than 0.01) was found between renal plasma flow and the relative increase in urinary excretion of sodium in the patients with heart failure. Treatment with captopril did not improve the natriuretic and diuretic effect of exogenous atrial natriuretic peptide, but resulted in an increase in filtration fraction after administration of atrial natriuretic peptide not present before captopril.(ABSTRACT TRUNCATED AT 250 WORDS)

Atrial Natriuretic Factor↗

PubMed1991

Mechanisms of sodium retention in heart failure: relation to the renin-angiotensin-aldosterone system.

Renal plasma flow (RPF), glomerular filtration rate (GFR), renal proximal tubular delivery of sodium and water evaluated by lithium clearance, and hormonal parameters were measured in 12 patients with congestive heart failure NYHA class II-IV before and after captopril treatment for 4 wk and in 13 healthy control subjects. RPF and GFR were significantly decreased in heart failure, whereas the filtration fraction (FF) was increased. Treatment with captopril increased RPF and decreased FF, whereas GFR was unchanged. Total and fractional urinary excretion of sodium were reduced in the patients compared with the controls, but increased after captopril. Fractional excretion of lithium was normal in heart failure and was increased by captopril. Atrial natriuretic peptide, guanosine 3',5'-cyclic monophosphate, and aldosterone in plasma were significantly elevated in heart failure and were reduced by treatment with captopril. Plasma renin activity was increased in patients, correlated inversely with RPF, and increased further after captopril treatment. It is concluded that the reduced sodium excretion in heart failure was caused by a combination of diminished glomerular filtration and enhanced tubular reabsorption beyond the proximal tubule and that treatment with captopril increased urinary sodium excretion partly due to an attenuated sodium reabsorption in the proximal tubule. The present data in patients with congestive heart failure are consistent with an increased intrarenal angiotensin II generation and an elevated plasma level of aldosterone being involved in the pathogenesis of the glomerular hemodynamic changes and the enhanced distal tubular reabsorption, respectively.

Adult↗

PubMed1990

Cardiac metabolic effects of heparin differentiate between patients with normal and stenotic coronary arteries.

We studied the effects of heparin, given as 12,500 units intravenously, on cardiac metabolism during catheterization of the coronary sinus at rest and during repeated rapid atrial pacing in 8 patients with stable angina pectoris, positive stress tests and coronary arterial disease and in 8 patients with normal coronary arteries without objective signs of ischemic heart disease. Heparin did not influence angina, ST-segment depression or myocardial lactate production induced by pacing in the group with diseased coronary arteries. In both groups, heparin increased the arterial levels (70%) and the myocardial uptake (40-50%) of free fatty acids, the latter only during non-ischemic conditions. Myocardial net uptakes of glucose, lactate and glutamate and the release of alanine were reduced by heparin in the subjects with normal coronary arteries but not in those with ischemic heart disease. Myocardial oxygen consumption was unchanged. In the patients with normal coronary arteries, the levels of free fatty acid in the arteries were positively related to myocardial uptake of fatty acids and the release of citrate but inversely related to cardiac uptake of lactate and glucose. These relations were lacking in the patients with diseased coronary arteries. The metabolic effects of heparin on the heart, therefore, were diminished in patients with ischemic heart disease when compared to controls. This is probably due to an altered regulation of substrate preference in ischemic hearts.

Alanine↗

PubMed1977

Bone changes in hyperthyroidism: interrelationships between bone morphometry, thyroid function and calcium-phosphorus metabolism.

Iliac-crest biopsies were obtained from 40 untreated hyperthyroid patients after double-labelling with tetracycline. Histomorphometric analyses were performed on undecalcified and decalcified bone sections. The morphometric and chemical data were compared with those in normal control groups and the results of the morphometric analyses were related to thyroid function and to chemical quantities of calcium-phosphorus metabolism. The bone turn-over was increased in the hyperthyroid patients with an increase both in bone resorption and bone formation. Serum alkaline phosphphatase was increased and positively correlated to the amount of osteoid and to the extent of tetracycline-labelled surfaces. The osteoclastic resorption was positively and the bone formation inversely correlated to thyroid activity. This might explain the reduced amount of trabecular bone found in hyperthyroidism. The most striking feature was, however, a pronounced increase in osteoclastic activity in cortical bone followed by increased porosity. The osteoclastic resorption in cortical bone was positively correlated to serum concentrations and urinary excretions of calcium and phosphorus. This indicates that increased cortical osteoclastic resorption is mainly responsible for bone mineral mobilisation in hyperthyroidism.

Adolescent↗

PubMed1976

The insulin receptor in normal and obese persons.

Using [125I]insulin at 172 pmol/1 (1 ng/ml) the binding of insulin to mononuclear leucocytes isolated from peripheral blood was studied. Our present study comprised 21 healthy subjects (22-33 years old, 90-110% of ideal weight) and a comparable group of 22 obese subjects (20-37 years old, minimum 150% of ideal weight). A significant difference in insulin binding was found between the two groups, the mean specific insulin binding fraction in normals being 1.92 +/- 0.58 (s) X 10(-2) and that for the obese 1.19 +/- 0.41 (s) X 10(-2) (P less than 0.01). No correlation was found between body weight and the number of insulin receptors in the obese subjects. However, the number of insulin receptors was negatively correlated to fat cell size (P less than 0.05). Insulin receptors in subjects were also negatively correlated to fasting plasma insulin (P less than 0.05). Insulin receptors were studied in 11 obese subjects before and after 10 days of fasting. A significant increase in the number of insulin receptors was observed with a simultaneous decrease in plasma insulin to normal values. The results indicate that obesity complicated by hyperinsulinism is associated with a decrease in the number of insulin receptors compared with the normal. This finding may in part explain the decreased insulin sensitivity of the hyperinsulinaemic obese.

Adult↗