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Biomedical subjects

J P Bagger

Publications and source records attributed to J P Bagger.

At least 19 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↗
PubMed1990

Placebo-controlled, double-blind study of the effect of verapamil in intermittent claudication.

The clinical effect of verapamil was tested in 24 patients with intermittent claudication in a randomized, placebo-controlled, double-blind, crossover study. Slow-release verapamil or placebo was given for two periods of three weeks. The walking distance, systemic blood pressure, and ankle-brachial blood pressure index were measured. Furthermore, a possible change in peripheral vascular tone was provoked by hyperventilation. The walking distance rose after both verapamil (40%) and placebo (31%) (p less than 0.01 for both) but tended to increase only after verapamil (7%) as compared with placebo. Blood pressure fell equally after both verapamil and placebo (p less than 0.05 for both). Verapamil did not influence the ankle-branchial blood pressure index. No signs of vasoactivity in the lower extremities were seen after hyperventilation. Although the greatest individual improvements in walking distance were seen after verapamil administration, it was not possible to predict positive responders among the patients.

Adult↗
PubMed1989

Antianginal and cardiac metabolic effects of low-dose glucose infusion during pacing in patients with and without coronary artery disease.

Anginal threshold and cardiac metabolism during infusion of glucose, 350 mg/min, were compared with control values before, during, and after pacing in nine patients with coronary artery disease (CAD) and nine patients without coronary artery disease (non-CAD). Pacing induced no ischemia in non-CAD patients; in CAD patients, intolerable angina developed in less than 5 minutes. However, glucose infusion in the latter group increased the time to onset of angina (110 +/- 24 seconds before infusion versus 140 +/- 24 seconds following infusion) and decreased the extent of ST segment depression (1.8 +/- 0.3 mm before infusion versus 0.9 +/- 0.2 mm following infusion, p less than 0.01) following pacing. In all subjects, arterial levels and cardiac uptake of glucose rose by 100% (p less than 0.001) and those of free fatty acids fell by 50% (p less than 0.01). Arterial lactate and uptake of lactate by nonischemic myocardium increased by 30% (p less than 0.05). During pacing in CAD patients, this elevated uptake was outweighed by similar increases of lactate release from ischemic areas, leaving mean negative global exchanges unaltered. In CAD patients solely, rebuilding of cardiac glycogen after pacing was suggested from augmented citrate efflux in the control period but not during glucose infusion, suggesting a glycogen-sparing effect. Arterial concentrations and net cardiac fluxes of oxygen, glutamate, and alanine remained unaltered. In conclusion, beneficial effects of glucose during ischemia are associated with increased aerobic and anaerobic glycolysis, saving of glycogen, and decreased lipolysis.

Alanine↗
PubMed1989

Cardiac metabolic and hemodynamic effects of insulin in patients with coronary artery disease.

To assess the effects of insulin in stable coronary artery disease (CAD), 2 U i.v. insulin was given to 9 control and 10 CAD patients during coronary sinus catheterization. Hemodynamic and metabolic data were obtained before and for 90 min after insulin injection. Insulin induced no changes in heart rate, mean aortic pressure, rate-pressure product, coronary sinus flow, or coronary resistance. Metabolic changes were similar in both groups and included 1) 30% decrease of arterial glucose (P less than .001) and 3-fold increase of myocardial glucose uptake (P less than .001), 2) 1.5- to 2.5-fold elevation of arterial lactate (P less than .001) and myocardial lactate usage (P less than .001), respectively, 3) 50-70% suppression of arterial levels (P less than .001) and myocardial uptake of free fatty acids (P less than .01), and 4) 10% reduction of myocardial net oxygen consumption (P less than .05). Myocardial citrate efflux increased in the CAD patients (P less than .05), whereas alanine release rose only in control patients (P less than .01), suggesting that glucose enters glycogen production in the CAD patients and pyruvate production in the control patients to a high degree. Myocardial glutamate uptake remained unchanged. In conclusion, insulin sensitivity was not altered in CAD. The insulin-induced shift from myocardial free fatty acid to carbohydrate usage may be beneficial to the ischemic heart by increasing glycogen stores, saving oxygen, and inhibiting an excess free-fatty acid concentration, which may be toxic during ischemia.

Alanine↗
PubMed1988

Altered global myocardial substrate preference at rest and during pacing in coronary artery disease with stable angina pectoris.

In 21 control subjects with atypical chest pains and normal coronary arteries and in 64 patients with stable angina and coronary artery disease (CAD), myocardial exchanges of free fatty acids, glucose, lactate, citrate, glutamate, alanine and oxygen were determined before, during and after pacing. At rest, myocardial uptake of fatty acids was 50% lower in CAD patients than in the control subjects (p less than 0.001), whereas uptakes of glucose and lactate were twice as high (p less than 0.01). CAD patients showed increased myocardial glutamate uptake (p less than 0.001) and alanine release (p less than 0.001). In control subjects, myocardial fatty acid uptake was directly related (r = 0.54, p less than 0.01), whereas uptakes of glucose (r = -0.42, p less than 0.05) and lactate (r = -0.46, p less than 0.05) were inversely related to arterial fatty acid levels. Citrate release was inversely related to glucose uptake (R = 0.44, p less than 0.05). These relations were absent in CAD patients. Glutamate consumption correlated only with glucose uptake in CAD patients (p less than 0.001) but did so with lactate uptake and alanine release in all individuals (p less than 0.001). Pacing caused angina in the CAD patients but not in the control subjects. Pacing induced no metabolic changes among control subjects but provoked myocardial lactate release in 40 CAD patients, including an additional decrease of fatty acid uptake (p less than 0.05) and increase of glucose uptake (p less than 0.05) compared with resting levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Relation of left ventricular function and Na,K-pump concentration in suspected idiopathic dilated cardiomyopathy.

The possible relation between Na-K-pump concentration and left ventricular (LV) function was studied in 24 patients with suspected idiopathic dilated cardiomyopathy. This was done by measurement of 3H-ouabain binding to biopsies obtained during left-sided heart catheterization. In all patients light microscopy of biopsies was compatilel with dilated cardiomyopathy. Nineteen patients had impaired LV function as defined by NYHA/WHO and a Na,K-pump concentration of 331 +/- 19 pmol/g wet weight, whereas 5 patients had normal LV function and a Na,K-pump concentration of 559 +/- 62 pmol/g wet weight (p less than 0.001). The correlation between Na,K-pump concentration and ejection fraction was highly significant n = 24, r = 0.81, p less than 0.001). There was no correlation between volume fraction of collagen tissue and Na,K-pump concentration in the biopsies (n = 24, r = -0.08, p less than 0.80), indicating that the decrease in Na,K-pump concentration with dilated cardiomyopathy is not the simple outcome of increased fibrosis in the myocardium. The results indicate that the decrease in Na,K-pump concentration may be of importance for myocardial dysfunction and suggest a simple biochemical assessment of dilated cardiomyopathy by measurement of 3H-ouabain binding.

Adult↗
PubMed1988

Hemodynamic and cardiac metabolic changes during nicardipine-induced myocardial ischemia.

After 10 mg nicardipine IV a patient with stable angina developed chest pain and ST-segment depression accompanied by excessive tachycardia, low arterial blood pressure, and initially decreased coronary sinus blood flow. Measurements of arterial concentrations and cardiac exchanges of lactate, glucose, free fatty acids, glutamate, and alanine showed alterations indicative of severe ischemia.

Angina Pectoris↗
PubMed1987

Usefulness of ST deviation induced by prolonged hyperventilation as a predictor of cardiac death in angina pectoris.

One hundred ninety patients with chronic angina for an average of 2 years were followed. Forty-seven had at least 1 mm of ST deviation in response to provocation of coronary vasoconstriction by prolonged hyperventilation (group I); 143 had no ST deviation (group II). The angiographic response to this test was studied in 21 patients from group I, and revealed 25 to 100% diameter reduction; in group II 9 patients showed a 5 to 14% diameter reduction. In group I, 15 patients (32%) died (hazard rate = 0.17 deaths/patients X years) vs 18 (13%) in group II (hazard rate = 0.06) (p less than 0.01). Seven patients in group I (15%) and 3 in group 2 (2%) died while waiting for surgery (p less than 0.01). All patients who died had coronary stenoses of at least 70%. A Cox regression analysis, using 24 variables (invasive and noninvasive), showed a positive hyperventilation test (ST deviation at least 1 mm), low ejection fraction and systolic blood pressure of at least 160 mm Hg to be independent predictors of death (p less than 0.05). Considering only deaths in non-operated patients (patients waiting for surgery and patients not planned to undergo operation), a rate-pressure product/100 of 150 or less at exercise stress testing, left ventricular end-diastolic pressure of 15 mm Hg or more and duration of angina less than 1 year were also independent predictors of death. Thus, the hyperventilation test may be useful for identifying angina patients who are at high risk of cardiac death due to dynamic coronary obstructions.

Adult↗
PubMed1987

Metabolic and hemodynamic effects of nicardipine during pacing-induced angina pectoris.

During repeat exercise testing in 10 patients with stable angina, individual optimal doses of nicardipine were determined. Hemodynamic values and cardiac metabolism were studied during 2 pacing periods carried out before and after this dose (mean 5.3 mg). Postpacing ST-segment depression diminished (1 mm) after nicardipine administration (p less than 0.05), whereas pacing time to onset of angina did not change. Nicardipine administration increased heart rate 16% (p less than 0.005) and reduced systolic (10%) and diastolic (8%) blood pressures (both p less than 0.005). Coronary blood flow increased 16% (p less than 0.05) and coronary vascular resistance decreased 24% (p less than 0.01). Myocardial oxygen consumption was unchanged despite an 11% decrease in rate-pressure product during pacing (p less than 0.02). In the control state before nicardipine administration, metabolic signs of ischemia included release of lactate across the heart in 7 patients, decreased mean free fatty acid and glutamate uptake and alanine release during pacing, together with increased glucose uptake and citrate release during recovery. After nicardipine lactate release decreased in 5 of the 7 patients, pacing no longer changed free fatty acid, glutamate and alanine uptake/release from the level at rest. During recovery glucose uptake was reduced and citrate release was unaffected. The hemodynamic data indicate that nicardipine is a systemic and coronary vasodilator, increasing oxygen supply to the ischemic myocardium. The metabolic results indicate a change in substrate utilization toward that of normal heart, suggesting improved aerobic energy supply.

Alanine↗
PubMed1987

Atrial natriuretic peptide during pacing in controls and patients with coronary arterial disease.

At rest, during cardiac catheterization, aortic plasma levels of immunoreactive atrial natriuretic peptide did not differ between 10 controls with atypical chest pains and normal coronary arteries and 9 patients with stable angina pectoris and coronary arterial disease (55.2 +/- 19.8 vs. 64.8 +/- 19.8 pg/ml, NS). Nor did atrial natriuretic peptide values differ between the two groups during or after atrial pacing (150 beats/minute), which induced electrocardiographic and metabolic signs of acute myocardial ischaemia in the patients with coronary arterial disease but in none of the controls. Pacing, when carried out for more than 300 seconds, induced an increase of plasma atrial natriuretic peptide that correlated with duration of pacing (r = 0.80, P less than 0.001), and similarly in controls and patients with coronary arterial disease. In a second part of the study, which included 2 controls and 2 patients with coronary arterial disease, post-pacing coronary sinus concentrations of atrial natriuretic peptide were 10-20 times higher than peripheral levels (415- greater than 890 pg/ml). The concentration of atrial natriuretic peptide rose as blood from the caval veins (34 +/- 7 pg/ml) entered the right atrium (56 +/- 24 pg/ml), but thereafter was unchanged in the pulmonary artery (51 +/- 3 pg/ml) and the aorta (46 +/- 9 pg/ml). In conclusion, the results gave no evidence for ischaemic heart disease without congestive cardiac failure to be associated with altered levels of atrial natriuretic peptide. It was confirmed that atrial pacing stimulates the secretion of atrial natriuretic peptide which is produced by the heart and released via the coronary sinus into the circulation.

Atrial Natriuretic Factor↗
PubMed1987

Dose-related haemodynamic effects of nicardipine during rest and exercise and variable anti-anginal effects in patients with chronic stable angina.

The effects of increasing doses of i.v. nicardipine (2.5, 5.0 and 7.5 or 10.0 mg) on blood pressure, heart rate and exercise performance were studied in 12 patients with chronic effort angina. Plasma nicardipine concentrations correlated closely with the infused doses (r = 0.90). Resting haemodynamic changes after nicardipine included a dose-related fall in systolic (5%, 13%, 15%) and diastolic (0%, 6%, 8%) blood pressure and a rise in heart rate (10%, 19%, 30%). Rate-pressure product was slightly increased after the highest dose (10%). During exercise, maximal systolic blood pressure decreased (3%, 9%, 9%) and heart rate increased (2%, 4%, 9%) but the rate-pressure product remained unchanged. Exercise tolerance improved in 10 patients as indicated by prolonged exercise duration in all, delayed appearance of ST-segment depression in 6, decreased maximal ST-segment depression in 5, and abolished (N = 3) or diminished (N = 4) anginal pain at the end of exercise after optimal nicardipine dose. Five of the 10 patients obtained maximum benefit after the highest dose. The other five patients improved after 2.5 or 5.0 mg but deteriorated (N = 4) or had no further benefit when the dose was increased (N = 1). One patient deteriorated even after the lowest dose, whereas one patient neither improved nor deteriorated after any dose. The patients who deteriorated after low or high doses tended to be more severely diseased than those who tolerated the maximal dose well. The results stress the importance of individual dose titration of nicardipine to ensure maximum benefit in patients with chronic effort angina.

Angina Pectoris↗