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Biomedical subjects

H Wesseling

Publications and source records attributed to H Wesseling.

At least 91 records · Page 5Linked to original sources
PubMed1988

Digoxin-felodipine interaction in patients with congestive heart failure.

A possible interaction between felodipine and digoxin was studied in 23 patients with congestive heart failure before and after 8 weeks treatment with both drugs. A modest, non-significant increase in serum digoxin level 2 h postdose (+15%) was found in the felodipine group (n = 11) compared to placebo (n = 12), with no change in the trough and 6 h postdose levels. There was a bimodal distribution of the observed changes in serum digoxin level 2 h postdose: a significant increase (p less than 0.001) was observed only in patients with a high plasma felodipine level, which may have been caused by changes in the absorption rate in those patients. Changes in the elimination of digoxin after felodipine therapy appeared unlikely, since the trough and 6 h post-dose levels were unchanged. Analysis of the clinical characteristics, haemodynamics and laboratory values revealed no significant differences between the subgroups. The observed increase in serum digoxin warrants monitoring the trough and peak levels digoxin in patients with congestive heart failure who are also being treated with felodipine.

Aged↗
PubMed1988

Value of New York Heart Association classification, radionuclide ventriculography, and cardiopulmonary exercise tests for selection of patients for congestive heart failure studies.

To evaluate the necessity of an objective cardiopulmonary exercise test in the selection procedure of patients for heart failure studies, 50 patients with congestive heart failure New York Heart Association (NYHA) class II and III and a left ventricular ejection fraction less than 40% were subjected to a cardiopulmonary exercise test. The results of the exercise test were compared with the independent clinical estimation of NYHA class and data of measurements obtained at rest. The NYHA classification separated the patients with a mild to moderate impairment of aerobic capacity from patients with a moderate to severe impairment of aerobic capacity very well, but 32% of the NYHA class II patients had a near normal aerobic capacity, and 29% of the NYHA class III patients had a very severe impairment of aerobic capacity, more compatible with NYHA class IV. Only data from exercise measurements showed differences between groups. The determination of maximal aerobic capacity for an objective assessment of patients' performance at exercise is necessary for a proper selection procedure of patients for heart failure studies.

Adult↗
PubMed1988

Effect of metoclopramide on dopamine-induced changes in renal function in healthy controls and in patients with renal disease.

1. The effects of intravenous metoclopramide on baseline values and dopamine dose-response curves for renal haemodynamics and natriuresis were investigated in healthy volunteers and patients with renal disease. 2. Dopamine infusion alone, in doses ranging from 0.25 to 8 micrograms min-1 kg-1, resulted in a dose-dependent increase in effective renal plasma flow (ERPF) and glomerular filtration rate (GFR) with a fall in filtration fraction (FF) in eight hydrated healthy volunteers and, to a lesser degree, in 12 patients with renal disease. An increase in natriuresis (urinary excretion of sodium, UNa+V), fractional excretion of sodium (FENa+) and diuresis (urine flow rate, UV) was found in both groups for doses of 2 micrograms min-1 kg-1 and higher. 3. Metoclopramide infusion did not alter baseline values of GFR, ERPF or FF, but shifted the dopamine dose-response curve for ERPF and FF in the healthy volunteers. Metoclopramide induced a fall in UNa+V and FENa+ in both groups (fall in baseline FENa+ from 1.52 to 0.71 during metoclopramide in healthy volunteers and from 1.23 to 0.56 in patients; P less than 0.01) and blunted the natriuretic response to subsequent dopamine infusion. The fall in UNa+V during metoclopramide infusion showed a strong correlation with baseline GFR (r = -0.944). In the patients, the response for the fractional excretions of beta 2-microglobulin and gamma-glutamyltransferase was comparable with that of FENa+. 4. Dopamine infusion induced a fall, and metoclopramide led to rise, in plasma aldosterone concentration. 5. We conclude that metoclopramide acts as a dopamine antagonist at the renal level in man.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Differential influences of angiotensin converting-enzyme inhibitors on the coronary circulation.

The effects of captopril and zofenoprilate (the active form of the prodrug zofenopril and also a sulfhydryl-containing angiotension converting-enzyme inhibitor) on coronary flow in the isolated rat heart were compared with the effects of a nonsulfhydryl converting-enzyme inhibitor, ramiprilate (the active form of the prodrug ramipril) and of sulfhydryl-containing compounds with no converting-enzyme inhibiting properties such as glutathione, cysteine, and the (R,S)-isomer of captopril. Drug concentrations of the angiotensin converting-enzyme inhibitors were equipotent in their effect on angiotensin I pressor response. Concentrations of the other compounds were equimolar with respect to the sulfhydryl group. Hearts treated with captopril, its isomer, zofenoprilate, cysteine, and glutathione showed significant increases in coronary flow by 5 min of perfusion. In contrast, ramiprilate treatment resulted in a slower increase in coronary flow that was only significant after 20 min of perfusion. The effect of ramiprilate was associated with a significant increase in 6-keto-prostaglandin (PG) F1 alpha overflow in the coronary effluent compared with that in saline-treated hearts, whereas captopril and glutathione had no significant effect on overflow of the measured cyclooxygenase products 6-keto-PGF1 alpha, thromboxane B2, and PGE2. The effects of captopril, zofenoprilate, and glutathione on coronary flow were dose dependent. These results corroborate the view that ramiprilate enhances coronary flow by affecting prostacyclin synthesis, mediated by an increase of endogenous bradykinin.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1987

Acute hemodynamic and hormonal effects of ramipril in chronic congestive heart failure and comparison with captopril.

Acute hemodynamic and hormonal responses to ramipril in comparison with captopril were studied in 10 patients with moderate to severe congestive heart failure in an open, randomized study. Both drugs were given to 5 patients each in 2 increasing doses on 2 successive days. After 5 mg of ramipril angiotensin converting enzyme (ACE) activity was significantly decreased during 24 hours with a maximum decrease 4 hours after administration. Mean arterial blood pressure decreased from 84 +/- 5 to 62 +/- 5 mm Hg at 4 hours and 71 +/- 4 mm Hg at 12 hours, respectively, after this dose. Capillary wedge pressure decreased from 19 +/- 1 mm Hg to 13 +/- 1 mm Hg at 4 hours with a maximum increase in cardiac output from 3.8 +/- 0.3 liters/min to 4.4 +/- 0.3 liters/min at 2 hours. No significant cardiac effects were present 8 hours after administration. After 10 mg of ramipril, cardiac and hormonal effects showed a quicker onset of action and longer duration compared with the 5 mg dose. Mean arterial pressure decreased to 61 +/- 6 mm Hg. Similar effects were seen after captopril, but with a significantly shorter duration. Mean arterial pressure decreased from 82 +/- 4 mm Hg to 64 +/- 5 mm Hg after 12.5 mg and to 58 +/- 6 mm Hg after 25 mg of captopril. In patients with congestive heart failure ramipril has the hemodynamic profile of a long-acting and potent ACE inhibitor. Significant cardiac effects are present during 4 to 8 hours and ACE activity is still significantly inhibited 24 hours after a single dose of ramipril.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1987

Does indirect consultation lead to overprescribing in general practice?

Indirect consultations (by telephone or receptionist) are of increasing importance in general practice and may result in more prescribing than during direct (face to face)-consultations. We analysed prescribing data for 14,660 disorders, presented in one week in 52 general practices. In general, a significant, but hardly relevant increase in prescribing during indirect consultations was observed. The effect varies strongly for different disorders and was especially relevant for repeat-prescriptions for the following conditions: musculoskeletal- and connective tissue diseases, endocrine, nutritional and metabolic disorders and disorders of the female genital tract.

Drug Prescriptions↗
PubMed1987

Suprofen versus paracetamol after oral surgery.

A randomized double-blind trial was performed to evaluate efficacy and tolerability of suprofen 200 mg (Suprocil) in comparison to paracetamol 500 mg after surgical extraction of a wisdom tooth. The study lasted 4 days per patient at the longest. Pain intensity and pain relief were evaluated by the patients using a visual analog scale. A total of 59 patients took part in the study; of these, 30 were on suprofen and 29 on paracetamol. The 30-min pain relief with paracetamol was superior to that obtained with suprofen. Roughly, the 90-min pain relief scores were somewhat higher for suprofen than for paracetamol. However, none of the differences were statistically significant. No significant difference was seen between the 2 treatment groups with respect to the frequency of the number of capsules taken per day. Broadly, the efficacy was good or excellent in 18 patients in each group. With suprofen, there were 8 moderate results and 4 insufficient ones. With paracetamol, 6 results were moderate and 5 insufficient or worse. No significant differences between the 2 treatments was seen. Tolerability was rated good by all but 1 patient in each treatment group; with suprofen, 1 result was moderate, while with paracetamol, 1 result was poor. Adverse reactions occurred in 3 patients on suprofen and in 2 patients on paracetamol, though these reactions could not be related to the use of the drug itself.

Acetaminophen↗
PubMed1987

Concentration-dependent protection by captopril against myocardial damage during ischemia and reperfusion in a closed chest pig model.

We previously reported concentration-dependent protection of captopril against ischemia-reperfusion injury in the isolated rat heart. In order to study these effects in vivo, we developed a closed-chest pig model. Reversible occlusion of the left coronary artery was achieved with a PTCA catheter during one hour. Captopril (C) i.v. was given in two different concentrations (0.6 mg/kg/10 min + 0.3 mg/kg/2 hr and 6 mg/kg/10 min + 3.0 mg/kg/2 hr) during the experiments to 11 and 10 pigs, respectively, versus 12 controls, who received only saline. Due to malignant ventricular arrhythmias, nine pigs died during ischemia. At the end of the reperfusion period of two hours, eight pigs were alive in each group. In the C-treated pigs, maximum creatine kinase after two hours of reperfusion was significantly lowered to 6,337 +/- 709 U/L in the high dose group versus 8,285 +/- 851 U/L in the low dose group and 9,635 +/- 1,115 U/L in the saline group. A reduction of local inosine overflow in the coronary sinus was seen. Maximum noradrenaline overflow after 5 min reperfusion diminished dose-dependently to 695 +/- 284 and 3,129 +/- 1,728 pg/ml in the C treated groups versus 4,693 +/- 2,277 pg/ml in the saline group. Mean arterial blood pressure and cardiac output decreased significantly during ischemia and reperfusion, but no significant differences occurred between the treated and untreated groups. Reperfusion arrhythmias, mainly accelerated idioventricular rhythm disturbances, were comparable among the three groups. We conclude that in vivo administration of C reduces myocardial damage upon reperfusion after one hour of ischemia in a dose-dependent way.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Captopril-induced increase in coronary flow: an SH-dependent effect on arachidonic acid metabolism?

The effect of captopril (80 micrograms/ml) on coronary flow in the isolated rat heart was compared with the effects of a non-sulfhydryl-converting enzyme inhibitor, ramipril (15 micrograms/ml), and of a sulfhydryl-containing compound with no converting enzyme-inhibiting properties, glutathione (112 micrograms/ml). Drug concentrations were equipotent in their effect on angiotensin I pressor response and equimolar with respect to the sulfhydryl group. Cyclooxygenase products or their stable metabolites (TXB2, 6-keto-PGF1 alpha and PGE2) were measured in the coronary effluent. Furthermore, the effect of mepacrin (1 microM), indomethacin (1 microM), and FPL 55712 (10 microM) on the changes in coronary flow induced by captopril was studied. Both captopril- and glutathione-treated hearts showed a significant increase in coronary flow already after 5 min treatment. After 60 min treatment, coronary flow was further increased to 185 +/- 9% for captopril-treated hearts and to 210 +/- 11% for glutathione-treated hearts when compared to saline treatment. Ramipril treatment resulted in a slower increase in coronary flow, which was significant after 20 min treatment. After 60 min treatment, this increase was 122 +/- 3% when compared to saline-treated hearts. This effect of ramipril was associated with a significant increase in 6-keto-PGF1 alpha overflow when compared to saline-treated hearts. Captopril and glutathione had no significant effect on overflow of the measured cyclooxygenase products. The effect of captopril and glutathione on coronary flow appeared to be dose dependent in an equimolar range. Simultaneous mepacrin treatment diminished the effect of captopril on coronary flow; indomethacin had no effect, and FPL 55712 potentiated the effect of captopril.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Nifedipine in Raynaud's phenomenon: relationship between immediate, short term and longterm effects.

Sixteen patients with Raynaud's phenomenon (8 with primary Raynaud's, 8 with systemic sclerosis including 3 patients with CREST) were treated for 4 weeks in a double blind crossover study with nifedipine, 20 mg twice daily. Treatment resulted in improvement of symptoms (p less than 0.05), a lower frequency of attacks (p less than 0.05) and a tendency to a shorter duration of the attacks. Photoelectric plethysmography during nifedipine treatment showed greater amplitudes on cooling (p less than 0.05) and a better and faster recovery on rewarming (p less than 0.05) than during placebo. The immediate effect of nifedipine, 10 mg sublingually, on the amplitude of the plethysmogram, finger temperature, heart rate and blood pressure did not correlate with the effect of maintenance treatment. Dose titration based on therapeutic effect and side effects resulted in a dose of 20 mg daily for 5 patients, 40 mg for 7, and 80 mg daily for 3 patients. Longterm treatment (16-20 weeks) resulted in sustained efficacy, both by subjective and objective standards (plethysmography).

Adult↗
PubMed1986

Effects of diltiazem on reperfusion-induced arrhythmias in vitro and in vivo.

The effects of the calcium antagonist, diltiazem, on myocardial injury during ischemia and reperfusion were studied both in vitro, in the isolated rat heart, and in vivo, in a closed-chest pig model. In the isolated rat heart, administration of diltiazem before or at the onset of ischemia resulted in a dose-dependent reduction of the incidence and duration of ventricular fibrillation. This reduction was associated with a dose-dependent reduction in overflow of ATP catabolites (adenosine, inosine, hypoxanthine and xanthine). Both changes were significant at concentrations of 3 X 10(-7) M diltiazem and higher. When 3 X 10(-7) M diltiazem was administered upon reperfusion no effect on the incidence of ventricular fibrillation and on ischemia induced total purine overflow was observed. However, the duration of ventricular fibrillation and purine overflow at 5 min after reperfusion were significantly reduced. In the pig experiments all untreated animals (n = 8) showed accelerated idioventricular rhythm (AIVR) upon reperfusion which lasted for 22 +/- 5 min after which sinus rhythm returned. Only two out of five treated animals (450 micrograms/kg/2 h) had an AIVR. Upon reperfusion both groups showed a substantial rise in noradrenaline concentration in the coronary sinus blood, but after 5 min this was significantly less in the treated group. Creatine kinase-kinetics were not altered by diltiazem, but the maximum creatine kinase level was significantly reduced. Within 4 days after the acute experiment 50% of the untreated animals died suddenly, whereas no sudden deaths occurred in the diltiazem group (P less than 0.05). Seven days after the acute experiment, sustained ventricular tachycardia could be induced with programmed electrical stimulation in three out of four surviving untreated pigs. In none of the diltiazem treated pigs was ventricular tachycardia inducible. The results of this study show that the calcium antagonist diltiazem can beneficially influence the events during ischemia and during reperfusion, both in vitro and in vivo; this benefit is associated with a reduction of ATP catabolism, creatine kinase release and noradrenaline overflow. Furthermore, diltiazem reduces electrical instability in the chronic phase of myocardial infarction.

Adenosine Triphosphate↗
PubMed1986

Concentration-dependent protection by captopril against ischemia-reperfusion injury in the isolated rat heart.

The purpose of this study was to investigate the protective effects of captopril at three concentrations (1, 10 and 80 micrograms/ml) against reperfusion injury after 15 min of coronary ligation in the isolated perfused rat heart. During ischemia, the apex displacement (AD) and pressure rate index (PI) decreased markedly and only in the presence of 80 micrograms captopril less reduction of the PI was obtained (p less than 0.05). Upon reperfusion, the AD and PI improved significantly in all captopril treated hearts, depending on the concentration used, whereas the untreated hearts showed a further deterioration (p less than 0.05). Ventricular fibrillation upon reperfusion occurred in 6/6 untreated hearts, but only in 4/6 hearts at 1 microgram/ml, in 2/6 hearts at 10 micrograms/ml and 0/6 hearts at 80 micrograms/ml captopril with a significantly shorter duration (p less than 0.05). In control hearts a marked overflow of purines and norepinephrine was found in the coronary effluent upon reperfusion. In contrast, captopril decreased purine overflow, most at 80 micrograms/ml, and norepinephrine levels were undetectable at all concentrations. These results indicate concentration-dependent protective effects of captopril after local ischemia and reperfusion, already present at therapeutic levels. Reduction of cellular injury and suppression of NE release appear to play an important role in the improvement of mechanical function and the reduction of reperfusion arrhythmias.

Angiotensin II↗