PubMed Health⌕ Search

Biomedical subjects

F Waagstein

Publications and source records attributed to F Waagstein.

140 records · Page 8Linked to original sources
PubMed1977

Intravaginal electrical stimulation. Clinical experiments on bladder inhibition.

The effect of intravaginal electrical stimulation (IVS) on the bladder in 17 patients with motor detrusor instability was explored. Isotonic volume registrations and cystometries were used for evaluation of volume increase and inhibition of abortive detrusor contractions. With either one or the other method, bladder inhibition was found in all patients, but with both methods only in 6. During isotonic volume registration, the volume increase showed considerable variations ranging between 4 to 465%, and during cystometry between 11 to 3500%. Bladder inhibition proved to be most effective when using a frequency of 10 Hz.

Adult↗
PubMed1976

Effect of cardioselective beta-blockade on heart function and chest pain in acute myocardial infarction.

Systolic time intervals and the a/H ratio were recorded in 20 patients with uncomplicated acute myocardial infarction over a period of five days. The initial high heart rate and systolic blood pressure and the short PEP and ICT indicating a sympathetic overactivity were spontaneously normalized during the first week of infarction. LVET was reduced indicating a fall in stroke volume and the a/H ratio was unchanged at the high levels suggestive of elevated preload or LVEDP. In 10 patients with acute myocardial infarction and recurrent chest pain recordings on noninvasive parameters were made before and 30 min after intravenous injection of practolol. In addition, 7 patients with chest pain, classified as acute myocardial infarction, were given practolol. The average dose of practolol was 17.9 mg ranging from 5 to 30 mg. An almost immediate and pronounced relief of pain was observed in all patients and no signs of impaired left ventricular function appeared. The product of systolic blood pressure and heart rate was decreased by practolol and the PEP and the ICT were prolonged to normal values while no changes were seen in LVET and a/H ratio. On 126 occasions practolol was given in dosages ranging from 5 to 30 mg (mean 8 mg) to 75 patients with acute myocardial infarction and recurrent chest pain. A satisfactory pain relief was seen on 108 occasions. It is suggested that an inappropriate sympathetic overactivity is an important factor in provoking recurrent chest pain in acute myocardial infarction. Administration of the beta-adrenergic blocking agent practolol resulted in pain relief due to reduction of heart work and in severity of myocardial ischemia. The beta-blocking agent was well tolerated in the present study. Continuous beta-blockade during the whole hospital stay to patients with acute myocardial infarction seems to be a very attractive therapy in order to preserve the ischemic myocardium and limit the size of infarction.

Acute Disease↗
PubMed1976

Double-blind study of the effect of cardioselective beta-blockade on chest pain in acute myocardial infarction.

A double-blind study including three different cardioselective beta-blockers, practolol, H 87/07 and metoprolol, was performed in 54 patients with acute myocardial infarction and chest pain shortly after onset of symptoms. Transmural infarctions were found in 42 patients while 12 patients had nontransmural infarctions. Chest pain and the product of heart rate and systolic blood pressure were significantly reduced in the beta-blocker groups whereas no changes were seen after saline. All patients with nontransmural infarctions and 14 out of 29 with transmural infarctions got pain relief lasting for at least 30 min. None of the patients developed signs of left ventricular backward failure, shock, or bradycardia. A decrease in ST segment elevation was observed in all the transmural infarctions after beta-blockade. No changes in ST segment elevation were found after analgesics when given after saline, but in some cases an increase was seen in this parameter when analgesics were given due to insufficient pain relief after beta-blockers or due to return of chest pain. It is suggested that pain relief by beta-blockers indicates decrease of myocardial ischemia.

Acute Disease↗
PubMed1975

Effect of chronic beta-adrenergic receptor blockade in congestive cardiomyopathy.

Adrenergic beta-blocking agents were given to 7 patients with advanced congestive cardiomyopathy who had tachycardia at rest (98 plus or minus 13 beats/min). The patients were on beta-adrenergic receptor blockade for 2 to 12 months (average 5-4 months). One patient was given alprenolol 50 mg twice daily and the other patients were given practolol 50 to 400 mg twice daily. Virus infection had occurred in 6 of the patients before the onset of symptoms of cardiac disease. All patients were in a steady state or were progressively deteriorating at the start of beta-adrenergic receptor blockade. Conventional treatment with digitalis and diuretics was unaltered or reduced during treatment with beta-blocking agents. An improvement was seen in their clinical condition shortly after administration of the drugs. Continued treatment resulted in an increase in physical working capacity and a reduction of heart size. Noninvasive investigations including phonocardiogram, carotid pulse curve, apex cardiogram, and echocardiogram showed improved ventricular function in all cases. The present study indicates that adrenergic beta-blocking agents can improve heart function in at lease some patients with congestive cardiomyopathy. Furthermore, it is suggested that increased catecholamine activity may be an important factor for the development of this disease, as has been shown in animal experiments.

Adult↗
PubMedDate not supplied

Effect of metoprolol on activity of beta-adrenoceptor coupled to guanine nucleotide binding regulatory proteins in adriamycin-induced cardiotoxicity.

Prevention of cardiotoxicity without interfering with the therapeutic efficacy of adriamycin is a very crucial question. We have investigated the activity of beta-adrenoceptor coupled to guanine nucleotide binding regulatory proteins (G-proteins) and Ca(2+)-ATPase activity in experimental adriamycin-induced cardiotoxicity and the influence of metoprolol treatment on these variables. Adriamycin was administered to rats intravenously as a single dose of 6 mg/kg, and metoprol was continuously given by means of implanted osmotic pumps. beta-Adrenoceptor characteristics were measured by radioligand-binding experiments and by basal and stimulated adenylyl cyclase activity. Northern blot and dot blot analysis was used to quantify G-protein mRNA. It was shown that adriamycin did not induce any change in the total beta-adrenoceptor density, nor did the high affinity agonist binding to beta-adrenoceptor change. Adriamycin did not induce any alteration in the amount of mRNA encoding for stimulatory (Gs) or inhibitory (Gi) G-proteins. Also, basal and stimulated adenylyl cyclase activities were identical in the different experimental groups. In contrast, the Ca(2+)-ATPase was shown to increase in adriamycin-treated rats compared to control rats (45 +/- 3.8 versus 23 +/- 1.2 mumol Pi/mg/h, P less than .01). Metoprolol was shown to normalize this increase (29 +/- 2.1 mumol Pi/mg/h). Thus, it may be concluded that in experimental adriamycin-induced cardiotoxicity, despite Ca(2+)-overloading, the beta-adrenoceptor-G protein-adenylyl cyclase system remains intact. Metoprolol seems to prevent Ca(2+)-overloading independently of the beta-adrenoceptors studied here.

Adenylyl Cyclases↗
PubMedDate not supplied

Effects of nifedipine on arterial concentration and myocardial extraction of catecholamines during pacing-induced angina pectoris.

We studied nine patients with arteriosclerotic coronary heart disease (Group I) and 10 patients with normal coronary arteries (Group II) to elucidate mechanisms by which nifedipine affects catecholamine arterial levels and myocardial extraction at rest and during pacing. Nifedipine induced signs of general and coronary vasodilatation and improved myocardial lactate metabolism during pacing. Noradrenaline arterial concentration increased significantly after nifedipine in both groups (p less than 0.01). In Group I, the values were 40-50% higher compared with Group II. The net myocardial extraction of noradrenaline was not significantly affected by nifedipine, except during pacing in Group II, in which an increase in myocardial release was seen (p less than 0.05). In Group I, there was no correlation between arterial concentration of noradrenaline and myocardial release, while there was a significant negative correlation in Group II (p less than 0.0001). Adrenaline arterial concentration and myocardial extraction were not altered by nifedipine, but there was a positive significant correlation in Group I between arterial concentration and myocardial extraction of adrenaline (p less than 0.001). In conclusion, nifedipine increased noradrenaline levels in both groups of patients, probably reflecting a rise in sympathetic activity. Because myocardial lactate production turned into extraction in patients with coronary artery disease, the increased sympathetic tone evidently did not outweigh the beneficial antianginal effects of nifedipine.

Adult↗
PubMedDate not supplied

Effects of felodipine on pacing-induced angina pectoris.

We determined hemodynamics and myocardial lactate extraction in 11 patients with severe coronary disease after 0.010 (D1), 0.015 (D2), and 0.025 nmol/min (D3) of the arteriolar dilator felodipine during pacing-induced angina pectoris. Plasma concentrations of felodipine after the 3 doses were 12 (5), 25 (6) and 43 (8) nmol/ L, respectively. At corresponding pacing rates, mean blood pressure fell from 126 (24) to 90 (15) mm Hg at D3 (p less than 0.01) and pulmonary capillary wedge pressure was reduced from 14 (10) to 9 (8) mm Hg (p less than 0.05). Cardiac output increased at all three doses (p less than 0.01). The reduction of systemic vascular resistance at D3 was 49% (p less than 0.01) and of coronary vascular resistance 35% (p less than 0.05). At D1, there was no change in lactate extraction, while 8/10 lactate producers improved at D2 and D3. ST depression was diminished at all three doses (p less than 0.05) at the control pacing rate. During maximal pacing rate at D3, the myocardial oxygen consumption was 14% above control level (N.S.). Thus, felodipine was beneficial in most patients at higher dosage. Ventricular unloading and improved coronary perfusion might explain some of these positive effects.

Aged↗
PubMedDate not supplied

Inhaled nitric oxide in the evaluation of heart transplant candidates with elevated pulmonary vascular resistance.

The reversibility of elevated pulmonary vascular resistance in heart transplant candidates is currently evaluated with intravenous vasodilators. The aim of this study was to evaluate the effects of increased concentrations of inhaled nitric oxide (20, 40, and 80 ppm) on central hemodynamics and right ventricular function in heart transplant candidates with elevated pulmonary vascular resistance (> 2.5 Wood units). Comparison was made with intravenous vasodilators, sodium nitroprusside, and prostacyclin in doses that lowered the mean arterial pressure by about 15%. Inhalation of nitric oxide did not change systemic or pulmonary arterial pressure, cardiac output, right ventricular function, or systemic vascular resistance. Pulmonary capillary wedge pressure increased and transpulmonary pressure gradient and pulmonary vascular resistance decreased (-34% +/- 4% and -36% +/- 4%, respectively; p < 0.01) during 20 ppm nitric oxide, with no further effects at higher doses. Prostacyclin and sodium nitroprusside decreased pulmonary vascular resistance (-50% +/- 6% and -33% +/- 5%; p < 0.01). Prostacyclin reduced to some extent (p = 0.08) transpulmonary pressure gradient, which was not seen during sodium nitroprusside infusion. Systemic vascular resistance decreased during both sodium nitroprusside (-37% +/- 5%) and prostacyclin (-44% +/- 4%) infusion. The pulmonary vascular resistance/systemic vascular resistance ratio, used as an index of pulmonary selectivity, was decreased by nitric oxide (p < 0.01) but not by the intravenous vasodilators. Metabolic data indicate that inhaled nitric oxide is metabolized in the same way as that formed endogenously. In conclusion, inhaled nitric oxide is a selective pulmonary vasodilator that can be used safely in the hemodynamic evaluation of heart transplant candidates with elevated pulmonary vascular resistance.

Administration, Inhalation↗
PubMedDate not supplied

Prognosis of alternative therapies in patients with heart failure not accepted for heart transplantation.

BACKGROUND AND METHODS: This article describes the outcome of alternative therapies in patients with end-stage heart failure, New York Heart Association class III-IV, referred for heart transplantation evaluation but not accepted for the procedure. From January 1988 through September 1992, 233 consecutive patients with severe heart failure were admitted to the thoracic transplantation center at Sahlgrenska University Hospital. At the time of admission all patients received standard medical treatment for heart failure. During the pretransplantation evaluation, an attempt to optimize the medical therapy was made in all patients. RESULTS: Eighteen patients (8%) died before a decision concerning transplantation was made, and 146 patients (63%) were accepted for heart transplantation. There were 69 patients (30%) who were denied heart transplantation for various reasons, and they were subgrouped: patients with contraindications (group 1, n = 23) or without indication (group 2, n = 10) for heart transplantation, patients with a positive response to intensified medical therapy (group 3, n = 25), and patients who underwent coronary artery bypass grafting and/or valvular heart surgery (group 4, n = 11). The 1-, 3-, and 5-year actuarial survival rates were as follows: group 1, 26%, 16%, and 8%; group 2, 100%, 77%, and 39%; group 3, 96%, 67%, and 53%; and group 4, 64%, 36%, and 27%, respectively. The corresponding figures for patients who had a heart transplantation were 85%, 79%, and 75%, respectively. During the first 2 to 3 years of follow-up the survival of group 2 and group 3 patients was similar to that of patients who underwent transplantation. However, late survival was worse compared with the heart transplant group. CONCLUSIONS: These results suggest that by close follow-up it may be possible to postpone heart transplantation in a selected group of patients.

Adult↗