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Biomedical subjects

H Emanuelsson

Publications and source records attributed to H Emanuelsson.

At least 109 records · Page 6Linked to original sources
PubMed1989

Effects of diltiazem and isosorbide-5-mononitrate, alone and in combination, on patients with stable angina pectoris.

The anti-anginal effect of sustained release diltiazem, isosorbide-5-mononitrate (IS-5-MN) and their combination has been evaluated in 25 patients in 4 blinded treatment periods of 2 weeks each. The number of anginal attacks during each treatment period was reduced from a mean of 23 during placebo to 15 during diltiazem and 15 during combination therapy, but it was not significantly changed after IS-5-MN-20. A similar pattern was seen for nitroglycerin consumption and number of angina-free days. Maximal exercise capacity was also significantly improved following diltiazem and the drug combination, and it was not changed after IS-5-MN. ST segment depression was less pronounced after diltiazem and the combination compared to IS-5-MN. There was no difference in exercise capacity or ST segment change between diltiazem and the combination. The PR interval was slightly prolonged after diltiazem, but this was of no clinical importance. Adverse effects of diltiazem treatment were rare. Headache was common following IS-5-MN (13 patients) and the combination (11 patients). Thus, sustained-release diltiazem was of value in the treatment of chronic stable angina pectoris, whereas IS-5-MN was not effective, either as a single therapy or in combination with diltiazem. The reason for the inefficacy of IS-5-MN is not known, but the development of tolerance and an inadequate dose are possible explanations.

Adult↗
PubMed1989

Thoracic epidural anaesthesia in patients with unstable angina pectoris.

The effect of high thoracic epidural anaesthesia with intermittent epidural bolus injections of bupivacaine (2.5 or 5 mg ml-1) was studied in 28 patients with unstable angina pectoris. The majority of the patients had a history of previous acute myocardial infarction(s) and/or angina pectoris and severe coronary artery disease. All patients were treated with nitroglycerin infusion for greater than 24 h and were included in the study if they had chest pain, not caused by acute myocardial infarction, at bed rest or recurrent anginal pain at rest greater than 2 days after infarction. 4.4 +/- 0.3 ml of bupivacaine induced a blockade of the upper seven sympathetic segments (Th1-7) for 98 +/- 9 min. Heart rate decreased significantly from 70 +/- 3 to 64 +/- 3 beats min-1 while blood pressure was unaffected by thoracic epidural anaesthesia. In 27 patients (96%) the anaesthesia induced complete analgesia. Nitroglycerin infusion was discontinued definitely within 3 h in 26 patients (93%) and pain was thereafter controlled by means of thoracic epidural anaesthesia as the sole treatment in 23 patients (82%) and as the major treatment in 25 patients (89%). Twenty-one patients (75%) were fully mobilized and stabilized. Treatment with thoracic epidural anaesthesia lasted for 6.0 +/- 1.1 days. The number of daily epidural injections decreased significantly with time from 2.7 +/- 0.3 the first day to 0.9 +/- 0.3 the fourth day (P less than 0.01, n = 19). Two patients developed acute myocardial infarction during the anaesthesia treatment period, and one of these patients died.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Influence of naloxone on the effects of high frequency transcutaneous electrical nerve stimulation in angina pectoris induced by atrial pacing.

The influence of naloxone on the effects of high frequency transcutaneous electrical nerve stimulation in angina pectoris induced by atrial pacing was studied in 11 patients with severe coronary artery disease. The patients were catheterised and treated with transcutaneous electrical nerve stimulation on two occasions, double blind and in random order, with a single intravenous dose of saline or with a single intravenous dose of 50 mg naloxone. Treatment with transcutaneous electrical nerve stimulation increased tolerance to pacing and significantly improved lactate metabolism with placebo and with naloxone. The positive effects of transcutaneous electrical nerve stimulation were thus reproducible and not reversed by single intravenous doses of naloxone. The results indicate that the effects of transcutaneous electrical nerve stimulation on the heart are not mediated by beta endorphin but they do not exclude activation of more short-acting opioids such as delta or kappa receptor agonists (met-enkephalin or dynorphin or both) because naloxone has a low affinity for these receptors. Non-opioid mechanisms may also be important.

Aged↗
PubMed1989

Thoracic epidural anesthesia and central hemodynamics in patients with unstable angina pectoris.

The effects of high thoracic epidural anesthesia (TEA) on central hemodynamics as measured by pulmonary arterial catheterization were studied in nine patients with severe coronary artery disease and unstable angina pectoris. The patients were also treated with a combination of beta-blockers, calcium antagonists, and nitrates, as well as salicylates, low-dose heparin, and nitroglycerin infusion for greater than 24 hr. Management of pain with high TEA was started with the bolus epidural injection of 4.3 +/- 0.2 mL bupivacaine (5 mg/mL), which induced a sympathetic blockade from Th. During ischemic chest pain, pulmonary artery and pulmonary capillary wedge pressures were significantly increased. TEA, while relieving the chest pain, significantly decreased systolic arterial blood pressure, heart rate, and pulmonary artery and pulmonary capillary wedge pressures, without any significant changes in coronary perfusion pressure, cardiac output, stroke volume, and systemic or pulmonary vascular resistances. In some patients, ST-segment depression was less pronounced during TEA. Thus, during ischemic chest pain, TEA has beneficial effects on the major determinants of myocardial oxygen consumption, without jeopardizing coronary perfusion pressure. TEA may therefore favorably alter the oxygen supply/demand ratio within ischemic myocardial areas.

Aged↗
PubMed1988

Presence of serotonin in early chick embryos.

With biochemical analysis and with autoradiography based on injection of 5-[3H]hydroxytryptophan, it was possible to demonstrate the presence of serotonin (5-hydroxytryptamine) in early chick embryos as early as the pre-streak stage. The biochemical analysis which covered the early developmental period (0.5-6 days of incubation) revealed an elevated concentration of serotonin at gastrulation; from then it stayed at a lower and fairly even level. Autoradiographs of embryos at the pre-streak stage, the primitive streak stage, the head fold stage and the 4-6 somites stage indicated the presence of serotonin in intracellular yolk granules and in cell nuclei. Moreover, the amine appeared associated with microfilaments and microtubules, particularly in developing neural cells. Notably the elevated concentration of serotonin at gastrulation, but also the intracellular distribution of the amine during early organogenesis, indicates a prominent role for it in cell-shape changes and morphogenesis in the early chick embryo.

5-Hydroxytryptophan↗
PubMed1987

Inhibition of polyamine synthesis reduces the growth rate and delays the expression of differentiated phenotypes in primary cultures of embryonic mesoderm from chick.

Inhibition of polyamine synthesis in early chick embryos blocks their development at gastrulation. Analyses of arrested embryos show that mesodermal outgrowth and differentiation are drastically impaired. To study these effects in greater detail, we have used primary cultures of embryonic mesoderm from chick. The cultures were treated with alpha-difluoromethylornithine (DFMO), an enzyme-activated irreversible inhibitor of ornithine decarboxylase, the first and rate-limiting enzyme in polyamine synthesis. In control culture medium, mesodermal cells retained their in ovo outgrowth behavior and differentiation pattern. Addition of 10 mM DFMO to the culture medium, however, retarded attachment and outgrowth, and reduced the rate of proliferation of the mesodermal cells. Furthermore, the expression of differentiated phenotypes, such as beating heart tissue, erythroid cells, and adipocyte-like cells, was delayed. Simultaneous addition of 100 microM putrescine prevented or reduced the effects of DFMO, showing that these were indeed caused by polyamine deficiency. In the DFMO-treated mesoderm, DNA synthesis was markedly suppressed by the first day. Similar effects on RNA and protein synthesis developed at a later time. Our data suggest that a reduction in the concentrations of the polyamines decreases the rate of mesodermal cell proliferation, and as a consequence delays the expression of differentiated phenotypes.

Animals↗
PubMed1987

Localization of ornithine decarboxylase in the chick embryo during organogenesis.

The localization of ornithine decarboxylase (ODC), a key enzyme in polyamine biosynthesis and thus in cell growth, was determined in the 4.5-day-old chick embryo, using two independent methods of analysis. ODC protein was identified by indirect immunofluorescence with a monospecific ODC antibody, and catalytically active ODC was identified by autoradiography with alpha-(5-3H) difluoromethylornithine. Both methods revealed a basically similar distribution of ODC within the embryo. Among the organs, the brain exhibited the highest ODC levels. ODC levels were also high in spinal cord, mesonephric tubules and heart. Similar levels, but confined to limited areas, were found in liver tissue, head mesenchyme, and the oral and pharyngeal regions. Organs that exhibited high ODC levels are all engaged in rapid growth, as well as in extensive tissue remodeling and differentiation.

Animals↗
PubMed1987

Catecholamine metabolism during pacing-induced angina pectoris and the effect of transcutaneous electrical nerve stimulation.

The arterial levels of norepinephrine and epinephrine were estimated in 14 patients with severe coronary artery disease in order to assess the catecholamine metabolism during pacing-induced angina pectoris and to evaluate the effects of transcutaneous electrical nerve stimulation (TENS). Arterial levels of epinephrine and norepinephrine increased significantly during pacing to angina pectoris (p less than 0.05 and p less than 0.001, respectively), indicating that maximal atrial pacing induced an increase in sympathetic tone. At the corresponding pacing rate during TENS, myocardial lactate production was improved (p less than 0.01) and the ST segment depression was less pronounced (p less than 0.05). The maximal pacing rate during TENS was 141 +/- 24 compared to 123 +/- 19 (p less than 0.01) and the heart rate-blood pressure product was also significantly higher (p less than 0.01), suggesting an elevation of the anginal threshold by TENS. Systemic vascular resistance and systolic blood pressure were significantly reduced (both p less than 0.01). These beneficial results may be caused by a decrease in left ventricular afterload as reflected by a fall in systolic blood pressure and may be explained by reduced sympathetic activity. TENS may decrease the sympathetic activity either directly or indirectly as a consequence of pain inhibition. This hypothesis is supported by the fact that arterial levels of epinephrine and norepinephrine dropped during TENS in TENS responders.

Angina Pectoris↗
PubMed1986

Transcriptional inhibition in early chick embryos as a result of polyamine depletion.

In the early chick embryo, inhibition of polyamine synthesis by alpha-difluoromethylornithine (DFMO), an enzyme-activated irreversible inhibitor of ornithine decarboxylase, blocks development at gastrulation. This effect was paralleled by a marked suppression of RNA and protein synthesis. There was no major change in cell cycle distribution in DFMO-treated embryos. Nevertheless, analysis of DNA synthesis and mitotic index indicated a prolongation of the cell cycle, possibly affecting all the phases. The inhibition of RNA synthesis in polyamine-depleted embryos, as evaluated by [3H]uridine incorporation, was not a result of reduced uptake or expansion of the UTP pool, and there was no deficiency or major imbalance among the ATP, GTP, and CTP pools. On the basis of agarose gel electrophoretic analyses of the various RNA species, and experiments using RNA synthesis inhibitors with different modes of action (actinomycin D, alpha-amanitin, and 5,6-dichloro-1-beta-D-ribofuranosylbenzimidazole), it was concluded that the DFMO-induced gastrular arrest was due to general inhibition of transcription.

Amanitins↗
PubMed1986

Felodipine-induced dilatation of epicardial coronary arteries. A randomized, double-blind study.

Dilatation of large coronary arteries is of potential value in the treatment of angina pectoris. In this double-blind study, the acute effect of felodipine or placebo on coronary artery dilatation was studied in patients with severe angina pectoris with the aid of coronary arteriography. There were two parallel groups, one with 9 patients who received felodipine, the other with 12 patients who received placebo. Measurements of vessel diameters were performed at a proximal position of the affected artery, at the site of the stenosis, and distal to the lesion. The mean plasma felodipine concentration was 17+/-6 nmol/l. The systolic blood pressure was reduced from 156+/-15 to 145+/-13 mm Hg after felodipine (p less than 0.05), but was unaffected by placebo. The heart rate and arterial catecholamine levels were basically unchanged in both groups of patients. The proximal arterial segment was dilated 7% after felodipine (p = 0.05), the stenosis area 9% (N.S.) and the distal part of the vessel 7% (p less than 0.05). There were no changes in coronary diameters in the placebo group. In conclusion, felodipine dilates large coronary arteries, and this mode of action may be valuable in the treatment of patients with coronary artery disease, especially in cases where coronary spasm is a prominent feature.

Adult↗
PubMed1985

No adverse effects from high doses of felodipine to patients with coronary heart disease.

Although vasodilators may be of value in treating hypertension and heart failure, excessive vasodilation may worsen poststenotic myocardial perfusion in patients with coronary artery disease. In this study, 11 patients with ischemic heart disease were given 0.010, 0.015, and 0.025 mg/min of felodipine, a potent arteriolar dilator, and hemodynamics and myocardial lactate extraction were measured. Plasma concentrations at the three dose levels (D1, D2, and D3) were 11 +/- 4, 22 +/- 5, and 40 +/- 8 nmol/l, respectively. Mean heart rate rose from 61 +/- 13 to 79 +/- 10 beats/min at D3 (p less than 0.01) and mean arterial pressure was reduced from 113 +/- 25 to 86 +/- 13 mmHg (p less than 0.01). There was a marked increase in cardiac index at all three dose levels (p less than 0.05 to p less than 0.01). The systemic vascular resistance was reduced by 47% at D3 and coronary vascular resistance by 44% (both p less than 0.01). Myocardial oxygen consumption was not changed by felodipine. There were three patients with myocardial lactate production both before and after drug administration, but there were no ST-segment shifts or chest pain in any patient. In conclusion, felodipine seems to be a potent vasodilator and deterioration of myocardial metabolic function occurs infrequently. Our results suggest that felodipine can be safely administered even in high doses to patients with severe coronary artery diseases.

Coronary Circulation↗