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Biomedical subjects

K Landmark

Publications and source records attributed to K Landmark.

At least 19 recordsLinked to original sources
PubMed1992

[Magnesium therapy in acute myocardial infarction].

Several small, double-blind, randomized studies have shown that infusion of magnesium in patients with acute myocardial infarction reduces incidence of arrhythmias and mortality quite considerably. These beneficial effects are found in elderly patients too. Compared with placebo, magnesium infusion seems to increase myocardial salvage and protect against evolution of infarct. The mode of action of magnesium in reducing arrhythmias and mortality in acute myocardial infarction has not been clarified. Several factors may be involved. It has been shown that the antiarrhythmic effect of magnesium is related to a rapid rise in serum concentration. Magnesium possesses calcium-antagonistic properties, and reduces tone in smooth muscle cells. The use of magnesium decreases coronary artery spasm and total peripheral resistance, and increases cardiac output. Beneficial effects on blood platelets have also been reported. Magnesium therapy is cheap and easy to administer; contradictions include reduced renal function, disturbances in atrioventricular conduction and hypotension.

Arrhythmias, Cardiac↗
PubMed1992

Mononuclear cell magnesium and retention of magnesium after intravenous loading in patients with acute myocardial infarction.

A magnesium (Mg++) retention test was performed in 19 patients with acute myocardial infarction (AMI) 4-11 days after admission to the coronary care unit. The retention of Mg++ was 45 +/- 23% of the 30 mmol given intravenously. It has been proposed that a retention of more than 20% represents Mg++ deficiency. The mononuclear cell Mg++ concentration before the retention test was on an average slightly higher in the AMI patients than in 25 healthy volunteers (72.5 +/- 24.2 vs. 62.9 +/- 9.2 mumol g-1 protein) indicating no Mg++ depletion in the first group. The reason why patients during the phase of AMI show an increased retention of Mg++ is unknown, but changes in concentrations of several hormones and a reduction in blood glucose could be of importance. Serum concentrations of Mg++ were lower on admission than after 4-11 days. These initial reductions are probably due to increased concentrations of circulating catecholamines during the early hours of AMI.

Adult↗
PubMed1991

[Treatment of hypertension with the ACE inhibitor lisinopril. A multicenter study of patients with mild to moderate hypertension in general practice].

367 patients with mild-moderate hypertension were included in a multicentre study for the purpose of examining the antihypertensive effect of six weeks of treatment with the ACE-inhibitor lisinopril 10 and 20 mg once daily. Both low-dose and high-dose lisinopril significantly reduced sitting and standing blood pressure values. The fall in blood pressure in the sitting position was slightly but significantly greater among the high-dose group compared with the low-dose group (a 3 mm Hg fall difference in systolic values and a 1 mm Hg fall in diastolic values). No such differences were found in the standing position. Heart rate remained unchanged during lisinopril treatment. Episodes of possible first dose hypotension were reported in six patients. Approximately 90% of the patients in both groups were classified as responders according to defined criteria. The frequency of side-effects was low, and was equal in both treatment groups. An evaluation of reduction in blood pressure, and of response rate and side-effects suggests that an initial dose of 10 mg lisinopril once daily is sufficient, and that this dosage will control blood pressure in the majority of patients.

Adult↗
PubMed1986

Hypertrophic cardiomyopathy.

Hypertrophic cardiomyopathy is characterized by a hypertrophic and non-dilated left ventricle with disproportionate involvement of the intraventricular septum compared to the free walls, and by varying degrees of outflow obstruction during systole. Its symptoms and clinical course, pathogenesis and treatment are briefly discussed. It is speculated whether hypertrophic cardiomyopathy and hypertension are both caused by systemic disorders of calcium channels and calcium uptake and binding by cardiac and smooth muscle membranes, respectively.

Animals↗
PubMed1979

Disopyramide plasma levels in cardiac patients on maintenance therapy.

The antiarrhythmic agent disopyramide, in a dosage of 200 mg/8 h, was given to 7 cardiac patients. The drug was fairly rapidly absorbed, and the mean peak plasma concentration (3.5 microgram/ml) was measured 1 h after administration of the first dose. The mean biological half-life (7.8 h) was slightly prolonged compared to that reported in normal volunteer subjects. Mean steady state plasma concentrations within the therapeutic range were attained 24--32 h after the start of medication. The fluctuations in the plasma levels were in the order or 30 percent; however, a wide spread of the values was observed. The drug was well tolerated.

Adult↗
PubMed1979

Calcium, nifedipine and arrhythmias in isolated rat atria.

Arrhythmias were induced in isolated rat atrial muscle preparations by increasing the calcium concentration of the Ringer solution, while the potassium concentration was kept low. A rise in the resting tension occurred simultaneously. The release of aspartate aminotransferase (ASAT) from the fibrillating atria was not higher than the release from non-fibrillating atria pretreated with a calcium-antagonistic drug, nifedipine 100 microgram/l. It is suggested that calcium-induced rat atrial arrhythmias in the present experiments are caused by a direct effect on calcium influx through the excitable membrane and not as a result of myocardial lesion caused by calcium overload.

Animals↗
PubMed1979

The effect of nifedipine on the monophasic action potential and refractoriness of the right ventricle of the dog heart in situ after beta-adrenergic receptor blockade.

The effect of nifedipine, a calcium-antagonistic drug, was studied on the electrophysiology of the right ventricle in the dog heart in situ. Monophasic action potential recordings were obtained by the suction electrode technique and refractoriness was measured by means of programmed electrical stimulation. Pentobarbital anaesthesia was used. As the basic cardiac effects of nifedipine can be altered by the release of catecholamines from sympathetic nerves of the heart and vessels, the dogs were pretreated with the beta-adrenergic receptor blocking agent acebutolol which increased the action potential duration and the refractoriness. Intravenous injection of nifedipine 30 microgram/kg body weight decreased the times for 50 and 90 per cent repolarization of the monophasic action potential and to a smaller extent the effective and functional refractory period. It is suggested that nifedipine decreases the action potential duration and the refractoriness of the right ventricle of the dog heart in situ due to a direct effect of the drug on the myocardium.

Acebutolol↗
PubMed1979

Ectopic atrial tachycardia on swallowing. Report on favourable effect of verapamil.

A female patient who suffered from atrial tachycardia associated with the ingestion of food or drink was examined in our department. No signs of organic heart disease were discovered, oesophageal motility was normal, but X-ray revealed a small hiatal hernia. The arrhythmia started with an atrial extrasystole arising well outside the functional refractory period of the AV node, and it could be reproduced by inflation of a balloon. It is suggested that the arrhythmia is induced by a mechanical effect of the passage of food on the left atrial wall. Several drugs were tried in order to stop or relieve the complaints. None of them prevented or stopped the atrial tachycardia but verapamil and edrophonium chloride caused 2:1 AV block, and follow-up study has shown that sufficient doses of verapamil are able to relieve the patient's complaints.

Atrioventricular Node↗
PubMed1978

Acebutolol-induced changes in refractoriness and monophastic action potential of the right ventricle of the dog heart in situ.

The effect of acebutolol, a beta-adrenergic receptor blocking agent, on the electrophysiology of the right ventricle was studied in the dog heart in situ. Pentobarbital anaesthesia which is known to increase the sympathetic tone was used. Monophasic action potential recordings were obtained by the suction electode technique and refractoriness was measured by means of programmed electrical stimulation. A stepwise increase in the frequency of stimulation from 170 to 200, 230, and 260 per min caused a progressive decrease in the refractoriness as well as the duration of the monophasic action potential. Intravenous injection of acebutolol 2.0 mg.kg-1 increased the times for 50 and 90% repolarisation of the monophasic action potential. This increase is probably due to beta-adrenergic receptor blockade in the presence of alpha-adrenergic receptor stimulation. The effective and functional refractory periods, however, were increased to an even greater extent than the monophasic action potential duration. It is suggested that this is the result of a blockade of a catecholamine-induced increase in the velocity of the depolarisation.

Acebutolol↗
PubMed1978

Verapamil and pulmonary hypertension.

We report on the effect of verapamil in 12 patients suffering from pulmonary hypertension. The drug caused a slight, but statistically significant decrease in mean pulmonary artery pressure and in the work performance by the right ventricle. The mean pressure of the right atrium, the end-diastolic pressure of the right ventricle, the pulmonary arteriolar resistance, the cardiac index and the stroke volume were not significantly changed, however, and there was a wide spread of the values observed. In some patients the drug exerted a marked negative inotropic effect, with a concomitant increase in the pulmonary arteriolar resistance.

Adult↗
PubMed1978

Serum levels and electrophysiological effects of N-acetlyprocainamide as compared with procainamide in the dog heart in situ.

The electrophysiological effects of procainamide and its major metabolite N-acetylprocainamide were tested and compared on the heart of the anaesthetized dog by means of His bundle electrography and programmed electrical stimulation. Both drugs exerted a negative chromotropic effect. They also increased intra-atrial and intraventricular conduction times; procainamide was, however, the more potent of the two drugs. In contrast to procainamide, N-caetylprocainamide did not increase His-Purkinje and atrioventricular nodal conduction times, and at the lowest dose employed, atrioventricular nodal conduction times were decreased during atrial pacing. Both drugs increased the functional and effective refractory period of the right atrium and ventricle. N-acetylprocainamide increased the functional refractory period of the atrioventricular node, but to a lesser extent than procainamide.

Animals↗
PubMed1978

The effect of nifedipine on the sinus and atrioventricular node of the dog heart after beta-adrenergic receptor blockade.

The effect of nifedipine (BAY 1040), a calcium-antagonistic inhibitor of the electromechanical coupling process was tested on atrioventricular conduction and refractoriness of the dog heart in situ by means of His-bundle electrography and programmed electrical stimulation. The animals were anaesthetized with sodium pentobarbital. As the basic effects of the compound can be altered by release of catecholamines from sympathetic nerves of heart and vessels, the dogs were pretreated with acebutolol, a beta-adrenergic receptor blocking agent, which decreased heart rate and prolonged atrioventricular conduction and refractoriness. Nifedipine 1,6 and particularly 30 microgram/kg body weight increased the heart rate and decreased atrioventricular conduction time during atrial pacing, whereas atrioventricular conduction time during sinus rhythm and atrioventricular refractoriness were only affected by nifedipine 30 microgram/kg. In this respect, nifedipine differs distinctly from another calcium antagonistic compound, verapamil.

Acebutolol↗